Human Pentagons S-1 notes

“These notes consist of a summarization of Bailey 26Ed (few additions from

27Ed) of Unit 1,2,3,4,5,6,7,8,9,10.

Human Pentagon consists of 5 friends of batch D’21, please remember us in

your prayers. Jazaka-Allahu-Khair

Regards: Rutaba Mairaj, Rahima Azam, Fizza Rashid, Aiman Niaz, Mym Raza”

Dated: 30/Aug/2020.

Contents
Unit-1 ...................................................................................................................................................... 3
Chap 1: Metabolic response to injury ................................................................................................. 3
Chap 2: Shock and blood transfusion ................................................................................................. 3
Chap 3: Wounds, tissue repair and scars ............................................................................................ 7
Chap 4: Basic surgical skills and anastomoses .................................................................................. 10
Chap 5: Surgical infection ................................................................................................................. 21
Chap 6: Surgery in the tropics ........................................................................................................... 21
Chap 7: Principles of laparoscopic and robotic surgery .................................................................... 25
Chap 8: Principles of paediatric surgery ........................................................................................... 28
Chap 9: Principles of oncology .......................................................................................................... 28
Chap 10: Surgical audit and clinical research.................................................................................... 31
Chap 11: Surgical ethics and law....................................................................................................... 33
Chap 12: Patient safety ..................................................................................................................... 33
Unit 2..................................................................................................................................................... 36
Chap 13: Diagnostic imaging ............................................................................................................. 36
Chap 14: Gastrointestinal endoscopy ............................................................................................... 36
Chap 15: Tissue diagnosis ................................................................................................................. 36
Unit-3 .................................................................................................................................................... 36
Chap 16: Pre-operative preparation .................................................................................................. 36
Chap 17: Anesthesia & pain relief ..................................................................................................... 36
Chap 18: Care in the operating room ................................................................................................ 51
Chap 19: Peri operative management of the high-risk surgical patient ............................................ 54
Chap 20: Nutrition & Fluid therapy ................................................................................................... 58

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 Chap21: Post-operative care ............................................................................................................. 58
Chap 22: Day- Case surgery ............................................................................................................... 70
Unit 4 ..................................................................................................................................................... 73
Chap23: INTRODUCTION TO TRAUMA ............................................................................................. 73
Chap24: EARLY ASSESSMENT AND MANAGEMENT OF TRAUMA ...................................................... 78
Chap 25: Emergency Neurosurgery ................................................................................................... 84
Chap 26: Neck and Spine ................................................................................................................... 84
Chap 27: Maxillofacial trauma ........................................................................................................... 93
Chap 28: Torso Trauma ..................................................................................................................... 97
Chap 29: Extremity Trauma ............................................................................................................. 102
Chap 30,31 → add in IM, very similar............................................................................................. 111
Chap 32: Disaster surgery ............................................................................................................... 111
Unit 5................................................................................................................................................... 126
Chap 34: Sports medicine and sports injuries................................................................................. 126
Chap 35: The spine .......................................................................................................................... 130
Chap 36: Upper Limb- pathology, assessment, and management ................................................. 135
Chap 37: Hip and knee .................................................................................................................... 135
Chap 38: Foot and ankle ................................................................................................................. 139
Chap 39. Musculoskeletal tumors................................................................................................... 142
Chap 40. Infection of the bones and joints ..................................................................................... 143
Chap 41. Pediatric orthopedics ....................................................................................................... 143
Unit 6................................................................................................................................................... 153
Chap 42: 42. Skin and subcutaneous tissue .................................................................................... 153
Unit 7................................................................................................................................................... 158
Chap 43: Elective neurosurgery ...................................................................................................... 158
Chap 44: The eye and the orbit (not to be done) ........................................................................... 161
Chap 45: Cleft lip & palate: developmental abnormalities of the face, mouth and jaws............... 161
Chap 46: The nose and sinuses (not to be done) ............................................................................ 161
Chap 47: The ear (not to be done) .................................................................................................. 161
Chap 48: Pharynx, larynx, and neck (not to be done) ..................................................................... 161
Chap 49: Oropharyngeal cancer ..................................................................................................... 161
Chap 50: Disorders of salivary gland ............................................................................................... 166
Unit 8................................................................................................................................................... 166
Chap 51: thyroid and parathyroid glands ....................................................................................... 166
Chap 52: the adrenals and other abdominal endocrine disorders ................................................. 166
Chap 53: breast ............................................................................................................................... 166

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Unit 9................................................................................................................................................... 166
Chap 54. Cardiac surgery ................................................................................................................ 167
Chap 55. The thorax ........................................................................................................................ 167
Unit 10................................................................................................................................................. 167
Chap 56: arterial disorders.............................................................................................................. 167
Chap 57: venous disorders .............................................................................................................. 173
Chap 58: lymphatic disorders ......................................................................................................... 178

Unit-1
Chap 1: Metabolic response to injury
-in IM

Chap 2: Shock and blood transfusion

Ischemia-reperfusion syndrome:

During systemic hypoperfusion, cellular and organ damage progresses. Once normal circulation is
restored, the elements activated by hypoxia ( complements,neutrophils,microvascular thrombi) are
flushed back into the circulation where they cause further endothelial innury to organs such as lungs
and kidneys.

SEVERITY OF SHOCK

✒ Compensated shock: The body's cardiovascular and endocrine responses reduce flow to non-
essential organs ( skin, muscle, git), and direct flow to kidneys lung and brain. Only signs:
tachycardia, cool peripheries. There is adequate compensation to maintain central blood volume.
But if hypo-perfusion for more than 12 hrs, that may lead to increased incidence of multiple organ
failure and death due to ischemia-reperfusion syndrome

✒ Decompensation: loss of around 15 percent of circulating blood volume is within normal

compensatory mechanism. After 30-40 percent of volume has been lost, BP falls.

✒ Mild shock: tachycardia, tachypnea, mild reduction of urine output. BP normal, decreased pulse
pressure. Cool & sweaty with prolonged capillary refill times (except in septic distributive shock)

✒ Moderate shock: as shock progresses, renal compensatory mechanisms fail. So all of the above
plus significant decrease in urine output (below 0.5 mL/kg/hour) Mild hypotension. State of
confusion & drowsiness

✒ Severe shock: profound tachycardia & hypotension. Anuria. Unconcious with laboured
respiration

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✒ Capillary refill: not an accurate marker of shock. In hypovolemic shock, cool, pale peripheries &
generally prolonged. In septic shock, warm peripheries & it is brisk.

✒ Tachycardia: May not always accompany shock. Patients on beta blockers or those with
implanted pacemakers don't have tachycardia.

✒ BP: Hypotension is one of the last signs of shock. Children & fit young adults can be in profound
shock with normal blood pressure. Elderly pts normally hypertensive present with normal bp

✒ Pitfalls: the classic cvs signs may not be seen in everyone. So it's important to recognize shock in
absence of some of these.

CONSEQUENCES

✒ Unresuscitable shock:

When severe shock continues for prolonged treatment, without tx or inadequate tx, the patient
becomes unresuscitable. Compensatory mechanisms are lost. Myocardial and respiratory
depression, death ensues.

✒ Multiple organ failure: as a result of prolonged ischemia.

Lung- ARDS

Kidney

Acute liver insufficiency

Coagulopathy (dic)

Cardiovascular failure

There is no specific tx, only supportive like ventilation, dialysis etc. until there is recovery of organ
function.

RESUSCITATION

Conduct of resuscitation:

First ensure airway and breathing. Resuscitation should not be delayed, however the type of
resuscitation will depend on the type of and severity of shock. Hence quick clinical assessment
should be done. If there is initial doubt about the cause of shock, then assume it to be hypovolemic
and begin resuscitation then assess response.

In patients who are actively bleeding, it is useless to begin fluid therapy while hemorrhage
continues. So surgically manage the bleeding along with fluid therapy.

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Conversely a patient with bowel obstruction & hypovolemic shock must be adequately resuscitated
before surgery, otherwise surgical injury & hypovolemia induced will increase inflammatory
activation

Monitoring in shock:

✒ Cardiovascular: ECG, BP, O2 saturation, pulse waveform

✒ Central venous pressure: There is no normal CVP, hence we don't have a value to compare. We
just assess by looking at changes in response to fluid. After infusion of a fluid bolus, the normal
response will be a rise of 2-5 cmH2O, which gradually drifts back to the original level in 10-20 min.
Patients with no change are empty and require further fluid resuscitation.

✒ Cardiac output: Cardiac output monitoring allows assessment of not only output but also
systemic vascular resistance and preload. These can help differentiate between types of shock
(hypovolemic, distributive, cardiogenic). Measurement of cardiac output desirable in pts who do not
respond to first line therapy, or have cardiogenic shock/myocardial dysfunction

One technique for this is Doppler US

✒ Organ perfusion: the best measure of organ perfusion is urine output. The level of consciousness
is an important market of cerebral perfusion, but brain perfusion maintained until very last stages of
shock, so a poor marker of adequate resuscitation. Clinical indicator of perfusion of git and muscle
are lactic acidosis (lactate & base deficits) and mixed venous oxygen saturation.

✒ Base deficit and lactate: these two measures degree of lactic acidosis. Assessed through ABGs.
The degree of lactic acidosis is sensitive for diagnosis of shock and monitoring response to therapy.

✒ Mixed venous oxygen Saturation:

It is a measure of oxygen delivery and extraction from tissues.

Checked by placing line in right atrium and blood drawn.

In sepsis mixed venous saturation is more than 70 % because there is disordered utilization of
oxygen at the cellular level & arteriovenous shunting of blood at microvascular level Thus venous
blood has a higher oxygen concentration than normal.

Patients who are septic should therefore have mixed venous oxygen saturation above 70%. Below
this: septic, hypovolemic & cardiogenic shock

✒ Occult hypoperfusion: state of normal vitals yet continued hypoperfusion. Indicated only by
persistent lactic acidosis and low mvos. This state for more than 12 hrs has increased risk of
mortality.

HEMORRHAGE:

Surgical and non-surgical hemorrhage:

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Surgical hemorrhage is due to direct injury that can be corrected surgically or other techniques such
as angioembolization. Nonsurgical hemorrhage is the loss of blood from wounds or raw surfaces due
to coagulopathy and cannot be stopped by surgery (only packing done). Tx requires correction of
coagulopathy.

Degree & classification

Adults: 5L of blood

Hb level is a poor indicator of degree of hemorrhage, as it represents concentration & not absolute
amount. In early stages of rapid bleeding: Hb concentration is unchanged as whole blood is lost.
Later, fluid shifts from intracellular & interstitial spaces into vascular compartment, then Hb &
hematocrit levels fall

Classification of hemorrhagic shock:

Class 1) <15%

Class 2) 15-30%

Class 3) 30-40%

Class 4) >40%

But there is still variation among people so tx based on degree of shock according to vital signs,
preload assessment, base deficit & response to fluid therapy

MNM

✒ Identify hemorrhage: any shock should be assumed to be due to hypovolemia, and hypovolemia
should be assumed to be because of hemorrhage.

✒ Immediate resuscitative maneuvers: direct pressure over sites of external hemorrhage. Airway,
breathing, blood cross matching, transfusion. Emergency blood requested if required

✒ Identify the site: this is not to identify exact location definitively, but to define next step in
hemorrhage control (operation, angioembolization, endoscopic control). Clues in hx: previous
episodes, known aneurysm, non-steroidal for GI blood loss). Clues in examination: nature of blood-
fresh, melena; abdominal tenderness. Internal hemorrhage seen by chest & pelvic Xray, abdominal
U/S, diagnostic peritoneal aspiration)

✒ Control: arrest hemorrhage through surgical control, angiography, endoscopy suite, control
sepsis.

TRANSFUSION

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✒ Autologous blood: it is possible for someone undergoing surgery to predonate their own blood
up to 3 weeks beforehand for transfusion during surgery. Similarly, during surgery blood can be
collected in a cell-saver which washes & collects RBCs which can be returned to the patient.

✒ Complications from a single transfusion:

(In addition to those in IM)

-- air embolism, Thrombophlebitis

✒ Complications from multiple transfusions:

(In addition to IM)

-- iron overload

✒ Management of coagulopathy

- Correction of coagulopathy not necessary if no active bleeding & not anticipated

- coagulopathy following or during massive transfusion anticipated & managed aggressively

- When red cells are transfused for active hemorrhage, match each red cell unit with 1 unit of FFP &
1 of platelets (1:1:1)

-FFP if PT or PTT more than 1.5 time normal

-Cryoprecipitate if fibrinogen <0.8 g/L

-Platelets if platelet count <50× 109/mL

Pharmacological adjuncts to blood component therapy include Tranexamic acid and aprotinin.

Blood Substitutes

- Biomimetic or abiotic
- Biomimetic: mimic standard oxygen carrying capacity of blood & are Hb based
- Abiotic: synthetic oxygen carriers

Chap 3: Wounds, tissue repair and scars

TIDY VS UNTIDY WOUNDS

Tidy: incised, clean, healthy tissues, seldom tissue loss

Untidy: crushed or avulsed, contaminated, devitalized tissues, often tissue loss

Managing the acute wound:

- Examine the whole patient according to ATLS guidelines. Wound is examined, site and
possible damage. Assess movement and sensation. Tetanus cover should be noted.

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 - A bleeding wound should be elevated, and pressure applied. Clamps should not be put on
vessels blindly because nerve damage is likely & vascular anastomosis is rendered
impossible. Analgesia/anesthesia should be given in order to facilitate examination.
- After assessment a thorough debridement is essential. Copious saline irrigation or pulsed jet
lavage less destructive than knife or scissors when debridement done, care should be taken
not to implant dirt deeper. Abrasions, road rash, and explosions all require scrubbing brush
or even excision. The wound should be debrided to the limit of blood staining.
- In a tidy wound, repair of all damaged structures maybe attempted. Repair of nerves under
magnification (loupes or microscope) is by using 8/0 or 10/0 monofilament nylon. Muscle
viability is judged by colour, bleeding pattern & contractibility. Tendon repairs: early active
mobilisation minimises adhesions between tendon & tendon sheath
- Skin cover by flap or graft maybe required.
See summary box 3.3

SPECIFIC WOUNDS:

✒ Bites: most are puncture wounds or avulsions. Common sites in victims of human bites are ear,
tip of nose, lower lip. Boxing type injury of metacarpophalangeal joint from perforating contact with
teeth of victim Antibiotic prophylaxis maybe required in bites, bite wounds have high virulent
bacterial counts.

✒ Puncture wounds: such wounds should be explored to the limit of blood staining. X Ray maybe
done to check if retained foreign body in depth of wound.

✒ Haematoma: if large, painful or causing neural deficit, this may require release by incision or
aspiration. In gluteal/ thigh region: associated disruption of fat in the form of fat fracture. Untreated
hematoma may calcify so surgical exploration if symptomatic

✒ Degloving: when skin & subcutaneous fat are stripped by avulsion from underlying fascia, leaving
neurovascular structures, tendon or bone exposed. Examination under anesthetic is required.
Radical excision of all nonbleeding skin. Fluorescein given IV under anaesthesia. Under UV light
viable skin will show up as fluorescent yellowish green color, & nonviable skin for excision is mapped
out. Complication: anaphylactic shock due to fluorescein sensitivity. Therefore, excision done until
punctate bleeding seen

✒ High pressure injection injuries: the use of high-pressure devices in cleaning, degreasing and
painting can cause extensive closed injuries through small entry wounds. The liquid injected spreads
along fascial planes. Common sites: finger to forearm. Tx is surgical with wide exposure, removal of
the toxic substance and through debridement. Amputation after high pressure injection injuries-45%

LEG ULCERS

In developed countries, the most common chronic wound is leg ulcers. Causes are:

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 - Venous disease causing local venous HTN e.g. varicose veins
- Arterial disease: atherosclerosis or diabetes
- Arteritis associated with autoimmune diseases such as RA, Lupus
- Trauma
- Chronic infections- Tb/syphilis
- Neoplastic-squamous or BCC, sarcoma
Ulcer: break in epithelial continuity. Prolonged inflammatory phase: overgrowth of granulation
tissue. Necrotic tissue at centre of ulcer is called slough

A chronic ulcer unresponsive to dressings and simple treatment should be biopsied to rule out
neoplastic change. (mc: SCC known as Marjolin’s ulcer)

Tx the underlying cause. Surgical tx if non-op tx fails or intractable pain. Meshed skin grafts allow
mobilisation & escape of tissue exudate

Recurrence rate is high with venous ulceration. Regime of hygiene, elevation and elastic
compression is essential.

NECROTISING SOFT TISSUE INFECTIONS:

- Rae but fatal. Polymicrobial. Hx of trauma or surgery with wound contamination

- Sudden presentation & rapid progression. Deeper tissues involved so leads to late/missed
diagnosis
- 2 main types: clostridial (gas gangrene) & non-clostridial (streptococcal gangrene & necrotising
fasciitis
- Variant of necrotising fasciitis with toxic shock syndrome caused by streptococcus pyogenes & is
called flesh-eating bug.
- Signs and symptoms: unusual pain, edema beyond area of erythema, crepitus, skin blistering,
fever (often absent), grayish drainage (dishwater pus), pink/orange skin staining, focal skin
gangrene (late sign), shock, coagulopathy, multiorgan failure
- Tx: antibiotics with wide surgical excision

SCARS:

The immature scar is pink, hard, raised and often itchy. As collagen matures & becomes denser, scar
becomes acellular as fibroblasts & blood vessels reduce. It matures in a period lasting over a year.
Mature scar is paler, softer, flatter and itchiness diminishes. Tensile strength does not exceed 60-
80% of normal skin

✒ Atrophic scar: pale, flat, stretched. It is easily traumatized as epidermis and dermis are thinned.
Mostly on back & in areas of tension

✒ Hypertrophic scar: excessive scar tissue that does not extend beyond the boundary of the
original incision or wound. It results from prolonged inflammatory phase of wound healing & from
unfavourable scar sitting (i.e. across the lines of skin tension)

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✒ Keloid scar: excessive scar tissue that extends beyond the boundaries of the original incision or
wound. Associated with elevated growth hormone, deeply pigmented skin, inherited tendency &
certain areas of body e.g. triangle whose points are xiphisternum & each shoulder tip

Both Hypertrophic and Keloid scars have excess collagen with hypervascularity. Hypertrophic scar
improves with time, whereas Keloid scars do not.

Treatment of Hypertrophic and Keloid scars:

Pressure (local moulds or elasticated garments), silicone gel sheeting, steroid injection
(triamcinolone), excision and steroid, excision and radiation, intralesional excision (Keloid only), laser
to reduce redness, vit E or palm oil massage

AVOIDABLE SCARRING

- A dirt ingrained scar (tattooed) scar prevented by proper initial scrubbing & cleansing of wound.
Late tx: excision or pigment destruction by laser
- Mismatched or misaligned scars due to failure to recognise normal landmarks. Tx: excision &
resuturing
- Poorly controlled scars caused by poor alignment of deep structures such as muscle or fat, but
trapdoor or pin cushioned scars unavoidable unless circumferential wound excised initially. Tx:
scar excision & correct alignment. Trapdoor scar: excision of margins, repair using W or Z-plasty
- Monofilament sutures removed early (3-5 days) minimise scarring
- Fine sutures (6/0 or smaller) placed closed to wound margins leave less scarring

CONTRACTURES:

Where scars cross joints or flexion creases, a tight web may form restricting the range of movement
at the joint. This may be referred to as a contracture and can cause hyperextension or hyperflexion
deformity. In the neck, interferes with head extension. Tx maybe simple like multiple z-plasties, or
complex like grafts or flaps. Splintage & intensive physiotherapy required post op.

Chap 4: Basic surgical skills and anastomoses

BASIC SURGICAL SKILLS AND ANASTOMOSES
PATIENT POSITIONING & SAFETY ON THE OPERATING TABLE

• Patient placed on table to maximise exposure for procedure.

• Categorised as:
1) Transfer to & from operating table
• Transfer of anaesthetised patient is critical as significant risks
• Additional risk: obese, elderly & emaciated
2) Positioning on the table
• Placement of passive diathermy electrode (pad) to minimise risk of electrosurgical
burns & accounting for metallic prostheses & pacemaker

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 • Ancillary equipment (energy generators, suction, laparoscopic stack systems)
appropriately located
• Operating lights in optimal starting position
3) Pressure areas
• At risk from pressure sores: diabetes, immunodeficiency, obesity, malnutrition
• Prone to injury: heels, sacrum, other bony prominences
• These areas should receive particular attention
4) Nerve injury
• Certain areas of the body where an anaesthetised patient can be exposed to
neurapraxia, sometimes can be permanent & disabling
• Areas: brachial plexus, ulnar nerve, common peroneal nerve
• Ensure these areas are protected
5) Compartment syndrome
• Acute postoperative compartment syndrome, as a result of under perfusion, usually
during prolonged surgery, often with elevation of leg
• Pain, reduced power, swelling, numbness & tingling
• Tx: prompt surgical fasciotomy
Considerations for laparoscopic surgery

• Steep angles of tilt to the side, or Trendelenburg & reverse Trendelenburg positions required to
move abdominal viscera. Danger that patient can slide or fall off. Ensure patient safety
• Side boards or arm restraints avoided as can interfere with laparoscopic instruments
• Restraints placed to avoid risk of nerve injury
• Suction bean bags & anti slip mats help secure patient

SKIN INCISIONS

• Made with scalpel with the blade being pressed down firmly at right angles to the skin & then
drawn gently across the skin in desired direction to create clean incision
• Do not incise skin obliquely as such a shearing mechanism leads to necrosis of undercut edge
• Incision facilitated by tension applied across line of incision by fingers of non-dominant hand
• Blades for skin incision usually have curved margin, while those used for arteriotomy or drain
site have a sharp tip.
• Scalpels at all times passed in a kidney dish rather than direct hand-to-hand process
• Diathermy, laser and harmonic scalpels can be used instead of blades when opening deeper
tissues, as they reduce blood loss & save operating time, reduce post-operative pain
• Four factors should be considered regarding skin incision:
1) Skin tension lines (Langer’s lines): These represent orientation of dermal collagen fibres and any
incision placed parallel to these lines results in a better scar.

2) Anatomical structures: incision should avoid skin creases and bony prominences if possible and
take underlying structures into consideration.

3) Cosmetic factors: ultimate cosmetic result should be bore in mind.

4) Adequate access for the procedure: incision functionally active for procedure

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Sometimes, circular incision necessary in areas where direction of Langer’s line is not apparent. Once
circular incision is made, it converts into elliptical, indicating lines of tension. Then circular incision is
converted to elliptical. ‘An elliptical incision must be at least 3 times as long as it is wide’ for wound
to heal without tension. Sometimes dog ears remain in corner of elliptical incisions, so it is picked up
with skin hook & excised as shown.

ABDOMINAL INCISIONS

In abdomen, transverse incisions are preferred as they minimize post-op complications (fewer
respiratory complications & better cosmetic outcome). Incision should be deep as subcutaneous
tissue and muscles have to be crossed & peritoneum displayed. Mass closure of abdominal wall:
large bites & short steps in closure. For closure, non-absorbable or very slowly absorbable sutures
should be used. Length of the suture material should be 4 times the length of wound, to prevent
abdominal dehiscence or incisional hernia

LAPAROSCOPIC SURGERY

• Benefits: less post-operative pain, better cosmesis, earlier return of normal physiological
function, shorter hospital stay, earlier resumption of normal activities
• Basic principles of trocar site placement in laparoscopic surgery:
1) Umbilicus preferred for primary trocar insertion because skin here is fused to peritoneum
2) An open or semi-open technique preferred by most surgeons (minimises possibility of injury
to underlying viscus)
3) Scars avoided as bowel is more adherent to undersurface; open insertion away from
umbilicus is safer if midline scar. Scar at umbilicus: relative contraindication (causes post-
operative peritonitis)
4) Secondary trocars should be inserted & removed under direct vision to observe port site
bleeding. 2 handed technique used to avoid sudden trocar movements, as can puncture
viscus
5) All trocars placed perpendicular to abdominal wall. Oblique insertion-increased pressure

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 6) A hand’s breadth (patient’s hand) either side of midline is rectus sheath which contains
epigastric vessels. Place non-midline trocars lateral to rectus sheath, in midclavicular line, to
avoid epigastric vessels
7) Where possible, smaller diameter trocars should be used. All trocar sites greater than 5 mm
undergo suture closure of fascial layers to reduce hernia
8) Bladed trocars avoided near blood vessels
Technique for laparoscopic primary trocar insertion

1) Umbilical cicatrix everted with tissue grasping forceps

2) Umbilical stalk palpated inferior to everted cicatrix, while maintaining cephalad traction
3) A curved transverse incision made inferior to cicatrix
4) Umbilical stalk exposed with dissection to reveal decussation of fibres above junction with
linea alba
5) Vertical incision through decussation, taking care not to incise fascia & not enter peritoneum
6) Blunt haemostat pushed through pre-peritoneal fat & peritoneum. Surgeon feels a pop as
instrument enters peritoneal cavity
7) Trocar pushed through same point of insertion as haemostat in same direction
8) Laparoscopic camera confirms successful placement in peritoneal cavity before insufflation
with CO2 gas
9) Co2 gas started at low flow (1-4 L/minute), max pressure: 15mm Hg, max flow rate:
20L/minute
10) Patients with scars from previous abdominal surgery, safest technique: full open approach
at Palmer’s point, 3cm below left subcostal margin in mid clavicular line
11) Obese patients with scars: optical blunt trocar used to enter peritoneal cavity under vision

WOUND CLOSURE

Types of wound healing:

1. Clean uninfected wound heals by primary intention, requires apposition of the edges.
2. When wound is left open it heals by secondary intention, by granulation tissue formation
(weeks or months)
3. Tertiary intention or delayed primary intention is used when there's a high probability of
wound getting infected. Wound is left open for few days, if infection has resolved, wound
closed to heal by primary intention or skin grafting done

SUTURE MATERIALS

• Desired characteristics: easy to handle, predictable tensile strength, sterile, glides through
tissues easily, secure knotting ability, inexpensive, minimal tissue reaction, non-capillary,
non-allergenic, non-carcinogenic, non-electrolytic, non-shrinkage
5 qualities:

1.Physical structure: suture material maybe monofilament or multifilament. Monofilament suture

material is smooth but difficult to knot easily. Such material easily damaged by needle holder or
forceps. While multifilament or braided sutures are easily knotted but they're not smooth. So they

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can be coated with silicone to make them smooth. Also have greater surface area so bacteria can
lodge and cause infections

2. Strength: depends open the constituent material, its thickness & how it is handled. For e.g.
absorbable sutures are weaker than non-absorbable. Catgut lasts a week while PDS may last for
several weeks. Non-absorbable sutures also degrade with time. Non-absorbable of biological
material such as silk never used in vascular anastomoses for fear of late fistula formation

3. Tensile behavior: some are elastic, material will return to its origin length once any tension is
released. Others are plastic, where this doesn't happen. Some demonstrate memory so that they
keep curling up in the shape they adopted in the packaging. A sharp gentle pull on suture material
diminishes this memory. The more memory a suture has, the lower is the knot security. Sutures
loose 50% of strength at the knot

4. Absorbability: sutures for use in biliary tract and urinary tract need to be absorbable in order to
minimize risk of stones. But a vascular anastomosis requires a non-absorbable suture, these are used
where persistent strength is required (monofilament e.g. polypropylene) Also in vascular
anastomosis braided material is avoided because platelet adherence causes distal embolisation

5. Biological behavior: biological sutures such as catgut are proteolyzed, can cause local irritation so
seldom used. Synthetic polymers are hydrolysed & their disappearance is more predictable

BARBED SUTURES: have helped reduce the need for knot tying such as in laparoscopic surgery. These
have uni/bi-directional barbs that secure the suture in the tissues

SUTURE TECHNIQUES

1. Interrupted sutures: needle inserted at right angles to incision & then passed through both
aspects of suture line & exit again at right angles (figure 1). To avoid enlarging needle hole, needle is
rotated through tissues rather than dragged. Distance from entry point of needle to edge of wound
same as depth of tissue being sutured & each successive sutured placed at twice this distance.
(figure 2)

Figure 1 Figure 2

2. Continuous suture: first suture like an interrupted suture but rest of sutures inserted in
continuous manner. At the end of the wound, it is secured by tying Aberdeen knot or by tying

14
the free end to the loop of last suture to be inserted

3. Mattress sutures: may be vertical/horizontal & produce eversion/inversion of wound edge. Initial
suture as for interrupted suture, then needle moves horizontally or vertically & traverses both edges
of wound again. Very useful in producing accurate approximation of wound edges

4. Subcuticular suture: this is used in the skin where cosmetic appearance is important & where skin
edges are approximated easily. Small bites of subcuticular tissue, taken on alternate sites of wound,
then gently pulled together, thus approximating wound edges without risk of cross-hatched
markings of interrupted sutures

NEEDLES

Current needles are eyeless or atraumatic, with suture material embedded in shank of needle.
Needle has 3 parts: shank, body, point. Needle is grasped by needle holder 1/3rd to ½ of the way
back from the rear of the needle, avoiding shank & point. The closer the needle holder is to the tip of
the needle, greater the accuracy of suture placement, & less the degree of rotation of hand
required.

Body of needle: round, triangular, flattened

Point of needle: round with tapered end, conventional cutting which has cutting edge facing inside
of needle’s curvature or reverse cutting where cutting edge is outside

Cutting needles: when tough or dense tissue is sutured (skin & fascia)

Blunt-ended needles: closure of abdominal wall to decrease risk of needle stick injuries

Half-circle needles: GIT, J-shaped: vagina, quarter-circle: eye, compound curvature: oral cavity

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KNOTTING TECHNIQUES

General principles:

-The knot must be tied firmly, but without strangulating the tissues

- Knot must be unable to slip or unravel

- Must be as small as possible, to minimise amount of foreign material

- tightened without exerting pressure on tissues being ligated i.e. the knot should be bedded down
carefully only exerting pressure against counter-pressure from index finger or thumb

-During tying, the suture must not be 'sawed’ as this weakens the thread.

-When tying an instrument knot, it should only be grasped at the free end, as gripping thread with
artery forceps or needle forceps can damage material & break it

-The standard surgical knot is the reef knot. Multiple rows are required for security.

- Granny knot: involves 2 throws of the same type of throw & is a slip knot. Used to achieve right
tension, followed by standard reef knot for security

- For added security: surgeon’s knot using a 2-throw technique

- In continuous suture. Aberdeen knot used for final knot

-When the suture is cut after knotting, the ends should be left about 1-2 mm long to prevent
unraveling.

ALTERNATIVES TO SUTURES

1.Skin-adhesive strips

Can be used where there is no tension and not too much moisture, for the skin e.g. wide excision of
breast lump

2. Tissue glue

To use this, wound needs to be cleaned, dry, with near perfect hemostasis and under no tension.
When it is applied it polymerises to form a firm adhesive bond.

16
Other glues: involve fibrin & work on the principles of converting fibrinogen to fibrin by thrombin
with crosslinking by factor XIII, and addition of aprotinin to slow breaking of fibrin network by
plasmin. Used for hemostasis in liver, spleen, dural tears, In ENT and ophthalmic surgery

3. Laparoscopic wound closure: done with sutures or glue

4. Clips

Skin clips produce a very neat scar with good wound eversion. They can be placed faster than
sutures but are more expensive and maybe uncomfortable for the patient.

4. Stapling devices

In the GI tract, stapling devices tend to apply two rows of staples to produce a sound anastomosis.

•End-to-end anastomoses: circular stapling devices allow tubes to be joined together & such
instruments used in esophagus & lower rectum. No extraneous tissue is allowed to become
interposed between 2 bowel walls on closing the stapler
• Transverse anastomoses: provide 2 rows of staples for a single transverse anastomosis.
Useful for closing bowel ends, & larger sizes used to create gastric tubes & gastric partitioning
• Intra-luminal anastomoses: used in fashioning a gastro-jejunostomy or jejuno-jejunostomy &
is used in ileal pouch formation
• Other devices: staple/ligate blood vessels.
LAPAROSCOPIC STAPLING DEVICES: inserted down trocars in laparoscopic surgery

PRINCIPLES OF ANASTOMOSES

1.Bowel Anastomoses

• Ensure good blood supply to both bowel ends before and after formation of anastomoses.
Ideally bowel ends should be pink & bleeding prior to anastomosis. Gold standard for a good
blood supply for any anastomosis is the presence of arterial bleeding from the marginal vessel
immediately adjacent to the cut end of the bowel & the absence of venous congestion
• Ensure the Anastomoses is under no tension. Suture bites 3-5mm deep & 3-5mm apart. Suture
materials should be of 2/0-3/0 size & made of an absorbable polymer which can be braided or
monofilament. Braided, coated sutures are best
• Avoid risk to mesenteric vessels by clamps or sutures.
• Only bowel of similar diameter is brought together to form an end-to-end anastomosis. In major
size discrepancy side-to-side anastomosis is done. When size discrepancy is not marked,
enlarges the lumen of distal, collapsed bowel & allow end-to-end anastomosis
• Use atraumatic bowel clamps to minimize contamination
• After anastomoses, mesentery closed to avoid risk of internal hernia
• Interrupted and continuous single-layer suture techniques are adequate and safe.
• Stapling devices are an alternative when speed is required, or access is a major factor

2. Vascular Anastomoses

• Extremely accurate closure required as must be watertight

17
• Non-absorbable monofilament suture material should be used e.g. polypropylene
• A smooth intimal suture line is essential, to minimise risk of thrombosis & embolus
• Suture size depends on vessel calibre: 2/0 for aorta, 4/0 for femoral artery, 6/0 for popliteal to
distal arteries
• Knots require multiple throws (6-8) for security
• If any significant manipulation is necessary, atraumatic forceps are utilized.
• Vascular clamps should be applied with great care, especially for calcified vessels
• Suture must pass from within outwards on the downflow aspect of the anastomosis to avoid
creating an intimal flap & fix any atherosclerotic plaque. The tip of the needle is inserted at right
angles to surface of intima & the curve of the needle followed to prevent vessel trauma
• Once closure is complete, distal clamp is released first, before final watertight knot is made. This
allows backflow to clear any clot or air from the anastomosis. Then proximal clamp released,
minimises risk of distal embolus.

3. Laparoscopic anastomosis
• Same principles are applied: good blood supply, avoidance of tension & gentle tissue handling
• If ends of bowel adequately mobilised, & specimen extraction site present, an extra corporeal
anastomosis performed using open surgical technique
• If one or both ends cannot be exteriorised, an intra corporeal anastomosis is performed

DRAINS

Drains are inserted to allow fluid or air that might collect at operation site or in wound to drain
freely to the surface. The substances to be drained include blood, serum, pus, urine, faeces, bile or
lymph. Adequate drainage of fluid prevents the development of cavities that may delay wound
healing. Principles:

-Open drains that utilize the principle of gravity

- semi-open drains that work on the principle of capillary effect

- Closed drains systems that utilize suction

May be placed through wound or separate incision. Drains may also act as a signal for post operative
hemorrhage or anastomotic leakage, provide a track for later drainage

However, use of drains is associated with increased intra-abdominal and wound infections,
anastomosis insufficiency, abdominal pain, increase hospital stay, decrease pulmonary function

Specialist Drains

Chest Drains: used for pneumothorax, pleural effusion, haemothorax or to prevent collection of fluid
or air after thoracotomy. Once drain inserted, it is connected to an underwater sealed drain. Allows
air to leave pleural cavity but cannot be drawn back in by negative pressure created in intra thoracic
cavity

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T-Tube drains: After exploration of common bile duct, a T-Tube maybe inserted into the duct which
allows bile to drain while the sphincter of oddi is in spasm post-op. Once sphincter relaxes, bile
drains normally down bile duct into duodenum

Image guided drainage: For many intra-abdominal collection or abscesses, , drains may be inserted
under US or CT guidance.

Removal of drains

• A drain should be removed as soon as it is no longer required, because if left in it itself can
predispose to fluid collection as a result of tissue reaction.
Removal

o Drain for peri-operative bleeding= 24 hrs (e.g. thyroidectomy)

o Drain for serious collection= 5 days (e.g. mastectomy)
o Drain for infection= until infection has subsided or drainage is minimal
o Drains put in to cover colorectal anastomoses should be removed at about 5-7 days
o Bile duct T-tubes= 10 days. Can be removed earlier if T-tube cholangiogram shows free flow
of bile into duodenum. 10-day period to minimise risk of biliary peritonitis
o Suction drain should have suction taken off prior to removal of drain. Blocked drain difficult
to pull out. Released by twisting or flushing with sterile saline
o During removal of chest drain, patient is asked to breath in & hold breath (Valsalva). So no
air is sucked into pleural cavity as tube is removed

PRINCIPLES OF DIATHERMY: ELECTROSURGERY

• Heat produced depends on: intensity of current, wave form of current, electrical property of
tissues through which current passes, sizes of the 2 electrodes
• Two types. In Monopolar diathermy (mc) single electrode is used. While in bipolar, two
electrodes are present which are represented by the limbs of a pair of diathermy forceps. Only
the tissue held between limbs of the forceps heats up. The pattern is used when it is essential
that the surrounding tissue should be free from the risk of being burned or having current
passed through them

Effects of diathermy

Used for 3 purposes

Coagulation: the sealing of blood vessels, to stop bleeding (heating effect leads to cell death by
dehydration & protein denaturation. If intracellular temperatures reach boiling point during
coagulation, an unwanted cutting effect occurs)

Cutting: used to divide tissues during bloodless surgery (when sufficient heat is applied to the tissue
to cause cell water to explode into steam)

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Fulguration: the destructive coagulation of tissues with charring. (A combination of cutting and
coagulation)

Complications of diathermy

-Electrocution

-Explosion: sparks can ignite any volatile or inflammable gas/liquid. Alcohol based skin preparations
can catch fire if allowed to pool on patient. Should not be used in presence of explosive gases
including those that occur naturally in colon

-Burns: most common type of diathermy accidents. Occurs when current flows in some way other
than which the surgeon intended. More common in Monopolar than bipolar. May occur as a result
of faulty application of the indifferent electrode with inadequate contact area, patient being earthed
by touching any metal object, faulty insulation of the diathermy leads, accidental

- Channeling: normally current passes at tip of active electrode, but if current passes up a narrow
channel or pedicle to active electrode excessive heat maybe produced causing, for e.g., coagulation
of the penis in a child undergoing circumcision, coagulation of spermatic cord

- Pacemakers: diathermy currents interfere with the working of a pacemaker, which can be
dangerous to health.

- Laparoscopic surgery= burns are a hazard here, due to the lack of visibility of the instrumentation
Such burns occur by:

✒ diathermy of the wrong structure because of lack of clarity of vision or misidentification

✒ Faulty insulation of any of the laparoscopic instrument.

✒ Intraperitoneal contact of the diathermy with another metal instrument or inadvertent

activation of pedal

✒ Retained heat in the diathermy tip touching susceptible structures such as the bowel.

✒ capacitance coupling. Phenomenon when capacitor is created by having an insulator sandwiched

between 2 metal electrodes. Created in situations when there is metal laparoscopic port &
diathermy hook is passed through it. The insulation of hook acts as sandwiched insulator, & by
means of electromagnetic induction, diathermy current flowing through hook can induce a current
in the metal port, which can damage intraperitoneal structures. If plastic port used, then the danger
of capacitance coupling is decreased

3 types of advanced energy devices: bipolar electrosurgery, harmonic scalpel, combination devices

PRINCIPLES OF HARMONIC SCALPEL

It is an instrument that used Ultrasound technology to cut tissues while simultaneously sealing them.
During use, the scalpel vibrates and cuts through tissues, effecting hemostasis by sealing vessels and
tissues by means of protein denaturation caused by vibration rather than heat. Cutting precision

20
even through thickened scar tissue, enhanced visibility as less smoke produced compared to
electrosurgery. Takes longer time than diathermy. Diathermy can coagulate bleeding vessel anytime;
this coagulates as it cuts. Blood vessels sealed at lower temperature so less thermal damage to
surrounding tissue Good recovery, reduced operating time. Commonly used in laparoscopic
procedures & open procedures

BIPOLAR ELECTROSURGERY DEVICES

It is a vessel sealing system. It fuses vessel walls to create a permanent seal in open & laparoscopic
surgery. Uses a combination of pressure & energy. Ligasure system uses body’s own collagen &
elastin to both seal & divide allowing surgeons to decrease instrument handling

COMBINATION ENERGY DEVICES

Ultrasonic vibration & bipolar diathermy

Chap 5: Surgical infection

Chap 6: Surgery in the tropics

Tropical infections & infestations

ASIATIC CHOLANGIOHEPATITIS
• Also called oriental cholangiohepatitis, caused by infestation of hepatobiliary system by
Clonorchis sinensis
• Organism resides in snails & fish, which act as intermediate hosts
• Infection in humans: ingestion of infected fish & snails, when eaten raw or improperly cooked

PATHOLOGY

• Parasite matures into adult worm in intrahepatic biliary radicles (can reside here for many years)
• Dilated intrahepatic bile ducts, with epithelial hyperplasia & periductal fibrosis
• Lead to dysplasia which may cause cholangiocarcinoma (most serious complication)
• Eggs/dead worms act as nidus for stone formation in gall bladder or CBD, which thickens &
dilates in later stages
• Cause of intrahepatic bile duct stones: parasite producing mucin-rich bile. Dilated intra hepatic
bile ducts lead to cholangitis, liver abscess, hepatitis

CLINICAL FEATURES

• Remains dormant for years. Non-specific features: fever, malaise, anorexia, abdominal
discomfort
• Fever with rigors (ascending cholangitis), obstructive jaundice, biliary colic, pruritis (from stones
in CBD)
• Obstruction of pancreatic duct by adult worm: acute pancreatitis

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 INVESTIGATIONS

• Abnormal LFTs
• Confirmation: examination of stool or duodenal aspirate shows eggs or adult worms
• U/S: uniform dilation of small peripheral intrahepatic bile ducts, with minimal dilation of
common hepatic & common bile ducts. Increased echogenicity & non-shadowing echogenic foci
in bile ducts: worms or eggs
• ERCP: confirms these findings

TREATMENT

• Drug of choice: praziquantel & albendazole

• Cholecystectomy with exploration of CBD. Repeated washouts during exploration as CBD is
dilated & contains stones, biliary debris, sludge & mud. After this: choledochododenostomy
• Some surgeons: roux loop instead of choledochododenostomy, which is brought to the
abdominal wall called an ‘access loop’ (allows radiologist to deal with future stones)
• Prevention: hepatobiliary U/S as a screening procedure to recent migrants from endemic areas

FILARIASIS
• Mainly caused by parasite Wucheria bancrofti carried by the mosquito
• In 10% by Brugia malayi & Brugia timori
• Once host bitten by mosquito, matured eggs enter the human circulation to hatch & grow into adult
worms; process of maturation takes a year
• Adult worms mainly colonise lymphatic system

DIAGNOSIS

• Mainly affects males

• Acute: episodic attacks of fever with lymphadenitis & lymphangitis. Sometimes, adult worms felt
subcutaneously
• Chronic after repeated acute attacks over several years
• Adult worms cause lymphatic obstruction, causing massive lower limb edema
• Obstruction to cutaneous lymphatics: skin thickening (like peu d’ orange appearance)
• Secondary streptococcal infection is common
• Recurrent attacks of lymphangitis: fibrosis of lymph channels, causing grossly swollen limb with
thickened skin producing elephantiasis
• Bilateral lower limb filariasis associated with scrotal & penile elephantiasis. Before that:
hydrocele
• Chyluria & chylous ascites
• Mild form of disease causes dry cough (tropical pulmonary eosinophilia)
• Investigations usually not needed as clinically very obvious
• Eosinophilia
• Nocturnal peripheral blood smear: microfilariae
• Parasite also seen in chylous urine, ascites, hydrocele fluid

TREATMENT

• Early stages before gross deformity: diethylcarbamazine

• Early stage of limb swelling: pneumatic compression repeated over prolonged period
• Hydrocele: excision & eversion of sac with if necessary, excision of redundant skin

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POLIOMYELITIS
• Enteroviral infection, enters by inhalation or ingestion

DIAGNOSIS

• Targets anterior horn cells causing LMN paralysis. Lower limb muscles affected more than UL. 1-
2% patients develop paralytic symptoms
• Fever & muscle weakness: Guillain-Barre syndrome excluded. Has sensory signs & symptoms.
CSF analysis to differentiate between both

MANAGEMENT

• Treatment is mainly medical & supportive in early stages. Surgery done only after very careful
assessment as most patients learn to live with their disabilities
• Surgery done for paralysis in the form of tendon transfers & arthrodesis

TROPICAL CHRONIC PANCREATITIS

• Affects younger generation from poor socioeconomic strata in resource poor countries
• Etiology: malnutrition, dietary, familial & genetic causes

ETIOLOGY & PATHOLOGY

• Cassava (tapioca) is consumed as a staple diet by people from a poor background (as inexpensive
& readily available). It contains derivatives of cyanide that are detoxified in the liver by sulfur
containing amino acids. The less well-off among the population lack such amino acids in their
diet. This causes cyanogen toxicity causing this disease
• Firm & nodular pancreas with extensive periductal fibrosis, with intraductal calcium carbonate
stones & dilated ducts
• Microscopically: fibrosis of pancreas as a whole
• High incidence of pancreatic cancer in these patients

DIAGNOSIS

• Usually 40-year-old male from poor socioeconomic background

• Clinical presentation: abdominal pain, thirst, polyuria, gross pancreatic insufficiency (steatorrhea
& malnutrition)
• Initial blood & urine tests confirm patient has type 1 DM. Known as fibrocalculous pancreatic
diabetes
• Serum amylase only elevated in acute presentation
• Plain abdominal radiograph: typical pancreatic calcification in the form of stones in duct
• U/S & CT scan: confirms diagnosis
• ERCP as an investigation only done when also combined with therapeutic approach to remove
ductal stones in pancreatic head

TREATMENT

• Mainly medical: treatment of diabetes with insulin, pancreatic enzymes, management of

malnutrition
• Tx of pain by analgesic ladder: non-opioids, then weak & then strong opioids, then referred to
pain clinic
• Surgery reserved for intractable pain

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• Operation: removal of stones with side-to-side pancreaticojejunostomy to a Roux loop.
Pancreatic resection is a last resort

TUBERCULOUS CERVICAL LYMPHADENITIS

DIAGNOSIS

• Any of cervical group lymph nodes involved: jugulodigastric, submandibular, supraclavicular,

post triangle
• Evening pyrexia, cough & malaise. Failure to thrive in a child
• Typical clinical feature: matted lymph nodal mass
• Late stages: cold abscess- painless, fluctuant mass, not warm (no signs of inflammation).
Denotes underlying castration
• If untreated this abscess bursts, producing bilocular mass with cross fluctuation – ‘collar-stud
abscess’
• Eventually bursts through skin, discharging pus & forming tuberculous sinus. Watery discharge

INVESTIGATIONS

• Raised ESR, CRP, low Hb, interferon gamma release assays

• Sputum for C/S, Ziehl-Neelsen staining
• Aspiration of pus from cold abscess for C/S. If mass in early stages of adenitis: excision biopsy

TREATMENT

• Involvement of other systems excluded. Treatment is mainly medical

TYPHOID

• Caused by Salmonella typhi

• Enters GIT by poor hygiene & inadequate sanitation

PATHOLOGY

• After ingestion of contaminated food/water, organism colonises Peyer’s patches in terminal

ileum causing hyperplasia of lymphoid follicles followed by necrosis & ulceration
• Microscopy: erythrophagocytosis with histiocytic proliferation
• In untreated: ulcers cause perforation & bleeding

DIAGNOSIS

• Persistent high temperature & patient is very toxic

• Blood & stool cultures confirm diagnosis
• Widal test is obsolete
• Practical & cheap kits available for rapid detection: multi-test dip S ticks, Tubex & TyphiDot
• After the 2nd week, signs of peritonitis denote perforation, confirmed by free gas in radiograph

TREATMENT

• Resuscitation with IV fluids & antibiotics in ICU. Metronidazole, cephalosporin & gentamycin
used
• Laparotomy is then carried out. Procedures: closure of perforation after freshening the edges,
wedge resection of ulcer area & closure, resection of bowel with or without anastomosis,

24
 closure of perforation & side-to-side ileotransverse anastomosis, ileostomy or colostomy where
perforated bowel is exteriorised
• Having found a perforation, always look for others
• Thorough peritoneal lavage done. Linea alba is closed leaving rest of abdominal wound open for
delayed closure
• Prognosis of perforation better if it occurs in 1st week than if it occurs later as pt is less
nutritionally compromised & body’s defences are more robust.

Chap 7: Principles of laparoscopic and robotic surgery

PRINCIPLES OF LAPROSCOPIC AND ROBOTIC SURGERY

Minimal access surgery is a way of performing surgery with shortened operating time, reduced
wound access trauma, less disfiguring than conventional techniques.

Types:

1.Laproscopy: A rigid endoscope (laproscope)is introdcued through a port into the peritoneal cavity.
This is insufflated with CO2 to produce a pneumoperitoneum.

laproscopic procedures have revolutionized the surgical management if cholelithiasis.

2. Thoracoscopy: to gain access to thoracic contents.

3. Endoluminal endoscopy: endoscopes are introduced into hollow organs.

4. Perivisceral endoscopy: examples are medistinoscopy, retroperitoneoscopy, and retroperitoneal

approaches to the kidney, aorta and lumber sympathetic chain.

5. Arthroscopy

ADVANTAGES

There is decreased wound size as compared to open surgery, as the latter requires larger
exposure for safe dissection.

Since there is smaller wound, so reduction in wound infection, dehiscence, bleeding, herniation
and nerve entrapment.

Decrease in wound pain

Improved mobility

Improved vision

Decreased heat loss (in open surgery, exposure of the body cavity to the atmosphere causes
cooling and fluid loss by evaporation, all of which contributes to morbidity. But this happens very
less in MAS).

25
LIMITATIONS

Reliance on remote vision and operating

Loss of tactile feedback, hence take longer to learn

Technically demanding

Intraoperative bleeding is difficult to control, because blood obscures the field of vision.

Extraction of large specimens is difficult, either a natural orifice like rectum ornmouth is used or
novel route needs to be created.

ROBOTIC SURGERY

Advantages include better visualization using stereoscopic views, elimination of hand tremor and
improved maneuvering as a result of the “robotic wrist” and the “robotic hand”

PREOPERATIVE EVALUATION

(Similar to open surgery)

History: patient must be fit for general anesthesia and open surgery if necessary. Potential
coagulation disorders are particularly dangerous in laproscopic surgery (since difficulty with
bleeding-control)

Examination

Prophylaxis against thromboembolism

Urinary catheters and nasogastric tubes: not required much in laproscopic surgery.

Informed consent

THEATRE TOOLS

At least two high resolution LCDs monitors, laproscopic kit for maintaining pneumoperitoneum and
the audio visual kit. Image quality is vital.

GENERAL PRINCIPLES

Creating a pneumoperitoneum

26
Two methods: Open and closed. Closed involves blind puncture using needle. Even though this is
fast, it has risk of intestinal or vascular injury.

Open method is safer and preferred, albeit time consuming. A 1 cm incision is made at the level of
umbilicus. Dissected deep till fascia is reached, then Hasson trocar is inserted. This allows entry into
peritoneal cavity.

Pre-op problems

Previous abdominal surgery: surgical scars need to be assessed and if adhesions present then
they need to be tackled.

Obesity: generally very safe and effective in obese patients. However there are technical
difficulties like reaching the operative region, obtaining pneumoperitoneum etc. Increased thickness
of the subcutaneous fat make things difficult.

Operative problems

Perforation of gallbladder: more common with laproscopic technique than with open technique.
Closure should be attempted prior to extraction, if there is stone spillage, they must be removed.

Bleeding: as mentioned above, bleeding creates a difficult situation in laproscopic surgery.

Best way to handle bleeding is to prevent it from happening at all. Risk factors:

-cirrhosis

- inflammatory conditions

- patients on anti-platelets or anticoagulant

- coagulation defects

If bleeding starts from a major vessel, then immediately use electrocautery or clip the vessel. When
vessel isn't identified due to inpaired vision, compress the area, perform immediate suction and
irrigation, and another port may need to be inserted.

Electrosurgery:

During laproscopy electrosurgical injuries can be serious. Majority of them occur due to use of
monopolar diathermy , so Bipolar diathermy should be used instead.

Post-op care:

Post-op symptoms may include dull abdominal pain, nausea and vomiting, (referred from
diaphragm). Analgesics like paracetamol maybe required for pain post-op.

If there is severe pain, fever, tachycardia, then re-exploration maybe required.

27
In the absence of problems, patient can be discharged within 24 hrs.

Mobility: patients can get out of bed and to go to the toilet as soon as they have recovered from the
anesthetic. Such movements are remarkably pain free when compared with the mobility achieved
after an open operation.

SINGLE INCISION LAPROSCOPIC SURGERY (SILS)

A technique adopted by some surgeons to insert all the instrumentation via a single incision through
the umbilicus, using a multiple channel port. Since only one incsion is made, it's virutally called
scarless. But special port and instruments are required for this.

Chap 8: Principles of paediatric surgery

Chap 9: Principles of oncology
MALIGNANT TRANSFORMATION

- Cancer cells establish an autonomous lineage (resist signals that inhibit growth)
- Obtain immortality by evading apoptosis
- Acquire the ability to invade, disseminate and implant
- Evade detection
- Genomic instability
- Jettison excess baggage (excess proliferation)
- Change energy metabolism

Growth of a tumor:

It is postulated that cancer starts from a single transformed (containing all the required mutations)
cell, then that cell is capable of giving rise to an infinite number of identical cells.

The growth of a typical human tumor can be described by an exponential relationship, called
gompertzian growth. There are some clinical implications of gompertzian growth:

- The majority of growth of tumor occurs before it is clinically detectable

- By the time they are detected, tumors have passed the period of most rapid growth, that
period when they might be most sensitive to anti-proliferative drugs.
- Early tumors are genetically old, meaning plenty of time has passed for mutations to occur.
- Rate of regression of tumor will depend upon it's age

CAUSES OF CANCER

Interplay between nature and nurture. So there are some genetic factors (Gene mutations like APC,
DNA mismatch repair genes, RB, PTEN, p53, BRCA) as well as environmental factors (like tobacco,
alcohol, radiation, viral infections, inhaled particles)

28
MANAGEMENT OF CANCER

1.PREVENTION

Preventive strategies should be applied, especially to those at risk. For example avoigin alcohol,
tobacco, smoking/2nd hand smoking, unprotected sex, decrease weight, excercise regularly, treat
viral infections on time etc.

2. SCREENING

If disease is detected in an asymptomatic individual at an early stage then that's better because
treatment will be more effective. Criteria for screening:

Disease should have a recognizable early stage. It should be sufficiently common to warrant
screening.

The test should be sensitive, specific and inexpensive.

Adequate diagnostic facilities should be available for those with a positive test. Screening repeated
at intervals if disease is of insidious onset.

3. DIAGNOSIS & CLASSIFICATION

Precise diagnosis is crucial to the choice of correct therapy.

Cancer is a disease of cells and for accurate diagnosis, abnormal cells need to be seen. So biopsy is
required in a lot of cancers. Tumors are classified in different ways. Such as lymphomas are classified
as Hodgkin and non-hodgkin, and then further subtypes are present.

Some tumors are simply classified as G1, G2, G3 (Well, moderately, poorly differentiated
respectively.)

4. INV & STAGING

Staging is a process through which extent of disease is mapped out.

5. MULTIDISCIPLINARY TEAM

For management of most cancers, a multidisciplinary team is required. It will include: site-specialist
surgeon, surgical oncologist, medical oncologist, reconstructive surgeon, ragiotherapist, diagnostic
radiologist, pathologist, physiotherapist, clinical nurse specialist, counsellor, administrator.

29
PRINCIPLES OF CANCER SURGERY

-Diagnosis and staging: in some cases, diagnosis of cancer is made during surgery. For example in
patients with malignant ascites, laproscopy is done and tissue is obtained for diagnosis.

Laproscopy is also widely used for the staging of intra-abdominal malignancy.

Other examples in which surgery is essential for diagnosis include orchidectomy, lymph node biopsy
in lymphoma etc.

-Removal of primary disease: Radical surgery for localized cancer involves removal of primary tumor
and as much of the surrounding tissue and lymph node drainage as possible in order to not only
ensure local control but also to prevent spread of the tumor through lymphatics.

-Removal of metastatic disease: ex. Removal of liver metastases

- Palliation: in many cases, surgery may not bring cure, but good for Palliation.

PRINCIPLES OF NON-SURGICAL TREAMENT

Dose-response curve: Drugs and radiation can be quantified in units, and thus we can construct a
dose-response relationship for both harms and benefits. Using the curve we can calculate the dose
at which there will be maximal possibility of uncomplicated cure.

Treatment should have selective toxicity, meaning it should only be toxic to the tumor and spare the
normal tissues.

General strategies: occasionally radio and chemo maybe used for curative intent. But most if the
time we use these as adjuvant therapies after surgical removal, in order to reduce the risk of
recurrence.

RADIOTHERAPY

One if the issues with radiation is the acute effect on normal tissues and the late effects, which may
take many years to become apparent. Fractioned Radiotherapy is done to reduce the late effects;
the smaller dose per treatment, the less severe the late effects will be. But the problem with this is
that the overall treatment will take longer, and greater the opportunity for the tumor to proliferate
during tx.

5 ‘R’s of Radiotherapy

-Repair: if given sufficient time between fractionated doses, cells will repair the radiation-induced
damage

30
- Reoxygenation: Hypoxic cells (like tumor cells) are more radioresistant than normal well
oxygenated cells.

- Repopulation: as Radiotherapy kills cancer cells, rapid proliferation is stimulated. Therefore, overall
treatment durationshould be as short as possible.

-Redistribution: sensitivity of cells to respond depend on their position in the cell cycle. Radiotherapy
should be timed to coincide with vulnerable phases of cell cycle.

- Radiosensitivity: tumor cells differ in their sensitivity to radiation. Some are completely resistant, so
therapy doesn't work. Some are very sensitive and therapy is effective.

CHEMOTHERAPY

Chemo is often a palliative rather than curative therapy. But usage should be selective, meaning that
tx aimed at relieveing symptoms should not itself produce unacceptable symptoms.

Principles of combined therapy:

Use effective agents

Use agents with different modes of action

Use agents with non-overlapping toxicities.

END OF LIFE CARE

Some issues in this regard are: Euthanasia, living will, bereavement, support to allow death at home
etc.

Chap 10: Surgical audit and clinical research

SURGICAL AUDIT AND CLINICAL RESEARCH
Clinical audit is a process used by clinicians who seek to improve patient care. It involves comparing
aspects of care with defined standards, to assess performance. If something is lacking than change
can be brought about either by training or providing better equipment. Following steps are required
to establish an audit cycle.

1. Define the audit question in a multidisciplinary team

2. Identify current standards
3. Design the audit to measure performance against standards
4. Measure over an interval

31
 5. Analyze results and compare performance
6. Undertake Gap analysis:
A) If all standards are reached, reaudit after an interval
B) If there is need for improvement, identify possible interventions such as training
7. Reaudit.

RESEARCH STUDY: During the design of the audit project, it might become apparent that there is a
limited body of evidence available. In this case a research should be conducted.

Identifying a research topic: once an idea has been formed, come up with a question. Keep thinking
whether the question actually matters. Find related articles from internet databases.

Project design:

Qualitative research-- data often comes from patient narratives, and the psychosocial aspect of
disease and treatments.

Quantitative research-- a medical condition is analyzed using hard points such as death or major
complications.

Types of study-- observational, case control, cross sectional, longitudinal, experimental, randomised,
randomised controlled

Sample size: incorrect sample size can lead to errors in surgical trials (false negatives and false
positives).

Eliminating bias: one way to eliminate any bias in data collection is to have observers/recorders who
don't know which treatment has been used. One can also ensure that the patient is unaware of
treatment allocation.

Protocols: the study protocol should be constructed to define the research strategy. It should
contain a paragraph on the background of the research, aims and objectives, a clear methodology,
definitions of population and sample size and methods of analysis. It should also include patient
numbers, inclusion and exclusion criterias, and the timescale for the work.

Once it is finalized, formal peer review is needed.

Also, review by ethics committee is important.

--Statistical analysis

32
Evidence based surgery: it is a move to find the best ways of managing patients using clinical
evidence from collected studies.

Chap 11: Surgical ethics and law

RESPECT FOR AUTONOMY

Surgeons should respect the right if autonomy if the patients. This means that patients have the
right to make choices regarding their treatment. They can refuse to receive treatment if they want,
and the doctor has to respect that, despite personal preferences.

INFORMED CONSENT

There should be detailed information about:

- The condition and why it requires surgery

- The type of surgery proposed and how it may correct the condition
- The prognosis and side effects of surgery
- The unexpected hazards of surgery
- Any alternative treatment than the proposed surgery
- Consequences if not getting treated

Written material in the patients preferred language should be provided, and translator should be
present if not an English speaker.

Time should be given to the patient to make a decision. The consent should be taken by the surgeon
instead of a junior staff member. Make sure that the patient has understood what was explained,
avoid using technical language. Ask patients if they have further questions

The patient must:

- Be competent, i.e should be able to understand and make a choice about the treatment
- Not be coerced
- Be given sufficient info

If the patient is temporarily incapacitated and can't give consent, such as drunk or unconscious, then
life-saving procedures can be performed without consent. If the patient has made a legally valid
advanced decision refusing a particular treatment, then that decision should be honored.

In the case of children, consent is taken from parent/guardian. However, children should be given
appropriate info and should be consulted.

If competence is severely compromised by psychiatric illness then those charged with protecting
them just assume responsibility.

33
LIFE AND DEATH

There is no obligation to provide or to continue life-sustaining treatment if:

- Doing so is futile
- If patient is irreversibly close to death
- If the patient is permanently brain damaged and will never be able to engage in any form of
self-directed activity.

CONFIDENTIALITY

Surgeons must not discuss clinical matters with relatives of patient or other individuals without
explicit consent from the patient. Clincians may discuss pertinent matters realted to the case
amongst themselves, but the patient must know about this communication.

There are some instances when it is permitted to break confidentiality. For example, as a result of
court order, or in relation to the requirements of public health legislation.

MAINTAINING STANDARDS IF EXCELLENCE:

Surgeons must keep agining further education throughout their career in order to maintain excellent
patient care and treatment.

Chap 12: Patient safety

PATIENT SAFETY

PATIENT SAFETY INCIDENTS

- An adverse event_ incident resulting in harm to the patient

- A near miss_ an incident that could've resulted in harm but did not
- a no-harm event_ an incident that reached the patient but results in no injury

FACTORS THAT CONTRIBUTE TO INCIDENTS

Human factors- inadequate assessment, delay or error in diagnosis, error in giving treatment,
deficiency in training or experience, fatigue etc.

34
System failures- poor communication between healthcare providers, equipment failure, inadequate
staffing

-Errors can be viewed from a person centered or system approach

-The majority of near misses or adverspe events are due to system factors

-Understanding why these errors occur and applying lessons learnt will prevent future injuries to
patients

-error models (like Heinrich’s safety pyramid, Swiss cheese model, SHELL model) help to understand
the factors that cause incidents and direct us to where our defences need to be improved.

PATIENT SAFETY AT THE COALFACE

-Communicating openly with the patients and carers and obtaining consent

-Professional behavior and maintaining fitness to work. To determine competence, credentialing is a

way. To ensure clinicians are adequately prepared to safely treat patients.

-Reporting adverse events and near-misses.

-Patients advocacy units help to ensure that complaints of patients are easily reported and resolved.

-Staff communication, understanding the work environment and working well with it.

-Prescribing medicine safely. Medication errors are common and causes include inadequate
knowledge of patient condition, of medication, incorrect dosage calculation, illegible handwriting

COALFACE ERRORS

-Diagnostic and management errors

- Resuscitation errors

- prescription errors

- technical and operative errors

-Situation awareness, identification and teamwork errors

The wrong patient in operating room

Surgery performed on the wrong side

Wrong procedure performed

35
 Disagreements about proceedings

Failure to communicate changes in patient's condition

Retained instruments or swabs

All these events occur due to a lack of communication

Checklists: surgical safety checklists have been introduced to reduce errors. Specific checks need to
be carried out at three obligatory time points.

1.Sign in: before induction of anesthesia

2. Time out: before skin incision

3. Sign out: before patient leaves operating room

In these checks, detailed are reviewed like patient's name, site, procedure, consent, vitals checked,
anesthesia safety check done etc.

SECOND VICTIM

Making errors in medical and surgical management leads to a range of emotions in doctors like
distress, guilt, shame, fear and depression. This causes physical and psychological disturbances. And
this docs become the 2nd victims. Coping and accepting errors requires management.

Unit 2
Not to be done

Chap 13: Diagnostic imaging

Chap 14: Gastrointestinal endoscopy
Chap 15: Tissue diagnosis

Unit-3
Chap 16: Pre-operative preparation
Chapter 16

36
Steps of pre-operative Patient assessment
History
Physical examination of all systems
Examination specific to surgery
General and specific investigations
Airway assessment
risk assessment & consent

Principles of history taking

Listen: What is the problem? (Open questions)
Clarify: What does the patient expect? (Closed questions)
Narrow: Differential diagnosis (Focused questions)
Fitness: Comorbidities (Fixed questions

Inv:
Full Blood Count
Urea & electrolyte
ECG
Clotting screen
Chest radio
Urinalysis
B-HCG
Blood glucose & HbA1c
Arterial blood gases
LFTs

• Urea and electrolytes. Urea and electrolytes (U&E) are needed before all major operations, in most
patients over 60 years of age

• Electrocardiography. Electrocardiography (ECG) is required for those patients aged over 60 years

• Chest radiography. A chest x-ray is not required unless the patient has a significant cardiac history,
cardiac failure, severe chronic obstructive pulmonary disease (COPD) etc

• Urinalysis. Dipstick testing of urine should be performed on all patients to detect urinary infection

• b-Human chorionic gonadotrophin. Pregnancy needs to be ruled out in all women of childbearing
age.

37
Pre-operative risk assessment: CVS (revised cardiac risk index)

• At preoperative assessment, it is important to identify the patients who have a high perioperative
risk of myocardial infarction (MI) and make appropriate arrangements to reduce this risk
• These patients include those who have suffered coronary artery disease, congestive cardiac failure,
arrhythmias, severe peripheral vascular disease, cerebrovascular disease or renal failure,
especially if they are undergoing intra-abdominal or intrathoracic surgery.

For patients with symptomatic valvular heart disease or poor left ventricular function, an echo
should be performed.
Pressure gradients across the valves, dimensions of the chambers and contractility can be
determined using echocardiography; an ejection fraction of less than 30 per cent is associated with
poor patient outcomes

In pre-operative assessment The patient should be referred to a cardiologist if:

• A murmur is heard and the patient is symptomatic.

• The patient is known to have poor left ventricular function or cardiomegaly.
• Ischaemic changes can be seen on ECG even if patient is not symptomatic (silent MI).
• There is an abnormal rhythm on the ECG, tachy/bradycardia or a heart block that may lead to
cardiovascular compromise

HTN IM

• Prior to elective surgery, blood pressure should be controlled to near 160/90 mmHg

• If a new antihypertensive is introduced, a stabilisation period of at least 2 weeks should be

allowed.

MI

Elective surgery should be postponed for three to six months after a proven myocardial infarct to
reduce the risk of perioperative reinfarction

Stent

• Patients may have had coronary stents inserted for IHD and should be asked about effectiveness of
the treatment, concurrent antiplatelet medications, e.g. clopidrogel and/or aspirin.

• If surgery cannot be postponed and the risk of significant perioperative bleeding is low, the dual
antiplatelet therapy can be continued during surgery

Pre-operative assessment in ptnt with dysrhytmias?

******AF:
• start beta blockers, digoxin, Can channel blockers to control rate and rhythm
• stop warfarin 5 days preoperatively to have INR of 1.5 or less
******
• cardioversion and overpace modes may be turned off (switch on after surgery)
*******
• Symptomatic heart blocks and asymptomatic second- (Mobitz II) and third-degree heart blocks, if

38
discovered at preoperative assessment clinic, will need cardiology consultation and temporary
pacemaker insertion.

Pre-operative steps required in ptnt with valvular heart disease?

• the patients with severe aortic and mitral stenosis may benefit from valvuloplasty before
undergoing elective non-cardiac surgery.

Pre-operative steps required in ptnt with anemia & blood transfusion?

• txtd w/ iron and vitamins

• <8Hb --> transfusion
• group & save (google: A group and save is the sample processing • It consists of a blood group and
an antibody screen to determine the patients group and whether or not they have atypical red cell
antibodies in their blood.)

Two flights of stairs

Arozullah Respiratory failure index

• The patient’s current respiratory status should be compared with their ‘normal state’. Note should
be made of regular treatment, records of peak expiratory flow rates (PEFR), use of steroids, home
oxygen and continuous positive airway pressure (CPAP) ventilation; check for evidence of right heart
failure.

Pre-operative steps required in ptnt with resp problems: smoking?

• Information should be provided to indicate perioperative risks associated with smoking

asthma?

• It is important to establish the severity of the asthma

• Patients should continue to use their regular inhalers until the start of anaesthesia.
• Brittle asthmatics may also need extra steroid cover.

COPD? • pre op --> xray, abgs

• stabilize ptnt
• Patients on steroid treatment, or oxygen therapy, or who have a forced expiratory volume in
the first second (FEV1) less than 30 per cent of predicted value (for age, weight and height) have
severe disease and may have respiratory failure in the postoperative period.
• Preoperative chest x-ray or scans are useful in patients with known emphysematous bullae,
pulmonary cancer, metastasis or effusions
• An arterial blood gas analysis may also be useful as it can give an indication of carbon dioxide
retention
• Patients with significant COPD who are undergoing major surgery will need to be referred to the
respiratory physicians for optimisation of their condition.

inf?
• Elective surgery should be postponed if the patient has a chest infection.

• It should be treated with antibiotics and physiotherapy and the operation rescheduled after 4–6
weeks

Pre-operative steps required in ptnt with GIT diseases: issues with NPO? solid 6 hrs liquids 2 hrs

39
• Patients are advised not to take solids within 6 hours and clear fluids (isotonic drinks and water)
within 2 hours before anaesthetic to avoid the risk of acid aspiration syndrome.

• Infants are allowed a clear drink up to 2 hours, mother’s milk up to 3 hours and cow or formula
milk up to 6 hours before anaesthetic.

• If the surgery is delayed, oral (until 2 hours of surgery) or intravenous fluids should be started
especially in the vulnerable groups of patients, e.g. children, elderly and diabetics

• Patients can continue to take their specified routine medications with sips of water in the nil by
mouth period

ptnt with GIT diseases: regurgitation risk?

• Patients with hiatus hernia, obesity, pregnancy and diabetes are at high risk of pulmonary
aspiration even if they have been NBM before elective surgery.
• Clear antacids, H2-receptor blockers, e.g. ranitidine or proton pump inhibitors, e.g. omeprazole,
may be given at the appropriate time in the preoperative period

in ptnt with GIT diseases:liver disease?

• In patients with liver disease, the cause of the disease needs to be known, as well as any evidence
of clotting problems, renal involvement, and encephalopathy
• Elective surgery should be postponed until any acute episode has settled (e.g. cholangitis).
• The blood tests which need to be performed are liver function tests, coagulation, blood glucose,
urea and electrolyte levels.
• The presence of ascitis, oesophageal varices, hypoalbuminaemia, sodium and water retention
should be noted as all these can influence choice and outcomes of anaesthesia and surgery

in ptnt with Genitourinary diseases: renal?

• Underlying conditions leading to chronic renal failure should be stabilized

• treat H↑, ↓Ca and ↑K of greater than 6 mmol/L.
• After the final dialysis before surgery, a blood sample should be sent for FBC and U&E.

• Underlying conditions leading to chronic renal failure, such as diabetes mellitus, hypertension and
ischaemic heart disease, should be stabilised before elective surgery.
• Appropriate measures should be taken to treat acidosis, hypocalcaemia and hyperkalaemia of
greater than 6 mmol/L.
• Arrangements should be made to continue peritoneal or haemodialysis until a few hours before
surgery. After the final dialysis before surgery, a blood sample should be sent for FBC and U&E.
• Chronic renal failure patients often suffer chronic microcytic anaemic that is well tolerated,
therefore preoperative blood transfusion is usually not necessary.
• Acute renal failure can present with acute surgical problems, for example bowel obstruction
needing emergency surgery. In such patients, simultaneous medical and surgical treatment and
critical care unit support will be needed in the perioperative period.

in ptnt with Genitourinary diseases: uti?

utis common , txt with ab before elective surgery

for emergency AB started and ensure good urine output after surgery

40
• Uncomplicated urinary infections are common in women, while outflow uropathy with chronically
infected urine is common in men.
• These infections should be treated before embarking on elective surgery
• For emergency procedures, antibiotics should be started and care taken to ensure that the patient
maintains a good urine output before, during and after surgery

in ptnt with malnutrition?

Bmi <18.5: nutritional impairment

<15: significant hospital mortality
nutritional support for 2 weeks

• Body mass index (BMI) is weight in kilograms divided by height in metres squared.
• A BMI of less than 18.5 indicates nutritional impairment and a BMI of less than 15 is associated
with significant hospital mortality.
• Nutritional support for a minimum of 2 weeks before surgery is required to have any impact on
subsequent morbidity.
• If a patient is unlikely to be able to eat for a significant period, arrangements should be made by
the preoperative assessment team to start nutritional support in the immediate postoperative phase

in ptnt with obesity? delay surgery until ptnt has lost weight

• Morbid obesity is defined as BMI of more than 35 and is associated with increased risk of
postoperative complications.
• Patients should be made aware of risks involved and advised on healthy eating and taking regular
exercise.
• Associated sleep apnoea can be predicted by using a clinical scoring system of perioperative sleep
apnoea prediction (P-SAP) score or sleep apnoea studies. Patients should be asked to continue to
use a CPAP device for obstructive sleep apnoea and cholesterol-reducing agents in the perioperative
phase.
• If possible, delay surgery until the patients are more active and have lost weight. If this
fails, prophylactic measures need to be taken (such as preventative measures for acid
aspiration and deep vein thrombosis (DVT)) and associated risks need to be
explained prior to the surgery.

in ptnt with DM?

• Diabetes and associated cardiovascular and renal complications should be controlled to as near
normal level as possible before embarking on elective surgery
• Any history of hyper- and hypoglycaemic episodes, and hospital admissions, should be noted.
• HbA1c levels should be checked.
• Lipid-lowering medication should be started in patients who are in a high-risk group of
cardiovascular complications of diabetes.

• Patients with diabetes should be first on the operating list and if they are operated on in the
morning advised to omit the morning dose of medication and breakfast
• the patient’s blood sugar levels should be checked every 2 hours.
• For those on the afternoon list, breakfast can be given with half their regular dose of insulin (or
full-dose oral anti-diabetic agents) and then managed with regular
blood sugar checks as above.

41
• An intravenous insulin sliding scale should be started for insulin-dependent diabetes mellitus
undergoing major surgery or if blood sugar is difficult to control for other reasons.

in ptnt with adrenocortical suppression? supplementation with extra doses of steroids

perioperatively to avoid an Addisonian crisis.

Patients receiving oral adrenocortical steroids should be asked about the dose and duration of the
medication in view of supplementation with extra doses of steroids perioperatively to avoid an
Addisonian crisis.

in ptnt with coagulation problems:what are the risk factors for thrombophilia?

Patients with a strong family history or

previous personal history of thrombosis
should be identified.

They will need thromboprophylaxis in the

perioperative period (Table 16.3).

The progesterone-only pill should be

continued, however, the risks of continuing
the combined pill (slight increased risk of
significant thrombosis) should be weighed against the risks of an unplanned pregnancy.

Hormone replacement therapy (HRT) should be stopped 6 weeks prior to surgery.

What preoperative steps should be taken in low risk thromboembolism?

Patients with a low risk of thromboembolism can be given thromboembolism-deterrent
stockings to wear during the perioperative period.
• If it is felt that the neurological and cardiovascular thrombotic risks are low, antiplatelet agents
should be withdrawn (7 days for aspirin, 10 days for clopidogrel).

High-risk patients with a history of recurrent DVT, pulmonary embolism (PE) and arterial
thrombosis will be on warfarin.
This should be stopped before surgery and replaced by low molecular weight heparin or factor
Xa inhibitors.

Each hospital has guidelines which advise what type of DVT prophylaxis should be used for each type
of surgery
• If the thrombotic risks are perceived to be high and the patient is undergoing surgery with a high
risk of bleeding, aspirin alone should be continued.

in a ptnt with neurological disorders?

• Anticonvulsant and antiparkinson medication is continued perioperatively to help early
mobilisation of the patient.

• Lithium should be stopped 24 hours prior to surgery; blood levels should be measured to exclude
toxicity.
• The anaesthetist should be informed if patients are on psychiatric medications such as tricyclic
antidepressants or monoamine oxidase inhibitors, as these may interact with anaesthetic drugs

42
in ptnt with RA?
RA:
• Rheumatoid arthritis can lead to unstable cervical spine with the possibility of spinal cord injury
during intubation.
Therefore, flexion and extension lateral cervical spine x-rays should be obtained

• Rheumatologists will advise on steroids and disease-modifying drugs so as to balance

immunosuppression (chance of infections) against the need to stabilise the disease perioperatively
(stopping disease-modifying drugs can lead to flare up of the disease).

AS:
• In ankylosing spondylitis patients in addition to the problems discussed above, techniques of
spinal or epidural anaesthesia are often challenging.

SLE:
• Patients with systemic lupus erythematosis may exhibit a hypercoagulable state along with airway
difficulties.

Preoperative Airway assessment

• The ease or difficulty in performing airway manoeuvres can be predicted by simple examination
findings of full mouth opening (modified Mallampati class), jaw protrusion, neck movement and
thyromental distance.

• The Samsoon and Young modified Mallampati test is performed with the clinician sitting in front of
the patient, with the patient’s mouth open and tongue protruding.
(The higher the grade, the higher the risk in
obtaining and securing an airway)

Preoperative assessment in emergency surgery

• Medical assessment and treatments should be

started (e.g. according to the Advanced Trauma Life
Support (ATLS) guidelines) even if there is no time to complete those before the surgical procedure
is started.

43
 • Some risks may be reduced, but some may
persist and whenever possible these need to be
explained to the patient
Preoperative assessment : asking for consent
• Valid consent implies that it is given voluntarily
by a competent and informed person who is not
under duress
• In emergency situations or in an unconscious
patient, consent may not be obtained and the
procedure carried out ‘in the best interests of the patient’.
• Adults are presumed to have capacity to consent unless there is contrary evidence.
• For adults who are not deemed competent to give consent, treatment can still proceed in their
best interests by filling in an inability to consent form.
• Those under 16 years who demonstrate the ability to appreciate the risks and benefits fully are
deemed competent. This is known as Gillick

competence

Chap 17: Anesthesia & pain relief

Ground rules for anaesthesia

• Safe surgery is achieved by close teamwork between surgeon and anaesthetist
• Safety checklists make sure that things are not forgotten
• Risk assessment allows the best strategy to be chosen
• Anaesthetists are extending their care into the pre- and postoperative phase

44
ASA, RSI

• Rapid sequence induction (RSI) is a technique that allows the airway to be rapidly secured. It is
used when there is a high risk of regurgitation that may lead to pulmonary aspiration

• Rapid sequence induction (RSI) using a predetermined dose of intravenous anaesthetic agent
together with rapidly acting muscle relaxant is used in those with high risk of regurgitation in order
to secure the airway quickly.

Induction of G. anesthesia?

• Induction of general anaesthesia is most frequently done by intravenous agents. Propofol has
replaced thiopentone as the most widely used induction agent and can be used for maintenance of
anaesthesia.

• Inhalational induction using agents such as non-pungent sevoflurane is useful in children, needle-
phobic adults and those in whom a difficult airway is anticipated

• These patients will have a higher risk of developing airway obstruction

Maintenance of anesthesia?

Maintenance of anaesthesia, on the other hand, can be done using continuous infusion of
intravenous agent (propofol) or inhaled vapour such as isoflurane, sevoflurane or desflurane

• The use of nitrous oxide is declining despite its analgesic and weak anaesthetic properties due to
concerns over postoperative nausea and vomiting.

• It also increases the size of the air bubble causing adverse effects, for example in eye, ear and
abdominal surgery. Finally, it is possibly mutagenic and is a powerful greenhouse gas.

google: • Malignant hyperthermia is a severe reaction to certain drugs used for anesthesia. This
severe reaction typically includes a dangerously high body temperature, rigid muscles or spasms, a
rapid heart rate, and other symptoms. Without prompt treatment, the complications caused
by malignant hyperthermia can be fatal

Muscle relaxation for GA be acheived?

• Suxamethonium is the most commonly

used depolarising agent.

• It binds to the nicotinic acetylcholine

receptors resulting in opening of the cation
channel leading to depolarisation and rapid
relaxation of muscles.

• These properties are useful where rapid

endotracheal intubation is necessary to
protect the patient’s airway or short
duration surgery is performed

• Non-depolarising muscle relaxants act by

competitive blockade of postsynaptic
receptors at the neuromuscular junction

45
atracurium : allergies, can be used in liver & renal failure
vecuronium: no allergies, cannnot be used in liver & renal failure
rocuronium: for rapid infusion

Management of airway during GA?

Loss of muscle tone as a result of general anaesthesia means that the patient can no longer keep
their airway open.

Therefore, the patients need their airway maintained for them. The use of muscle relaxants will
mean that they will also be unable to breathe for themselves and so will require artificial ventilation

• The addition of a cuff to the endotracheal tube facilitates positive pressure ventilation and
protects the lungs from aspiration of regurgitated gastric contents

• Laryngeal mask:

Several varieties of LMA are available including reinforced, I-gel and an intubating LMA that aids
endotracheal intubation (Figure 17.3).

• The gold standard for intubation in difficult situations is the use of the fibreoptic intubating
bronchoscope, facilitated by topical local anaesthetic in awake patients or using general anaesthesia

• Double-lumen tubes and endobronchial tubes are used in procedures such as thoracoscopic,
pulmonary and oesophageal surgery to allow collapse of one lung (while ventilating the other) for
ease of surgery

• Ventilating bronchoscope and endobronchial catheters can be used to maintain oxygenation

during laryngotracheal surgery or bronchoscopy by using intermittent jets of oxygen

when is mechanical Ventilation during anaesthesia?

Mechanical ventilation is required when the patient’s spontaneous ventilation is inadequate or

when the patient is not breathing because of the effects of the anaesthetic, analgesic agents or
muscle relaxants.

• In volume control ventilation, a preset volume is delivered by the machine irrespective of the
airway pressure. The pressure generated will be in part dependent on the resistance and compliance
of the airway.

In laparoscopic surgery requiring the Trendelenburg position (the patient is positioned head down),
and in morbidly obese patients and those with lung disease, this may result in excessive pressures
being developed, which may lead to barotrauma (pneumothorax).

46
• In pressure control mode, the ventilator generates flow until a preset pressure is reached. The
actual tidal volume delivered is variable and depends on airway resistance, intra-abdominal pressure
and the degree of relaxation.

• Positive end expiratory pressure (PEEP) is often

applied to help maintain functional residual capacity
(FRC). This avoids lung collapse by opening collapsed
alveoli, and maintains a greater area of gas exchange
so reducing vascular shunting

What needs to be monitored during GA? recovering from GA? Local anesthesia

dose limit w/ adrenaline: {{c1::7mg/kg}}

dose limit w/o adrenaline {{c2::3mg/kg}}

local --> lbrp 3246

Dope: Lignocaine can be used for nerve blocks, has a

time of onset of {{c1::4}} minutes, and lasts between
{{c1::30}} minutes and {{c1::3}} hours.

What is the longest duration of analgesia for wound management? Bupivacaine

Bup bup bup like a heart (cardiotoxic) --> hearts beat the longest

Bupivacaine}} is a local
anesthetic that is associated
with severe
{{c1::cardiovascular}}
toxicity

spinal anesthesia

47
 Caution is needed in patients with
hypovolaemia and cardiovascular
disease.

The incidence of dural puncture

headache can be minimised by limiting
the number of punctures and use of fine
bore pencil tip needles designed to split
rather than cut the dura.

epidural anesthesia

• Continuous infusion (with a patient-

controlled bolus) of weak local
anaesthetic combined with opioids
(such as fentanyl) is routinely used for postoperative analgesia.

• Placement of an epidural catheter in the high thoracic region provides excellent analgesia for a
wide variety of upper abdominal and thoracic surgical operations enabling early mobilisation and
reducing respiratory complications.

Anking: What is the underlying pathophysiology of hypotension after administration

of epidural anesthesia? Vasodilation and venous pooling

sympathetic nerve fibers responsible for vascular tone may be blocked by the anesthesia resulting
in vasodilation and venous pooling → ↓ cardiac return

TAP block

• The technique has been shown to provide effective analgesia after a wide range of abdominal
surgery.

• Injection of local anaesthetic into the fascial plane between the internal oblique and transversus
abdominis muscles allows a block of all these nerves, and excellent anaesthesia of the anterior
abdominal wall (Figure 17.8).

chronic benign pain

• In surgical practice, the patient with chronic pain may present for treatment of the cause (e.g.
pancreatitis, malignancy) or concomitant benign pathology. Acute pain after surgery may progress to
chronic pain and is believed to be due to inadequate treatment of acute pain itself.

management of chronic benign pain

• Epidural injections are used for the pain of nerve root irritation associated with minor disc
prolapse along with active physiotherapy to promote mobility.

• Nerve stimulation procedures such as acupuncture, transcutaneous nerve stimulation, and spinal
cord stimulators
increase endorphin production in the central nervous system.

• Nerve decompression craniotomy rather than percutaneous coagulation of the ganglion is now
performed for trigeminal neuralgia.

48
Drugs in chronic non-malignant pain

• The tricyclic antidepressant drugs and anticonvulsant agents are often useful for the pain of nerve
injury, although side effects can prove troublesome and reduce compliance.

• Both pregabalin and gabapentin reduce spontaneous neuronal activity and are now used for
managing the neuropathic chronic pain.

Treatment of pain dependent on sympathetic nervous system activity

• Even minor trauma and surgery (often of a limb) can provoke chronic burning pain, allodynia,
trophic changes and resultant disuse due to excessive sympathetic adrenergic activity inducing
vasconstriction and abnormal nociceptive transmission.

• Management includes:

◘ a test response to systemic alpha-adrenergic blockade using intravenous phentolamine and/or

local anaesthetic injection of stellate ganglion or lumbar sympathetic chain.

◘ Percutaneous chemical lumbar sympathectomy with phenol/local anaesthetic is used for relief
of rest pain in
advanced ischaemic disease of the legs.

It has an added advantage as it assists in the healing of ischaemic ulcers by improving peripheral
blood flow.

chronic malignant pain

• Oral opiate analgesia is necessary when the less powerful analgesic agents no longer control pain
on movement, or enable the patient to sleep

• It is also important to distinguish between the addiction and dependence; the former being a
psychosocial phenomenon while the latter is a pure physiological response to a given drug

• Some patients experience ‘breakthrough pain’ : (acute, excruciating and incapacitating), which
occurs either spontaneously or in relation to a specific predictable or unpredictable trigger,
experienced by patients who have relatively stable and adequately controlled background pain.

Management:

• Oral morphine, often used for chronic pain, can be prescribed in short-acting liquid or tablet
form and should be administered regularly every 4 hours until an adequate dose of drug has been
titrated to control the pain over 24 hours. Once this is established, the daily dose can be divided into
two separate administrations of enteric-coated, slow-release morphine tablets (MST morphine)
every 12 hours

• Additional short-acting opioids (morphine/fentanyl) can then be used to cover episodes of

breakthrough pain.

Infusion of subcutaneous, intravenous, intrathecal or epidural opiate drugs

• The infusion of opiates is necessary if a patient is unable to take oral drugs

49
• Subcutaneous infusion of diamorphine is simple and effective to administer.

• Epidural infusions of diamorphine with an external pump can be used on mobile patients.

• Intrathecal infusions with pumps programmed by external computer are used, however, there is a
possibility of developing infection with catastrophic effects.

• Intravenous narcotic agents may be reserved for acute crises, such as pathological fractures.

Neurolytic techniques in cancer pain

Alternative strategies include:

• The development of anti-pituitary hormone drugs, such as tamoxifen and cyproterone, enables
effective pharmacological therapy for the pain of widespread metastases instead of pituitary
ablation surgery.

In the management of chronic pain, a multidisciplinary approach by a team of medical and nursing
staff working with psychologists, physiotherapists and occupational therapists can often achieve
much more benefit than the use of powerful drugs. Pain management programmes lay out a logical
structure for this.

Describe different topical anesthetics

• EMLA (eutectic mixture of local anesthetics). {{c1::This is a mixture of lignocaine and prilocaine for
application to the skin for venepuncture in children}}.
• Cocaine. {{c2::It may be called Mofatt’s solution and used in nasal surgery for anaesthesia and
vasoconstriction}}.
• Lignocaine 4%. {{c3::Spray to anaesthetise the airway during awake fibreoptic intubation}}

Common local anaesthesia techniques: Nerve blocks

• Interscalene block for {{c1::shoulder surgery}} produces excellent postoperative analgesia.

Complications include phrenic nerve block, Horner’s syndrome, as well as accidental intravascular
and spinal injection.
• Axillary brachial plexus block can be used as {{c2::the sole anaesthetic technique for upper limb
surgery (Figure 17.7).}}
• Femoral and sciatic nerve blocks are often used for{{c3::anaesthesia and analgesia for lower limb
surgery}}

nociceptive pain

• Nociceptive pain may result from musculoskeletal disorders or cancer activating cutaneous
nociceptors (pain receptors).
• Prolonged ischaemic or inflammatory processes result in sensitisation of peripheral nociceptors
and altered activity in the central nervous system leading to exaggerated responses in the dorsal
horn of the spinal cord.

50
 neuropathic pain

• It is classically of a ‘burning’, ‘shooting’ or

‘stabbing’ type and may be associated with
allodynia, numbness and diminished thermal
sensation.

• It is poorly responsive to opioids.

Summary box 17.11: Options for controlling

severe pain in malignant disease

Oral morphine using slow-release, enteric-

coated tablets
Slow infusion of opiates subcutaneously, by
epidural, or intrathecally
Neurolysis for patients with limited life
expectancy
Palliative hormone, radiotherapy, or steroids control pain from swelling

Chap 18: Care in the operating room

PREOPERATIVE PREPARATION IMMEDIATELY BEFORE SURGERY:

PATIENT PREPARATION:

● Both surgeon and anesthetist should examine patient

● Identity is confirmed
● Valid informed consent is taken
● Check for contraindications for surgery eg critical illness or remote infections
● Neurovascular examination should be performed
● Mark the site of operation with arrow
THEATRE TEAM PREPARATION :

● booking and scheduling elective and emergency surgery

● Theatre list (date , time , name of surgeon and anesthetist)
● For each operation patients name , hosp number and site of surgery and equipments must be noted
● Children and diabetics will go first and infectious patient be last as they contaminate theatre

IN THEATRE :

SURGICAL SAFETY CHECKLIST :

WHO safety check list given in 2008 has 5 steps

1. PRELIST BRIEFING :
Short meeting of staff and team to introduce themselves to patient and discussing patients issues positioning ,
allergies , antibiotics and thromboprophylaxis

2. SIGN IN :
List should be read prior to induction of anesthesia

● Confirm patients identity

● Mark surgery site
● Check medicine and anesthesia machines

51
 ● Allergy hx
● Airway problems and risks of aspiration
● Blood loss risk > 500 ml requires IV access

3. TIME OUT :
This must be performed before surgery starts i.e verbal communication between team , introduction and
discuss critical events plus managing temperature control , hair removal , glycemic control infection control
and scrubbing

4. SIGN OUT :
Checking WHO sign out list which include

● Procedure has been recorded

● Instrumentand swab count
● No equipments problems

5. POSTLIST DEBRIEFING :
Writing operating note which include :

● Patient details (name, age hosp no. ,Address)

● Date and time of operation
● Location of operation
● Name of procedure and method (incision , findings , complications , dressing)
● Surgeon , assistant and anesthetist
● Type of anesthesia
● Patients position
● Application of torniquet , antibiotics and catheter
● Post op time for recovery and follow up and discharge details

MANAGEMENT WITHIN THEATRE :

ANTIBIOTICS :

● antibiotics given less than an hour before surgery as prophylaxis for clean surgery involving prosthesis
insertion
● Discontinue antibiotic 24 hour post surgery
● Non prosthetic surgery requires no antibiotic prophylaxis

VTE :

● prevent dehydration
● Mechanical VTE prophylaxis ( compression stocking and intermittent pneumatic compression devices)
● Pharmacological VTE
● Regional anesthesia has less risk of VTE than general anesthesia

MONITORING :

● pulse , BP , temperature , respiration and other vitals

52
OPERATING ROOM ENVIRONMENT :

● VENTILATION :
air flow system filters air with 20 air changes per hour

While laminar air flow provides 100-300 air changes per hour and used in centres for implants to reduce
infection risk

● HUMIDITY AND TEMPERATURE :

Temperature of 20-24°C with humidity 50-60% is ideal

● PATIENT TRANSFER :
Coordinated with anesthetist to protect airway devices and other connections

● POSITIONING :
Pressure areas are given importance

1. Bony prominences
2. Nerves with superficial course eg common peroneal
3. Nerves at risk of stretching eg brachial plexus
4. Area at risk of developing conpartment syndrome
5. Eye protection

EQUIPMENTS :

● DIATHERMY :
Monopolar diathermy is used that is clean and dry , free of air , situated over well perfused muscle mass ,
avoid bony prominences and scars and distal to torniquet

Contraindicated in pacemakers , implantable defib , cochlear implant and spinal cord stimulators

● TORNIQUETS :
Use to reduce blood flow at the site.

Complications include neurovascular compression , skin injury and distal ischemia and reperfusion injury .

Precautions : avoid use in high risk patients and apply padding , minimum cuff pressure (100 mm of Hg for
upper limb and 150 for lower limb )

● URETHRAL CATHETER :
Sterile equipments must be used

TEMPERATURE CONTROL :

patient loses heat rapidly during surgery due to exposure to cold IV fluids and anesthetic gases , reduced
metabolic heat production and limited vasocontriction . To decrease risk of hypothermia room temperature
must be maintained .

HAIR REMOVAL :

Clipping reduce infection risk rather than shaving

GLYCAEMIC CONTROL :

53
Hyperglycemia perioperatively increases the post op wound infection risk and hypoglycemia lead to seizures
and death

INFECTION CONTROL :

Asepsis and universal precautions are followed :

● Protective non porous gloves , eye wear , mask , apron for staff
● Safe sharp handling techniques
● Staff vaccination for hep B
● Staff with infected wounds or active dermatitis should not work there

SCRUBBING :

● Hat , mask , eye protection should be worn and jewellery should be removed
● Nail and deep skin creases are cleaned with brush for 1-2 mins
● Hand and forearm is washed systematically 3 times and dried with sterile towel
● Folded gown is lifted away from trolley and allowed to unfold while the top is held
● Gloves are worn using one or two person technique
Standard scrub solution :

1. 2% chlorhexidine (effective for more than 4 hrs against gram positive and gram negative )
2. 7.5% povidone iodine (bacteriacidal , fungicidal and viricidal )
3. Alcohol

MOVEMENT IN THEATRE :

Scrubbed personnel should place hands over table , touch only sterile area

Unscrubbed personnel touch only unsterile area and avoid walking between patient and tray

ROLE OF ASSISTANT :

1. Prepping : removal of debris , washing and disinfecting patients skin

2. Draping : creating protective zone around operative site to avoid contamination . Diathermy and
suction equipments are attached to drape
3. Trainee : should write inportant steps in brief on board
4. At surgery : place and hold retractor and showing surgeon the field where they are working
5. After surgery : transfer patient safely off the table and write operatiin note

Chap 19: Peri operative management of the high-risk surgical patient

ASSESMENT OF HIGH-RISK PATIENT

➢ Patients who have a predicted mortality≥5% considered high risk

➢ After surgery, tissue destruction, blood loss, fluid shifts, changes in temp, pain and anxiety causes
increased demand of oxygen (from 110ml/min/m2→170ml/min/m2)
➢ This is met by increased cardiac output and tissue oxygen extraction. Pts not able to do so→oxygen
debt.
➢ Occult hypovolemia (from fluid shift and blood loss) →further impairment of o2 delivery
➢ Compensation by splanchnic vasoconstriction→gut ischemia

54
 ➢ Coronary or cerebrovascular disease→higher risk of MI and stroke
FACTORS CONTRIBUTING TO RISK

➢ Patient factors that predispose to high risk of morbidity and mortality:

• Previous severe cardiorespiratory illness e.g. acute MI, COPD or stroke

• Late stage vascular disease involving aorta
• Age>70 years with limited physiological reserve in one or more vital organs
• Extensive surgery for carcinoma
• Acute abdominal catastrophe with hemodynamic instability (e.g. peritonitis)
• Acute massive blood loss>8 units
• Septicemia
• Positive blood culture or septic focus
• Resp failure: Pao2<8kPa or FiO2>0.4 or mechanical ventilation>48 hours
• Acute renal failure: urea >20mmol or creatinine >260mmol/L

• Surgery specific estimates of risk:

High risk (cardiac risk>5%):
• Open aortic
• Major vascular
• Peripheral vascular
• Urgent body cavity
Intermediate risk (cardiac risk 1-5%)
• Elective abdominal
• Carotid
• Endovascular
• Aneurysm
• Head and neck
• Major neurosurgery
• Arthroplasty
• Elective pulmonary
• Major urology
Low risk(cardiac risk<1%)

• Breast
• Dental
• Thyroid
• Ophthalmic
• Gynecological
• Reconstructive
• Minor ortho
• Minor urology
Risk increases→if surgery performed as emergency

MANAGEMENT OF RISK

➢ When risks too high→less extensive or nonsurgical option

➢ Those with mortality>10% → managed in critical care
➢ Improve pts condition by optimising medical therapy

IDENTIFICATION OF HIGH-RISK PATIENT

55
ASA score

Grade Description

1 Healthy
2 Mild systemic disease, no functional limitation
3 Severe systemic disease, definite functional limitation
4 Severe systemic disease, constant threat to life
5 Moribund patients unlikely to survive 24 hours with or without operation
E emergency operation

This system does not account for age, nature of surgery and the term systemic disease in ASA grading system
brings element of subjectivity.

Metabolic equivalent

➢ Functional physical fitness judged by the ability to tolerate metabolic equivalent tasks (METs)
➢ One MET is equivalent to the oxygen consumption of an adult at rest(~3.5mL/kg/min)
➢ 1 MET=eating and dressing
➢ 4 MET=climbing 2 flights of stairs
➢ 6 MET=short run
➢ >10 MET=able to participate in strenuous sport
➢ Patients who can exercise at 4METs or above have lower risk of perioperative mortality.
➢ This also depends on a subjective assessment of the ability of a patient and may be overestimated by
them.
POSSUM SCORE

➢ Use to predict all-cause mortality in post-op critical patients as well as non cardiac morbidity
ACS NSQIP score

➢ Estimates chance of a complication or death after surgery

➢ Compares pts risk with an average patients’ risk
Cardiopulmonary exercise testing (CPET)

➢ Used as a screening tool to identify high risk patients.

➢ The oxygen consumption and carbon dioxide production of the patient are measured while they
undergo a 10 minute period of incrementally demanding exercise (usually on a cycle ergometer) up to
their maximally tolerated level.
➢ Principle→when a subject’s delivery of O2 to active tissue becomes inadequate, anaerobic
metabolism begins; lactate is buffered by bicarbonate and the resulting CO2 increases out of
proportion to the escalation in physical difficulty and O2 consumption.
➢ Anaerobic threshold (AT)→O2 consumption in ml/kg/min above which this occurs.
➢ Peak oxygen consumption is also measured
➢ When CPET not available→6-minute walk test, incremental shuttle walk test
OPTIMISATION OF THE HIGH-RISK PATIENT

➢ Stopping smoking, reducing alcohol intake, losing weight, improving nutrition, and/or Hb levels
➢ In high risk group→need for more complex investigations, review of medication or further surgery.
Ischemic heart disease

➢ Optimise oxygen supply and demand

➢ May require preoperative CABG or PCI
Minimising myocardial ischemia

➢ Anaesthesia technique to be used→ which dampens stress response to surgery and provides a good
degree of cardiac stability.
➢ Anaesthesia should avoid→tachycardia, systolic hypertension and diastolic hypertension

56
 ➢ Use invasive arterial bp monitoring
➢ Blood loss accurately monitored, Hb maintained at a level suitable for patient’s cardiac risk factors
➢ Admission to hdu for pts with IHD and supplemental oxygen therapy for 3-4 days
Cardiac failure

➢ Decompensated heart failure puts patient at risk of multi organ failure

➢ Highest risk→ejection fraction<35%
➢ Patient’s functional capacity should be assessed
➢ Anaesthesia→minimal myocardial depression and change in afterload during surgery
➢ Arrhythmias should be rapidly brought under control, correcting electrolyte abnormalities crucial in
this
Respiratory failure

➢ Surgery under GA→changes to respiratory physiology

➢ Functional residual capacity of lungs is reduced
➢ This combined with respiratory depressant affect of residual anesthetic agents, patients limited
mobility and pain from surgery causes atelectasis. This predisposes patient to post operative
respiratory infection.
➢ Other complications→bronchospasm, pneumothorax, ARDs, respiratory failure
➢ Preoperatively→bronchodilator therapy for reversible obstructive airway disease.
➢ Nutritional status optimised and albumin levels corrected
➢ Patients at increased risk of respiratory complications→physiotherapy for postural drainage, deep
breathing exercises and incentive spirometry
➢ General anaesthesia associated with more respiratory complications so regional considered when
possible
➢ Hypoxemia and CO2 retention leading to the need for reintubation is avoided in those at risk by
delaying extubation until analgesia, hydration and acid base status have been corrected.
Sepsis

➢ Needs urgent identification and treatment

➢ Resuscitative measures→broad spectrum antibiotics and treating hypotension, hypovolemia and
elevated lactate levels and IV fluids.
MINIMISING THE IMPACT OF SURGERY IN THE HIGH-RISK PATIENT

➢ Selection of surgical techniques influenced by patient risk factors. Some procedures not primarily high
risk but may become so in unsuitable patients.
➢ Example→laparoscopic surgery preferred for patients predisposed to post op resp complications, but
its effect on cardiac physio means can’t be used for patients at risk of cardiac complications.
➢ Trendelenburg positioning associated with adverse CVS and neuro complications such as myocardial
ischemia and increased ICP.
➢ Risk is minimised by attention to patient selection
ROLE OF CRITICAL CARE AND OUTREACH SERVICES

➢ Optimal care in high risk group extended to include post op support which for majority of patients
means admission to a critical care bed.
➢ Many patients in hospital at risk of being critically ill, early identification of these patients using early
warning scores could allow for early intervention→hence intensive care outreach services. Outreach
team bridges gap between critical care unit and ward.
CONSENT

➢ Both voluntary and informed

➢ Key principles
1. Give patient information required to make decision
2. Be tailored to individual patient
3. Explain all reasonable treatment options

57
 4. Discuss all material risks
➢ Consent should be written and recorded on a form. Key points of discussion recorded in case notes.
➢ For consent to be given→patient must have capacity (ability to understand information provided), to
retain and use the information to make a decision.
➢ Children presumed to have capacity at 16
ARRANGING THEATRE LISTS

➢ Children and diabetic patients placed at beginning of the list, life and limb threatening surgery should
take priority, cancer patients need to be treated early

Chap 20: Nutrition & Fluid therapy

*****ARTIFICIAL NUTRITIONAL SUPPORT*****

General characteristics
Indications for nutritional support:
• Any patient who has sustained 5–7 days of inadequate intake or
• who is anticipated to have no intake for this period should be considered for nutritional support.
○ The periods may be less in patients with pre-existing malnutrition. This concept is important because it
emphasises that the provision of nutritional support is not specific to certain conditions or diseases.
○ Although patients with Crohn’s disease or pancreatitis, or those who have undergone gastrointestinal
resections, may frequently require nutritional support, it is the fact that they have had inadequate intakes for
defined periods that is the indication rather than the specific disease process.

Enteral nutrition
• The term ‘enteral feeding’ means delivery of nutrients into the gastrointestinal tract.
• This can be achieved with oral supplements (sipfeeding) or with a variety of tube-feeding techniques
delivering food into the stomach, duodenum or jejunum.
• A variety of nutrient formulations is available for enteral feeding. These vary with respect to energy content,
osmolarity, fat and nitrogen content and nutrient complexity; most contain up to 1–2 kcal/mL and up to 0.6
g/mL of protein.
○ Polymeric feeds contain intact protein and hence require digestion, whereas
○ monomeric/elemental feeds contain nitrogen in the form of either free amino acids or, in some cases,
peptides. These are less palatable and are used much less frequently than in previous years.
○ Newer feeding formulations are available that include glutamine and fibre to optimise intestinal nutrition
or immunonutrients such as arginine and fish oils, but these are expensive and their use is controversial.

Sip feeding
Indications:
• Commercially available supplementary sip feeds are used in patients who can drink but whose appetites are
impaired or
• in whom adequate intakes cannot be maintained with ad libitum intakes.
These feeds typically provide 200 kcal and 2 g of nitrogen per 200 mL carton.
Complication:
• There is good evidence to demonstrate that these sip-feeding techniques are associated with a significant
overall increase in calorie and nitrogen intakes without detriment to spontaneous nutrition.
• The evidence that these techniques improve patient outcomes is less convincing.

Tube-feeding techniques
• Enteral nutrition can be achieved using
○ conventional nasogastric tubes (Ryle’s),
○ fine-bore feeding tubes inserted into the stomach,
○ surgical or percutaneous endoscopic gastrostomy (PEG) or,
○ post-pyloric feeding utilising nasojejunal tubes or
○ various types of jejunostomy.

58
•The choice of method will be determined by local circumstances and preference in many patients.
• Whichever method is adopted, it is important that tube feeding is supervised by an experienced
dietician who will calculate the patient’s requirements and aim to achieve these within 2–3 days of the
instigation of feeds.

Txt regimen:
• Conventionally, 20–30 mL are administered per hour initially, gradually increasing to goal rates within 48–
72 hours.
• In most units, feeding is discontinued for 4–5 hours overnight to allow gastric pH to return to normal.
Adv:
• There is some evidence that this might reduce the incidence of nosocomial pneumonia and aspiration.
• There is good evidence to confirm that feeding protocols optimise the tolerance of enteral nutrition.
Disadv:
• In these, aspirates are performed on a regular basis and if they exceed 200 mL in any 2-hour period, then
feeding is temporarily discontinued.
• Tube blockage is common. All tubes should be flushed with water at least twice daily. If a build up of solidified
diet occurs, instillation into the tube of agents such as chymotrypsin or papain may salvage a partially
obstructed tube.
Contraindications:
• Guidewires should not be used to clear blockages as these may perforate the tube and cause contiguous
damage.

Nasogastric tubes:
• Nasogastric tubes are appropriate in a majority of patients.

fine-bore feeding tube

• If feeding is maintained for more than a week or so, a fine-bore feeding tube is preferable and is likely to
cause fewer gastric and oesophageal erosions.
These are usually made from soft polyurethane or silicone elastomer and have an internal diameter of <3 mm.

Fine-bore tube insertion

• The patient should be semi-recumbent.
• The introducer wire is lubricated and inserted into the fine-bore tube (Figure 20.4).
Technique:
• The tube is passed through the nose and into the stomach via the nasopharynx and oesophagus.
• The wire is withdrawn and the tube is taped to the patient.
• There is a small risk of malposition into a bronchus or of causing pneumothorax. The position of the tube
should be checked using plain abdominal radiography (Figure 20.5).
Alternatively,
• 5 mL of air can be injected and a stethoscope used to confirm bubbling from the stomach.
• Confirmation of position by pH testing is possible but limited by the difficulty of obtaining a fluid aspirate
with narrow lumen tubes.

Gastrostomy

• ‘gastrostomy’: The placement of a tube through the abdominal wall directly into the stomach.
• Historically, these were created surgically at the time of laparotomy. Today, the majority are performed by
percutaneous insertion under endoscopic control using local anaesthesia, known as PEG
(percutaneous endoscopic gastrostomy) tubes (Figure 20.6).

Figure 20.6 Percutaneous endoscopic gastrostomy tube

• Methods of PEG are commonly used.

1. The first is called the ‘direct-stab’ technique

59
• in which the endoscope is passed and the stomach filled with air. The endoscopist then watches a cannula
entering the stomach having been inserted directly through the anterior abdominal wall.
• A guidewire is then passed through the cannula into the stomach. A gastrostomy tube (commercially
available) may then be introduced into the stomach through a ‘peel away’ sheath.
2. The alternative technique is the transoral or push-through
technique,
• whereby a guidewire or suture is brought out of the stomach by
the endoscope after transabdominal percutaneous insertion and is
either attached to a gastrostomy tube or the tube is pushed over a
guidewire.
• The abdominal end of the wire is then pulled, advancing the
gastrostomy tube through the oesophagus and into the stomach.
• Continued pulling abuts it up against the abdominal wall.

• If patients require enteral nutrition for prolonged periods (4–6

weeks), then PEG is preferable to an indwelling nasogastric tube; this minimises the traumatic complications
related
to in dwelling tubes.

PEG procedure-specific complications,(although these are uncommon.)

• Necrotising fasciitis and intra-abdominal wall abscesses have been recorded.
• Sepsis around the PEG site is more common and may necessitate systemic antibiotics or repositioning.
• A persistent gastric fistula can occur on removal of a PEG if it has been in place for prolonged periods and
epithelialisation of the tract has occurred. This
necessitates surgical closure.
-----------------Jejunostomy-----------------
• This can be achieved using nasojejunal tubes or by placement of needle jejunostomy at the time of
laparotomy.

Use:
• Some authorities advocate the use of jejunostomies on the basis that post-pyloric feeding may be associated
with a reduction in aspiration or enhanced tolerance of enteral nutrition.
• In particular, there are many advocates of jejunostomies in patients with severe pancreatitis, in whom a
degree of gastric outlet obstruction may be present, related to the oedematous head of pancreas.
In most patients it is appropriate to commence with conventional nasogastric feeding and progress to post-
pyloric feeding if the former is unsuccessful.

Disadvantages:
• Nasojejunal tubes often necessitate the use of fluoroscopy or endoscopy to achieve placement, which may
delay commencement of feeding.
• Surgical jejunostomies, even using commercially available needle-insertion techniques, do involve creating a
defect in the jejunum, which can leak or be associated with tube displacement; both of these complications
result in peritonitis.

-----------------Complications-----------------
• Most complications of enteral nutrition can be avoided with careful attention to detail and appropriate
infusion rates.
• Patients should be nursed semi-recumbent to reduce the possibility of aspiration.

Complications can be divided into

○ those resulting from intubation of the gastrointestinal tract and
• are more frequent with more invasive means of gaining access to the intestinal tract
○ those related to nutrient delivery.
• They include diarrhoea, bloating and vomiting.
• There is no evidence that the incidence of diarrhoea and bloating is reduced by the use of half-strength
feeds.
• It is important to introduce normal feeds at a reduced rate according to patient tolerance.

60
• Metabolic complications associated with excessive feeding are uncommon in enterally fed patients.
• nosocomial enteric infections associated with contamination of
feeds, which should be kept in sealed containers at 4°C and discarded
once opened.
• In all patients, it is essential to monitor intakes accurately as target
intakes are often not achieved with enteral nutrition.
• The complications of enteral nutrition are summarised in Summary
box 20.3.

-----------Parenteral nutrition--------------------
• Total parenteral nutrition (TPN) is defined as the provision of all
nutritional requirements by means of the intravenous route and
without the use of the gastrointestinal tract.
Indication:
• Parenteral nutrition is indicated when energy and protein needs
cannot be met by the enteral administration of these substrates.
• The most frequent clinical indications relate to those patients who have undergone massive resection of the
small intestine,
who have intestinal fistula or who have prolonged intestinal failure for other reasons

----------Route of delivery: peripheral or central venous access----------

• TPN can be administered either by a catheter inserted in the central vein or via a peripheral line.
• (In the early days ) hypertonic glucose--> had to be given into a central vein to avoid thrombophlebitis
• (in later days) These include the identification of safe and non-toxic fat emulsions that are isotonic;
pharmaceutical developments that permit carbohydrates, fats and amino acids to be mixed in single
containers; and a recognition that the provision of energy during parenteral nutrition should be a mixture of
glucose and fat and that energy requirements are rarely in excess of 2000 kcal/day (25–30 kcal/kg per day).
• These changes enabled the development of peripheral parenteral nutrition.

----------Peripheral----------
• Indication: Peripheral feeding is appropriate for short-term feeding of up to 2 weeks.

Technique:

1.Access can be achieved either by means of a dedicated catheter inserted into a peripheral vein and
manoeuvred into the central venous system (peripherally inserted central venous catheter (PICC) line) or
Adv:
○ The former method has the advantage of minimising inconvenience to the patient and clinician.
○ PICC lines have a mean duration of survival of 7 days.
Disadvantage
○ is that when thrombophlebitis occurs, the vein is irrevocably destroyed

2. by using a conventional short cannula in the wrist veins.

• In the alternative approach, intravenous nutrients are administered through a short cannula in wrist veins,
infusing the patient’s nutritional requirements on a cyclical basis over 12 hours.
• The cannula is then removed and resited in the contralateral arm.

• Peripheral parenteral nutrition has the advantage that it avoids the complications associated with central
venous administration, but suffers the disadvantage that it is limited by the development of
thrombophlebitis (Figure 20.7).
• Peripheral feeding is not indicated if patients already have an indwelling central venous line or in those in
whom long-term feeding is anticipated.

------------Central---------------
• When the central venous route is chosen, the catheter can be inserted
via the subclavian or internal or external jugular vein.

61
Different methods of gaining central access:
1. US (safest but not practical for everyone)
2. Cannulation of IJV/EJV: Most intensive care physicians and anaesthetists favour cannulation of internal or
external jugular veins as these vessels are easily accessible.
○ disadvantage : repeated movements result in disruption of the dressing with the attendant risk of sepsis.
3. The infraclavicular subclavian approach is more suitable for feeding , which optimises nursing care (Figure
20.8).
4.,Hickman lines : (for longer-term parenteral nutrition).
○ These are often inserted by a radiologist with fluoroscopic guidance or ultrasound.
○ They incorporate a small cuff, which sits at the exit site of a subcutaneous tunnel.
○ Adv: This is thought to minimise the possibility of line dislodgement and reduce the possibility of line
sepsis.

• Whichever technique is employed, a post-insertion chest x-ray is essential before feeding is commenced to
confirm the absence of pneumothorax and that the catheter tip lies in the distal superior vena cava to
minimise the risk of central venous or cardiac thrombosis.

5. An alternative technique for central intravenous access allows the PICC technique under ultrasound
guidance to cannulate the cephalic vein in the arm which facilitates passage of a catheter into
the bracheocephalic vein or superior vena cava. ○
○ Adv: it minimises the risks of insertion and ensures distance between the site of skin entry and the tip of
the catheter.
○ Disadv: Thrombophlebitis, however, can occur.

Catheters
1. Multi-lumen catheters can be used for the administration of TPN; one port should be employed for that
sole purpose and strict protocols of care employed.

----------Complications of parenteral nutrition----------

• The commencement of TPN may precipitate or accentuate underlying nutrient deficiency by encouraging
anabolism.
• Common metabolic complications include
○ fluid overload,: can be avoided by daily weighing of the patient. A weight change of >1 kg/day normally
indicates fluid retention.
○ hyperglycaemia,: common because of insulin resistance in critically ill patients. Even modest rates of
glucose administration may be associated with hyperglycaemia. Hyperglycaemic patients undergoing surgery
are known to run a substantially higher risk of infectious complications
○ abnormalities of liver function: the precise mechanisms are unclear, intrahepatic cholestasis may occur
and hepatic steatosis
and hepatomegaly have been reported.
Reducing the fat content or infusion of fat-free TPN may be required.
If liver enzymes continue to deteriorate, TPN should be temporarily discontinued.
○ vitamin deficiencies.

Other complications:
• overfeeding is a major factor in hepatic and other metabolic complications associated with TPN.
• Catheter-related sepsis
○ It may occur at the time of line insertion or afterwards by migration of skin bacteria along the external
catheter surface.
○Causes: manoeuvring of the catheter hub due to frequent manipulation is a common cause.
Seeding on the catheter at the time of bacteraemia from a remote source may also cause
catheter infection
○Dx: requires that the same organism is grown from the catheter tip as is recovered from blood and that
the clinical features of infection resolve on removal of the catheter.
Dx methods:

62
• Traditional methods: of confirming line sepsis have necessitated removal of the line with
subsequent bacteriological assessment.
• An alternative approach: is to use an endoluminal brush passed down the catheter and withdrawn into a
polythene sheath. The brush tip is cultured at the same time as performing blood cultures.
Catheter sepsis is confirmed if identical organisms are cultured from brush and blood.
• A second alternative : is to culture blood withdrawn through the catheter and compare this with peripheral
blood cultures. If the colony
count from the catheter sample is five or more times higher than that from peripheral blood then line sepsis is
probable.

Prevention of complications:
• Supplemental parenteral glutamine during parental nutrition should be considered, particularly in the
critically ill patient.

The complications of parenteral nutrition are summarised in Summary box 20.4.

Chap21: Post-operative care

The immediate postoperative period: recovery room

• The theatre team should formally hand over the care of the patient to the recovery staff.

• The information provided should include the patient’s name, age, the surgical procedure, existing medical
problems, allergies, the anaesthetic and analgesics given, fluid replacement, blood loss, urine output, any
surgical and anaesthetic problems encountered or expected.

• Patient’s vital parameters, consciousness, pain and hydration status are monitored in the recovery room and
supportive treatment is given (Figure 21.1).

• Specific monitoring, such as

○ Doppler flow for a free flap,

○ observations like neurological evaluation and

○ laboratory tests such as blood gas analysis may also be requested where necessary (Summary box 21.1).

**************SYSTEM-SPECIFIC POSTOPERATIVE COMPLICATIONS***************

----------Respiratory complications-------

The most common respiratory complications in the recovery room are

hypoxaemia, hypercapnia and aspiration.

Pneumonia and pulmonary embolism tend to appear later in the

postoperative period.

Postoperative hypoxia

• Hypoxia is defined as an oxygen saturation of less than 90 percent.

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• Clinical Features: Hypoxia may present as shortness of breath or agitation or as upper airway obstruction
(absence of air movement, seesaw motion of chest, suprasternal recession) or cyanosis or as a combination of
any of the above.

• Causes of Hypoxia in post operative period:

• Upper airway obstruction due to the residual effect of general anaesthesia, secretions or wound haematoma
after neck surgery.

•In obese patients or in those with acute or chronic lung disease,hypoxia develops more quickly.
• Laryngeal oedema from traumatic tracheal intubation, recurrent laryngeal nerve palsy and tracheal collapse
after
thyroid surgery.
• Hypoventilation related to anaesthesia or surgery.
• Atelectasis and pneumonia especially after upper abdominal and thoracic surgery (Figure 21.2).
• Pulmonary oedema of cardiac origin or related to fluid overload.

• Pulmonary embolism: this often presents with the sudden onset of chest pain and shortness of breath.

○ In the presence of a large embolism, there will be systemic hypotension,pulmonary hypertension and an
elevated central venous pressure (CVP) (Figure 21.3).

Treatment:

• Patients with hypoxia or imminent signs should be treated urgently.

• If the patient is breathing spontaneously administer oxygen at 15 L/min, using a non-rebreathing mask.

• A head tilt, chin lift or jaw thrust should relieve obstruction related to reduced muscle tone.

• Suctioning of any blood or secretions and insertion of an oropharyngeal airway may be needed.

• Call the anaesthetist as tracheal intubation and manual ventilation may also be needed.
Neck wound haematoma

• can become a life-threatening emergency, and must be evacuated immediately under local or general
anaesthetic.

• Along with the immediate management of hypoxia, appropriate antibiotics, chest physiotherapy and
bronchodilators will be needed to treat pneumonia.

• In the case of pulmonary oedema, diuretics should be started and a

cardiology opinion should be sought (Summary box 21.2).

**************SYSTEM-SPECIFIC POSTOPERATIVE
COMPLICATIONS***************

------Cardiovascular complications-------------
• Hypotension in the immediate postoperative period may be due to inadequate fluid replacement,
vasodilatation from subarachnoid and epidural anaesthesia or rewarming of the patient.
However, other causes of hypotension such as surgical bleeding, sepsis, arrhythmias, myocardial infarction,
cardiac failure, tension pneumothorax, pulmonary embolism, pericardial tamponade and anaphylaxis should be
also sought (Figures 21.4, 21.5 and 21.6).

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• Clinical features: Patients with hypotension are likely to have cold clammy extremities, tachycardia and a low
urine output ≤0.5 mL/kg per hour and low CVP.

• Txt: Hypovolaemia should be corrected with intravenous crystalloid or colloid infusions (see below under
Bleeding).

Myocardial ischaemia and infarction

General characteristics

• Patients with previous cardiac problems undergoing major surgery are at risk of developing an acute coronary
syndrome.

• They commonly present with retrosternal pain radiating into the neck, jaw or arms and may also have nausea,
dyspnoea or syncope.
• Typically, there is a ST-elevation in two continuous leads on the ECG or new left bundle branch block
(STEMI),though this may not always be present (non-ST-elevation myocardial infarction (NSTEMI)).

• However, serum troponin levels will be high in both types of MI (myocardial ischaemia and myocardial
infarction).

Txt:

• Start treatment with oxygen, glyceryl trinitrate, morphine and aspirin and involve a cardiologist.

• Beta-blockers and/or calcium antagonists may be started to reduce further episodes of ischaemia.

• Cardiologists may start coronary reperfusion therapy for STEMI in the form of primary percutaneous coronary
intervention or thrombolysis.
However, these should be discussed first with a senior due to the risk of bleeding after major surgery.

Arrhythmias
• Arrhythmia in the postoperative period can cause hypotension and ischaemia. Therefore, these patients will
need to be continuously monitored.

• Treatment should be delivered according to the Resuscitation Council peri-arrest guidelines, correcting
underlying causes including acid-base and electrolyte imbalance, hypoxia and hypercapnia (Summary box 21.3).

• Tachycardia (sinus or supraventricular) may be caused by anxiety, pain,

MI, hypovolaemia, sepsis or hypoxia in the postoperative period.

• Txt: Correct any underlying causes of the dysrhythmia and control the
heart rate with beta-blockers, amiodarone or cardioversion.

• Sinus bradycardia may be normal in athletes, but it may also be associated with hypoxia, preoperative beta-
blockers, digoxin and increased intracranial pressure.

• Txt: If the heart rate is 40 bpm or less, glycopyrrolate 0.2–0.4 mg or atropine 0.6 mg should be given
intravenously and the patient reviewed.

-------------Renal and urinary complications-----------------

---Acute renal failure----

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• About a quarter of cases of hospital-acquired renal failure occur in the perioperative period and are associated
with high mortality especially after cardiac and major vascular surgery (Table 21.1).

•Risk Factors:

○ Patients with known chronic renal disease, diabetes, liver failure, peripheral vascular disease and cardiac
failure are at high risk.

○ Perioperative events such as sepsis, bleeding, hypovolaemia, rhabdomyolysis or abdominal compartmental

syndrome can all precipitate acute renal failure (Summary box 21.4).

Treatment:

• If urine output is less than 0.5 mL/kg per hour for 6 hours,
○ check that the catheter is not blocked,

○ correct hypovolaemia,
○ correct metabolic and electrolyte disturbances, and stop nephrotoxic drugs.

• Stage I of kidney failure is associated with a rise in serum creatinine inc > x1.5 times from baseline or a greater
than 25 per cent decrease in GFR (glomerular filtration rate); aggressive treatment should be started at this
early stage to avoid further damage.

Urinary retention
• Causes:

○ Inability to void after surgery is common with pelvic and perineal operations or

○ after procedures performed under spinal anaesthesia.

○ Pain, fluid deficiency, problems in accessing urinals and bed pans, and lack of privacy on wards may
contribute to the problem of urine retention.

• The diagnosis of retention

○ may be confirmed by clinical examination and

○ by using ultrasound imaging.

• Treatment: Catheterisation should be performed prophylactically when an operation is expected to last 3

hours or longer or when large volumes of fluid are administered.

Urinary infection
• Urinary infection is one of the most commonly acquired infections in the postoperative period.

• Clinical features: Patients may present with dysuria and/or pyrexia.

• Risk factors:

○ Immunocompromised patients,

○ diabetics and

○ those patients with a history of urinary retention are known to be at higher risk.

• Treatment :

66
 ○ involves adequate hydration,
○ proper bladder drainage and

○ antibiotics depending on the sensitivity of the microorganisms.

**********COMPLICATIONS RELATED TO SPECIFIC SURGICAL SPECIALTIES***********

Abdominal surgery
• The abdomen should be examined daily for excessive distension, tenderness or drainage from wounds or
drain sites.

• In certain operations, such as those for intestinal obstruction, oesophageal and gastric procedures (but not in
lower intestinal operations), a nasogastric tube may be used.

• It is of particular value in those patients suffering from ileus or a marked level of altered consciousness who are
therefore liable to aspirate.

Paralytic ileus
• CF: Paralytic ileus may present with nausea, vomiting, loss of appetite, bowel distension and absence of flatus
or bowel movements.
Following laparotomy, gastrointestinal motility temporarily decreases.

• Treatment is usually supportive with maintenance of adequate hydration and electrolyte levels.

• Return of function of the intestine occurs in the following order: small bowel, large bowel and then stomach.

This pattern allows the passage of faeces despite continuing lack of stomach emptying and, therefore, vomiting
may continue even when the lower bowel has already started functioning normally.

Localised infection
Clinical Feature:

• An abscess may present with persistent abdominal pain, focal tenderness and a spiking fever.

• The patient may have a prolonged ileus.

• If the abscess is deep-seated, these symptoms may be absent.

• The patient will have a neutrophilic leukocytosis and may have positive blood cultures.

• Dx: An ultrasound or computed tomography (CT) scan of the abdomen should identify any suspicious
collection and will identify the subphrenic abscess which can otherwise be difficult to find (Summary box 21.5).

----------Orthopaedic surgery----------

• In patients who have undergone open reduction and internal fixation

of fractures, and especially if a tourniquet has been used,

the neurovascular status of the limb must be checked

○ every half an hour first in recovery and then

○ on the ward for at least a further 4 hours.

67
• Plasters should always be split for the first 24 hours (or until swelling starts to reduce) and

• the nurses given instructions to check and record distal circulation every 4 hours.

• If the patient has an external fixator, the pin sites should be checked daily for signs of infection.

• Radiographs are taken after the operation to check that the implants are correctly positioned and that
fractures remain reduced.

• Patients with compartment syndrome complain of pain out of proportion to that expected.

CF:

• It is not relieved by simple analgesics.

• Passive stretching of the muscles in the affected compartment produces severe pain.

• The limb is usually swollen and tense and, in the later stages, there may be
altered sensation distally.

• Distal pulses are only lost at a very late stage and so their presence does not
exclude a compartment syndrome.

• Dx: Intracompartmental pressure studies are not reliable so should only be

used in the unconscious patient.

The diagnosis is a clinical one and is made on suspicion not certainty (Summary box 21.6).

• Txt: If there is any possibility that a patient might have a compartment syndrome then all circumferential
dressings should be removed at once.

• If there is no immediate improvement in the pain, then a fasciotomy should be performed.

----------Neck surgery----------

Patients having neck surgery, e.g. thyroid surgery, must be observed for:
• accumulation of blood in the wound, which may cause rapid asphyxia.

• A check also needs to be made pre- and postoperatively for damage to the recurrent laryngeal nerve.

• The findings must be recorded in the medical notes.

----------Thoracic surgery----------
• Fluid intake should be restricted in patients undergoing a lobectomy or pneumonectomy as they are
susceptible to fluid overload in the first 24–48 hours postoperatively.

• Chest drains require regular review.

○ If the fluid in a chest drain swings then the drain has been inserted correctly in the pleural cavity.

○ If the chest drain continues to bubble, then a bronchopleural fistula probably exists.

• A haemothorax or pleural effusion (Figure 21.4) will reveal itself as a prolonged loss of blood or fluid,
respectively, into the drain.

• Cardiac patients require continuous electrocardiography monitoring postoperatively (Figures 21.5, 21.6 and
21.7).

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----------Neurosurgery----------
• Postoperatively, the patient should be kept under close observation.
• A rise in intracranial pressure may be signalled by a deterioration in the state of consciousness, as well as by
the appearance of new neurological signs.

• Some patients may have an intracranial monitoring device to allow for more sensitive monitoring.

----------Vascular surgery----------
• The patency of grafts and anastomoses in patients with femoropopliteal bypasses and abdominal aneurysmal
repairs needs to be checked by regular clinical assessment of the limbs and by Doppler ultrasound in the
postoperative phase.

----------Plastic surgery----------
• The viability of flaps is crucial and the perfusion needs to be monitored regularly.

• The blood supply may be compromised by position, dressings or collection of fluids or blood beneath the flap.

----------Urology----------
• Catheter patency must be checked regularly following urological surgery.

• In patients who have undergone transurethral resection of the prostate (TURP),

• continuous bladder irrigation may be used, and

• pulmonary oedema may develop if a large amount of irrigation fluid is absorbed into the circulation.

GENERAL POST OPERATIVE PROBLEMS AND MANAGEMENT

1. PAIN : (in anesthesia chap)

2. FLUID AND NUTRITION : (in nutrition chap)
3. NAUSEA AND VOMITING : (in IM)
4. BLEEDING :
● Patients BP , pulse , urine output , dressing and drains must be checked in first 24 hours after surgery
● In excess bleeding go for Clotting profile , bleeding time , blood cross match
● Imaging in massive bleeding : ct and ultrasound
● Management is done with pressure application then fluid resuscitation and radiological embolism
● Blood transfusion is given if Hb is less than 8 mg/dl or fibrinogen is less than 1 g/l or PT / APTT is 1.5
times normal . Platelet count should be maintained above 75×109 / L
● If transfusion reaction is suspected stop transfusing as it can cause hyperkalemia and fluid overload
5. DVT : (in IM)
6. HYPOTHERMIA AND SHIVERING :
● Anesthesia induces loss of thermoregulatory support
● Infusion of cold iv fluids can cause hypothermia
● Hypothermia leads to cardiac morbidity , hypercoagulable state , shivering that imbalance
oxygen supply and demand
● Treatment : rewarming
7. FEVER : (in IM)
8. PROPHYLAXIS AGAINST INFECTIONS :
● Patient having foreign body inserted or prosthetic valves surgery must have 3 dose antibiotics
● 1 is given 30 mins before knife to skin and 2 doses post operatively
9. PRESSURE SORES :

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 ● Site : sacrum , greater trochanter , heel
● Risk factors : poor nutrition , dehydration , immobile
● Management : early mobility , filter mattress
10. CONFUSIONAL STATE : this occurs after recovery from anesthesia i.e postoperative delirium (POD)
● Clinical features : anxiety , incoherent speech , clouding of consciousness , destructive
behaviour
● Risk factors : dementia , use of narcotics , benzodiazepine , alcohol , renal impairment ,
depression
● Precipitating factors : electrolyte and fluid abnormalities , blood loss
● Treatment : treat underlying cause , pain control and haloperidol
11. DRAINS :
● Drains prevent accumulation of blood , serous or purulent liquid
● Drains should be removed as soon as possible or when it is draining less than 25 ml/day
12. WOUND CARE :
● Within hours of wound closure dead space is filled with inflammatory exudate
● Within 48 hours epidermal cells bridge the gap
● Infected wound and hematoma requires treatment with antibiotics
● Skin clips and sutures are removed after 6-10 days of surgery
● Condition delaying the wound healing : vit C and vit A deficiency , steroids and uncontrolled
diabetes
13. WOUND DEHISCENCE : (in IM)
14. ENHANCED RECOVERY : post operative strategies for enhanced recovery include :
● Early physiotherapy and mobilization
● Early oral hydration and nourishment
● Good pain control
● Discharge planning and follow up

DISCHARGE OF PATIENT AND FOLLOW-UP :

● Discharge letter : diagnosis , treatment , laboratory result , complications , discharge plans , support
needed and follow up
.

Chap 22: Day- Case surgery

DAY SURGERY PATHWAY :

● Definition : admission and discharge of patient for specific procedure within 12 hours
● 23 hour stay : when patient requires an overnight admission
● the day surgery has increased due to advantage of health care delivery around the globe
● Provide patients preference and financial benefits by eliminating overnight hospital stay
● Unplanned overnight stays are prevented by ensuring patients fitness and safe home environment

70
TERMS USED IN AMBULATORY SURGERY :

● OUTPATIENT : not admitted to ward

● PROCEDURE ROOM SURGERY : surgery not requiring full sterile theatre
● DAY SURGERY : admitted and discharge within 12 hours
● OVERNIGHT STAY : 23 hours admission with early morning discharge
● SHORT STAY SURGERY : admission of upto 72 hours

SELECTION CRITERIA :

Day surgery be safely performed for minor and intermediate procedures

Procedures with intraoperative risks and complications require management in hospital integrated unit

Following are selection criteria :

1. MEDICAL CRITERIA :
following things are included in medical criteria

● AGE : there is no upper age limit . Healthy patients are managed with day surgery
● COMORBIDITY : stand alone unit often confine their criteria to ASA 1 and 2 , ASA 3 are more suitable
for hospital integrated unit .
cardiac , respiratory complications and HTN > 180/110 exclude day surgery

● OBESITY : BMI >30 is considered obese . BMI upto 40 for surface procedures and 30 for laproscopic
procedures is acceptable in advanced units

2. SURGICAL CRITERIA : patient undergoing procedure for 2 hours can safely undergo day surgery when
there is suitable control over pain and eating drinking
3. SOCIAL CRITERIA : suitable home circumstances , appropriate toilet facilities , home journey of less
than an hour , availability of adult care taker

PREOPERATIVE ASSESSMENT :

● Evaluation and optimization of patients fitness for surgery is called pre-op assessment
● Measurement of BMI , BP and medical history

PERIOPERATIVE MANAGEMENT :

● SCHEDULING : major procedures are scheduled early in the morning list to allow time for maximum
recovery . Complex cases may be delayed if day cases are scheduled first and vice versa

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 ● ANESTHESIA AND ANALGESIA : multimodal analgesia is required eg giving full oral dose paracetamol
and nsaid like ibuprofen (if no contraindication) -----> then TIVA (propofol) and short acting opiod (
fentanyl , alfentanil) is given in perioperative period
Avoid long acting opiod morphine to reduce risk of nause and vomiting

● POST OPERATIVE COMPLICATIONS : following complications are common :

1. Inadequate pain control

2. Heamorrhage : reactionary hemorrhage in 4-6 hours due to slippage of ligature and
secondary hemorrhage after 24 hours due to vessel erosion by infection
3. Nausea
4. Vomiting

Management of post op nausea and vomiting (PONV) :

patient with severe nausea and vomiting

Give IV fluid to hydrate the person (10-15 ml/kg/hr) and IV antiemetics (cyclizine and prochlorperazine)

Review after 1 hour

If still problem give second antiemetic eg ondansetron

Hydrate the patient and offer choice either to go home or stay in hosp

SURGERY :

● The risk of post op hemorrhage after tonsillectomy and laproscopic surgery is major cause of
overnight hospital stay
● Good surgical procedure requires minimal tissue traction and maintain good hemostasis
VOLUME SURGERY :

40% can be performed as day case surgery

● ABDOMINAL : anal lesion excision , hemorrhoidectomy , hernias , lap chole , fundoplication

● BREAST : mastectomy , sentinal nodes excision
● GENITOURINARY : prostectomy , orchidectomy, circumcision
● ORTHOPEDIC : carpel tunnel release , fasciotomy , therapeutic arthroscopy
● VASCULAR : varicose vein procedure , sympathectomy

DISCHARGE CRITERIA :

● Vital signs stable for 1 hour

● Correct orientation to time place and person

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 ● Adequate pain control with oral analgesia
● Know how to use analgesia
● Ability to dress and walk
● Minimal nausea and vomiting
● Taking oral fluids
● Minimal bleeding from wounds
● Has passed urine
● Has adult care taker at home for next 24 hours
● Emergency contact number supplied
● Written and verbal instructions about post-op care

Unit 4

Chap23: INTRODUCTION TO TRAUMA

WHAT IS TRAUMA:
• Definition: Trauma is the study of medical problem associated with physical injury i.e deleterious
effects of kinetic energy on human frame
• Variety of forces could lead to injury: thermal, ionizing radiations , chemicals , mechanical etc.
• The force involved in mos
• t of the injuries is mechanical
THE SCALE OF THE PROBLEM:
• trauma is the leading cause of death and disability in first 4 decades of life and is the 3rd most
common cause of death overall
• major vectors of traumatic injury→RTA, falls and intentional violence
• Injury severity score (ISS): major trauma→ISS>15
• Motor vehicle accidents are not the only source of trauma (young people mostly by RTAS caused by
high energy transfer), but the elderly fall victims from major group of hospital admitted injuries e.g.
proximal femoral fracture of which 30% die within 1 year of trauma.(low energy transfer→sustain
injuries from falls, fragility fractures)
• In case of children non accidental injury (NAI) e.g. child abuse is also the cause of death
• Fragility fractures are increasing as well
THE MANAGEMENT OF TRAUMA:
• IMPORTANCE OF TIME:
This is the most important feature in case of trauma. From time of impact to subsequent development of
pathology and body response up till recovery or death all have specific time frames:
1. At time zero patient is at normal baseline(seconds prior to application of external injury force).
Subsequent events(acute physiological response to injury, body;s internal mechanisms to maintain
homeostasis, healing, actions by health professionals) follow a timeline. Therefore, critical time
window in which we can intervene for a positive treatment outcome, before loss of compensatory
mechanisms.
2. Interventions:
i)emergency (life saving)
ii)acute (restoring hemodynamic stability)
iii)delayed or semi-elective, focusing on treatment of post fracture fixation complications
3. Seriousness and immediate impact of a specific clinical condition should be prioritised and treated in
systematic approach(what kills first should be managed first)
Advanced trauma life support (ATLS) works on the ‘time dependence principle’ defining management as
ABCDE
• airway
• Breathing

73
 • Circulation
• Disability
• Environment exposure
The overall timeline is divided into two parts:
1. Assessment time or diagnosis time: understanding and assessing the injury helps in making diagnosis
2. Response time: once diagnosis is made the life saving manoeuvres are matter of seconds to apply
Example of extradural hematoma displayed by figure:

Avg response time from diagnosis to surgical interventions is measured in hours. If one waits for clinical
symptoms to occur then response time will decrease deteriorating the condition.This means the response
should be initiated before we're sure of diagnosis to save life of patient

Time not only plays role in multiple injury patient but also for long term management in old age patients with
underlying cardiac, respiratory and other conditions which requires management and also for minor injuries to
manage treatment plan

But this may sometimes result in missing problems therefore all x-rays are viewed by radiologists and if their
findings differ from clinical findings then patient is recalled and assessed.
All clinical conditions characterised by a dynamic process. This implies that observation and analysis can
change rapidly, to an extent that interventions have to be modified accordingly. Therefore, initial primary
survey followed by secondary survey and tertiary clinical assesement, even after acute phase of treatment has
been completed successfully.

A plain language summary of the situation directed at the patient’s family doctor, but intelligible and available
to the patient’s or carers, should be available within 24 hours.
ASSESSMENT AND RESPONSE:
1. ASSESSMENT OF TRAUMA:
Initial assessment (besides clinical examination): analysis of interactions between the patient, the
mechanism of injury and the extent of injury sustained
‘Mechanism+patient=injury’
E.g.: 50-year-old restrained passenger in car involved in head on collision with another vehicle may sustain rib
fractures, sternal fracture, cardiac contusions, abdominal injuries. Clinician knowing mechanism can proceed
quickly in making the diagnosis and starting treatment.
If any factor is not adding up to produce outcome there is some misjudgement (for example reported
mechanism is underestimated) so, look for the reason
A. MECHANISM: it might be blunt or penetrating
MECHANISM OBVIOUS FEATURES COVERT INJURIES

Left sided impact from RTA • Lateral compression of pelvis • Splenic rupture
• left sided pneumothorax • extradural hematoma

Flexion distraction (lap • Chance fracture of lumbar • Duodenal rupture

belt) spine • Popliteal artery disruption
• dislocated knee • Cervical spine fracture

74
 • head injury

Electrocution • Burn on hand and collapse • Posterior dislocation of

shoulder

Dashboard impact • Knee wound • Posterior dislocation of hip

PENETRATING INJURIES:
1) Those caused by firearms
2) Those caused by sharp objects (necessary to take into account the length of the sharp object,
its surface area and the size of the entry point)
• incisional injury is readily evaluated for distal perfusion, peripheral nerve function, tendon
and muscle function
• If joint is penetrated consequences are different as there is high risk of septic arthritis, so
time frame is important in management
• All this requires knowledge of anatomy, esp. imp in penetrating wounds over torso, as not
easy to establish track sharp object has followed. Should be remembered abdominal
structures extend higher than anticipated, and as high as the level of the 5 th rib in expiration.
• Many abdominal contents penetrate into chest too
• Even cardiac injuries are treatable if recognized and managed early

• Firearms induce penetrating injuries, more difficult to comprehend than incisional injuries caused by
sharp objects
• Low velocity injuries also act as penetrating injuries under formula of E=1/2mv2 e.g. low velocity
bullet acts as knife injury
• High energy bullet injury crushes particles of body coming in its way producing lateral acceleration
away from the point of impact, this produces cavities of either type in the body:
▪ Permanent cavity: tissues remain away from the point of impact
▪ Temporary cavity: one that lasts for millisecond and not apparent on examination,
can contain foreign material
BLUNT INJURIES:
• Direct injuries: damage occurs at the site of impact e.g. hitting with nightstick cause
ulnar fracture
• Indirect injuries: damage occurs at distant site after transmission of force e.g. fall on
an outstretched arm here force is transmitted by soft tissues to bone so associated
injuries like radial head dislocation should be sought too
• Effects of direct mechanisms are easier to comprehend than those of indirect ones.
B. PATIENT FACTORS: children, adults and elderly are 3 different groups, so we anticipate different
injuries in these groups even if mechanism is same
• Factors like patient on anticoagulation therapy or osteogenesis imperfecta are responsible for
outcome of injury
• Past medical history, medication and allergy risk directs treatment and assessment.
C. INJURY:
EXTERNAL FACTORS
• Most obvious injuries are those which are visible externally
• E.g. Bruising to the scrotum of a motorcyclist suggests pelvic fracture, finger shaped bruises
on child’s arms or thighs suggests NAI, presence of a seatbelt mark on lower abdomen of
patient involved in car crash→damage inside abdomen. In burn injuries looking at facial hair
and nasal hair damage helps to call anesthetist before laryngeal edema occurs.

COVERT OR HIDDEN FACTORS

1. MECHANISM: sometimes when above formula fails to give reason for injury then look for hidden
factors
• Sometimes in order to escape illegal activities patients fabricate the mechanism
• Abuse cases

75
 • Child abuse and criminal violence
• Patients unable to give history of events e.g. unconscious
Misleads the clinician and leads them to look for wrong patterns of injury
Parameters that should alert clinician and raise suspicion of NAI:
• External signs of injury not consistent with mechanism reported
• Long bone fractures in a pre-ambulatory child
• Inconsistent or changing history
• Aggressive or unusual behaviour of carers at interview
• Posterior rib injuries
Clinician also should protect patient from further harm
2. PATIENT: if mechanism and injury are well known but not fitting in formula there is something in
patient that needs diagnosis
• Previous pathology e.g. bone neoplasia
• E.g. in old age patient the overt injury is femoral fracture, but hidden injury is TIA which leads
to fall
3. INJURY: when analysis of formula has failed to identify hidden injury 2 methods are used
• Look everywhere approach: this is called secondary and tertiary elements of ATLS and
involves a detailed secondary survey from top to bottom and at different time points (chest
and pelvic x-ray are part of primary survey) and includes CT, MRI, echo and U/S
• The focused exclusion approach: certain areas missed easily like scaphoid fracture, peri
lunate dislocation, posterior shoulder dislocation, tarsometatarsal dislocation are included in
this

2. RESPONSE TO THE TRAUMA:

• PATIENTS RESPONSE TO INJURY:

patient’s hemostatic mechanism responds to injury
o Temperature falls due to hemorrhage, exposure andinactivity, so temperature must be
maintained if thermoregulatory mechanism of body fails (covering patient with appropriate
blankets during transportation, resuscitation and in the theatre environment)
o Oxygen saturation is checked and maintained (inspired oxygen or ventilation)
o If BP falls the body response readjusts the blood to vital organs causing vasoconstriction in
other organs
o Blood loss→endogenous clotting factors are activated. Traumatised lung parenchyma cannot
tolerate surplus fluid, so reduction in crystalloid administration, and early transfusion of
blood products. Also, quickly identify and stop source of bleeding.
o Another important response to injury→activation of immune-inflammatory system.
Sometimes extravasation of lymphocytes takes place with possible auto destruction. clinical
decisions should aim to minimise risk of exaggerated immune-inflammatory response.
• MEDICAL RESPONSE TO INJURY:
o INITIAL MANAGEMENT:
▪ Call for trauma team if needed acc to ATLS protocol
▪ Equipment is adjusted
▪ Assess airway, respiration, BP, pulse and consciousness
▪ All patients should undergo physiological triage to reduce risk of being wrongly
assigned
o BEYOND THE FIRST HOUR:
▪ Primary survey of ATLS is associated with identification of problem
▪ Earlier only early total care philosophy was used, now damage control surgery is
also there
▪ Damage control surgery stages:
1)resuscitation 2) hemorrhage control 3) decompression 4) decontamination 5)
fracture splintage
• In the DCO concept, initially any long bone fractures and the pelvis are temporarily stabilised with the
use of external fixators. Definitive stabilisation of the fractures would take place usually 4 days later
when physiological state of the patient has been stabilised

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 CRITERIA FOR DCS (DAMAGE CONTROL SURGERY) CRITERIA FOR ETC (EARLY TOTAL CARE)
HYPOTHERMIA:<34◦C STABLE HEMODYNAMICS
ACIDOSIS:PH<7.2 NO NEED FOR VASOACTIVE, INOTROPIC SOLUTION
SERUM LACTATE >5MMOL/L NO HYPOXEMIA, NO HYPERCAPNIA
COAGULOPATHY SERUM LACTATE<2MMOL/L
BLOOD PRESSURE<70 MM HG NORMAL COAGULATION
TRANSFUSION APPROACHING 15 UNITS NORMOTHERMIA
INJURY SEVERITY SCORE>36 URINARY OUTPUT>1 ML/KG/HOUR

▪ Definitive surgery only carried out if patient is able to tolerate it

▪ Laparotomy, femoral nailing, tibial nailing is done first
▪ Monitor temperature, coagulation, base excess
▪ Record the plan on white board in operation theatre

LOCAL PROTOCOLS AND GUIDELINES:

• Regional guidelines refer to small areas of practice such as antibiotic prophylaxis for open fractures,
mass transfusion, pharmacotherapy for coagulation disturbances, steroids for spinal cord injuries,
clearance of cervical spine and angiographic embolization of pelvic fractures
• early policy for managing spine and the polytrauma is summarized as "suspect and protect"
• The policy of "clearing" the spine in obtunded patient:
o Cervical spine: fine quality CT scan of C0-T4 in coronal, sagittal and axial plane and assess the
power ratio of atlanto occipital junction
o Thoracolumbar spine T4 to distal: AP and lateral CT
• Pre-empt time-limiting steps to avoid delay
• Respond to evolving condition of patient
• Use charts to plot trend
PLANNING OF INDIVIDUAL OPERATION:
• the central part of surgeons’ work is operation
• Make rehearsals of a procedure this may allow hazards to be predicted and avoided
• White board practice in theatre
(Cephalosporin or gentamicin is given at induction)
• The appropriate surgical equipment’s for plan A, B, C should be clearly identified and kept in
close proximity to the OT

Diagnosis: open segment Equipment: Problem/ solution:

fracture left tibia • Radiolucent • Segment viable but too narrow for
table nail / proceed to bridge plate or
Procedure: • Tourniquet external fixator
• Excise wound with • Soft tissue tray • Segment nonviable / remove
plastic • Washout tray segment and put temporary
• Plan soft tissue cover (9litre washout) external fixator
• Secure nail entry • Reamer • Nail causing malalignment / remove
point • Cannulated tibial nail and place blocking screw
• Ream segment IM nail
through traumatic
wound In reserve: external fixator
• Statically lock nail / long plate
• Dress wound with a
bead pouch
• Continue antibiotic
until definitive wound
cover
RESPONSE TO MECHANISM OF INJURY:
• once the mechanism of injury is known strategy is made to prevent further incidents

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 • Legislation and education are required
RESPONSE TO PATIENT FACTORS:
• Older patients may be vulnerable to injury, owing to poor bone stock and other comorbidities
• Use of hip protectors and management of osteoporosis, addressing early the medical comorbidities
e.g. cataract surgery
• Treat underlying malignancy if that’s the primary cause of secondary trauma

Chap24: EARLY ASSESSMENT AND MANAGEMENT OF TRAUMA

early assessment and management of severe trauma begins in the prehospital environment. Forewarning the
receiving hospital allows activation of trauma team to prepare for the patient’s arrival.
Key information in pre-alert includes: basic demographic information (age and gender), mechanism of injury,
injuried identified and vital signs, including respiratory rate, pulse, bp, GCS.

EPIDEMIOLOGY:
• Trauma is most common cause of death between 1-44 years worldwide
• In addition to mortality it can cause long term complications and huge economic impact.
ROLE OF THE TRAUMA TEAM:

• Composition of team: doctors from emergency department, anaesthetics and/or critical care,
orthopaedics and general surgery. Now, radiologists and hematologists too.
• Code red trauma call-most severely injured patients.
• Trauma team:
• allows simultaneous and efficient application of ATLS principles to rapidly identify and treat life-
threatening pathologies, should be led by the most senior clinician, the most senior clinicians from
each specialty should attend code red trauma calls, the team leader should be trying constantly to
anticipate the next move.
ADVANCED TRAUMA LIFE SUPPORT (ATLS) :

• primary survey with simultaneous resuscitation: identify and treat what is killing the patient
• Secondary survey: proceed to identify all other injuries
• Definitive care: develop a definitive management plan
MECHANISM OF TRAUMA:

BLUNT:
o The most common cause of blunt trauma is motor vehicle accident e.g. car bonnet
o 10% increment in speed cause 40% rise in cases of fatality
o Use of seat belt reduces the risk of mortality by 45% but increases specific pattern of injury e.g. 4x
increase in thoracic trauma and 8x increase in abdominal trauma
o Factors reducing trauma: air bag, children less than 12 years be seated in back seats and <1 year in
rear facing child safety seats
PENETRATING:
o E.g. knife and gunshot injury
o Important factors are proximity to visceras, velocity of penetration, distance from the weapon to the
wound.
BLAST:
o E.g. bomb
o Terrorism is major phenomenon
CRASH:
o E.g. building collapse or plane crashes

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THERMAL:
o E.g. burn injury
ALCOHOL AND DRUGS:
o Drivers with illegal alcohol consumption increase risk of accidents.

ASSESSMENT AND MANAGEMENT OF SERIOUS INJURIES:

"Trimodal distribution of death " the 3 peaks as follows:
1. Immediate: 50% of all die due to massive head injury or cardiopulmonary insult
2. Early: death within first few hours due to failure of oxygenation of tissues or circulatory failure
3. Late: 20% die due to multiorgan failure or sepsis

PRIMARY SURVEY AND RESUSCITATION:

cABCDE PROTOCOL:

c: exsanguinating external hemorrhage:

• exsanguinating external hemorrhage from massive arterial bleeding needs to be controlled before airway
is managed. Most are due to gunshot wounds and blasts and are mainly seen in military practice.
• Bleeding must be controlled immediately by application of packs and pressure directly onto the bleeding
wound and artery. Hemostatic dressings that augment local coagulation are now available
• Failure to control bleeding in limb, then tourniquet applied proximal to the wound
• Once tourniquet is applied the limb becomes ischemic, the time for which the tourniquet is applied must
be recorded on the patient and pt requires urgent surgical control of bleeding to reperfuse limb

2.AIRWAY WITH SPINE PROTECTION:

• all trauma patients should have cervical spine immobilised and protected throughout
• immediate assessment of airway is made. If compromised, then:
a. Clearing the mouth and suctioning secretions or blood
b. Jaw thrust, chin lift or insertion of oropharyngeal or nasopharyngeal airway.
c. Nasopharyngeal or guedels airway is used provided that the patient will tolerate it
d. Head trauma with GCS <8 requires intubation
e. Consider every patient with head trauma having cervical spine injury until proven otherwise
f. Check the vocal response of patient to check airway patency

3.BREATHING AND VENTILATION:

Oxygen 100 % is administered using high concentration masks, all patients should receive high flow oxygen

a. Check functioning of chest wall, lungs and diaphragm for adequate ventilation
b. Check for signs of surgical emphysema, dilatation of neck veins, asymmetry of chest and excessive
respiratory efforts
c. Percussion and auscultation should be performed both in front and back of chest wall after log rolling
d. Life threatening injuries include: tension pneumothorax, massive hemothorax, flail chest and open
pneumothorax
I. Tension pneumothorax is immediately decompressed
II. Hemothorax and pneumothorax requires chest drains
III. Major vessel bleeding requires control

4.CIRCULATION AND CONTROL OF BLEEDING:

3 critical clinical observations
a. Conscious level: ALOC without significant head injury shows inadequate cerebral perfusion

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 b. Skin colour: pale skin and warm peripheries show hypovolaemia. Hypotensive patients treated as
hypovolemic until proven otherwise. Simultaneous fluid resuscitation and identification of
hemorrhage is done
c. Pulse: rapid thready pulse show hypovolaemia
d. While primary survey is being carried out secure 2 iv cannulas for fluid resuscitation
e. Blood should be taken for cross match and laboratory assessment including Hb, and venous lactate
f. A pelvic binder should be applied to all hemodynamically unstable patients following blunt trauma
and not removed until pelvic fracture has been excluded.

(27Ed) PERMISSIVE HYPOTENSION, MASSIVE TRANSFUSION PROTOCOLS AND TRANEXEMIC ACID

• Initial aim of resuscitation: maintain blood supply to vital organs

• For a short time achieved with a target systolic blood pressure of 70-90mm Hg (if head injury
>90)
• Done by small boluses of IV fluids (e.g. 250ml of O- blood or NS if blood not available), should
result in palpable radial pulse
• Excessive IV crystalloid or colloid solutions avoided because they cause hemodilution,
increase coagulopathy, increase risk or ARDS
• Key to this approach of permissive hypotension is that it is time limited, source of bleeding
identified ASAP
• Tranexamic acid decreases risk of mortality from bleeding. 1d given IV over 10 minutes,
followed by 1g dose over 8 hours. Given to all trauma patients suspected of having
significant hemorrhage including those with systolic bp of <110mm Hg or pulse of
>110/minute. Needs to be given within 3 hours.
IDENTIFICATION AND MANAGEMENT OF HEMMORHAGE
• Sites of major hemorrhage in trauma patients are the chest, abdomen, pelvis, long bones and external
hemorrhage
• Examinations and investigations should aim rapidly to confirm or exclude bleeding from these sites
• Whole body CT scan (WBCT) is the gold standard investigation in patients with signs and symptoms of
multiple injury or deranged physiology. A provisional hot report can be issued within minutes to
identify immediate life-threatening pathology. More detailed definitive report available within 30-60
mins.
• Some patients are so hemodynamically unstable that they need immediate surgical control of
hemorrhage before CT. The most likely sources are abdominal or pelvic bleeding. Chest radiograph
excludes catastrophic intrathoracic hemorrhage. Immediate pelvic radiograph is essential but should
not delay transfer to OT. A focused abdominal sonography for trauma (FAST) scan useful in this
scenario
• All patients undergoing immediate laparotomy in the OT should have a pelvic binder applied and not
removed. A correctly positioned pelvic binder at level of greater trochanters does not obstruct trauma
laparotomy. WBCT scan done after surgical control of hemorrhage.
5.DISABILITY:
a. Pupils are monitored for size and reactivity to light
b. GCS is measured
c. Patient observed if moving all 4 limbs
d. Core temperature is recorded
e. Patients are managed with cervical spine protection and protection of thoracolumbar spine using
standard log roll techniques until spinal injury excluded.
f. ALOC etiology: head trauma, Hypovolaemia, hypoglycaemia, alcohol these must also be excluded
6.EXPOSURE:
a. Spinal alignment must be assessed
b. Exposure can exacerbate hypothermia so warm air and blanket must be arranged. Also warmed
fluids for resuscitation
c. Trauma patients are frequently hypothermic which increases coagulopathy

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 d. (27ED) Log-rolling patients with severe pelvic fractures harms patient by disturbing established
blood clots, therefore, should not occur until pelvic fracture has been excluded.
e. If patient needs to be moved during primary survey, a 20 ͦ roll with inline spinal stabilisation used.
Nowadays ‘scoop stretchers’ used in place of this
f. Formal log rolling deferred after primary survey except in penetrating trauma where important to
identify presence of posterior torso wound.
g. Mechanical testing of pelvis in the ER (springing of the pelvis) should never be performed, as it can
disrupt blood clots.
ADJUNCT TO PRIMARY SURVEY:
o Blood tests: cbc, uce, clotting profile, glucose, toxicology, blood cross match
o ECG, pulse oximetry, ABG
o Two wide bore cannulas for IV fluids
o Urinary and gastric catheters
o Radiographs: CT, U/S and arteriography of spine chest and pelvis

SECONDARY SURVEY:
The secondary survey does not begin until after the primary survey has been completed, and all potentially
life-threatening injuries have been dealt with
The purpose of the secondary survey is to identify all other injuries and to perform enough head to toe
examination (AMPLE) (after life threatening injuries have been identified and managed during the primary
survey)
Patients may be intubated and unresponsive at this time, limiting accuracy, so in such patients’ tertiary survey
when extubated and alert to identify missed minor injuries
• Allergy
• Medication including tetanus status
• Past medical history
• Last meal
• Event of the incident
•
SECONDARY SURVEY PHYSICAL EXAMINATION:
1. Head and face: look for penetrating injuries, head fracture, bleeding, maxillofacial fracture, ocular
injury, zygomatic fracture, bleeding
2. Neck: inspect and palpate cervical spine anteriorly and posteriorly for hematoma, crepitus,
tenderness and gap on palpation
The spine is held immobilised until formally cleared clinically and radiographically
3. Chest: perform full percussion and auscultation of chest
4. Neurological: perform GCS regularly
5. Abdomen and pelvis: look for distension, bruising, penetration of wound, tenderness and guarding
Palpate the iliac crests for pain which might indicate pelvic instability, resulting from ring fractures
6. Extremities: deformed limb should be manipulated into near anatomical alignment and neurovascular
status is checked
It is often here that attention is diverted immediately when a dramatic injury to the limbs presents
itself (Figure 24.3). It is important to note that, unless there is severe haemorrhage, the injury to the
limb is not immediately life threatening and focus must be maintained on the primary survey and
‘ABCDE’ sequence
7. Log roll: this is performed to inspect the back and spinal stability
Inspect and palpate the entire spine from occiput to sacrum, looking and feeling for tenderness and
bony abnormalities. Identify any penetrating injuries or exit wounds from gunshot injuries and cover
these once they have been photographed. Percuss, palpate and auscultate the posterior chest wall.
RE-EVALUATION:

• it is an integral process in initial assessment of major trauma

• Continuous monitoring of vitals and urinary output

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 • It is also very important to stress that, should the patient’s condition change at any time during the
initial assessment, then the primary survey must be repeated from the beginning, since additional life-
threatening injuries may be declaring themselves
DEFINITIVE CARE AND TRANSFER:
• only given when initial care and resuscitation is completed
• early transfer to an appropriate care facility is the most important contributor to successful outcome
• Patient must be hemodynamically and cardiovascular stable
• Before definitive surgery life saving surgery is performed called " damage control surgery "(control of
hemorrhage, decompression of cavities, revascularisation of ischemic organs and limbs and removal of
contamination)
• Early total care- definitive management of patients’ injuries within 36 hours of injury after initial
resuscitation
• Damage control surgery- simultaneous resuscitation with early rapid life and limb saving surgeries
• DCS in abdomen-packing and control of hemorrhage, debridement and resection of devitalised tissue
and removal of contamination by foreign body or faeces.
• DCS (orthopaedic)- debridement of severe open fractures, rapid temporary splintage or stabilisation
of long bone fractures and decompression of limb compartment syndrome
• Revascularisation of a limb following arterial injuries appropriate for isolated injuries but in the severe
polytrauma patient amputation is better, as it increases threat to life.
• Physiological indices used to measure response to resuscitation: pulse rate<100/min, normal bp and
respiratory rate, urine output>30ml/hour. Should not have hypothermia (<35 ͦ C), no acidosis on
ABGs, normal coagulation screen.
• Lactate levels good indicator of tissue perfusion, should return to normal
VENOUS LACTATE
• Useful marker of resuscitation and physiological state.
• <2 mmol/L-resuscitated and suitable for early total care
• >3mmol/L- under resuscitated and should have further resuscitation or DCS if urgent surgery
• If 2-3mmol/L- trend should be noted (upwards or downwards) and other physiological markers
considered, to see if patient is suitable for definitive surgical procedures

SURGICAL SUBGROUP CONSIDERATIONS:

The initial management of any traumatised individual initially follows the same methodical ‘ABCDE’ pathway.
However, there are three very important subgroups which require special consideration: the paediatric, the
elderly and the pregnant.

1. PEDIATRIC TRAUMA:
injury is the leading cause of mortality among children and adolescents. Children have smaller BMI so there
may be greater force applied per unit surface area for given injury .and there is higher risk of hypothermia in
children
Airway and cervical control:
I. children have anteriorly placed smaller funnel shaped larynx, floppy epiglottis, short trachea
and large tongue
II. Nasopharyngeal intubation in children younger than 9 years is not performed as it may
damage cranial vault
III. Children have cricoid ring providing adequate seal so cuffed tubes are rarely used

Breathing and ventilatory control:

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 I. Resp rate dec with age.
II. Hypoxia is common cause of cardiorespiratory arrest causing respiratory
acidosis (hypoventilation causes a respiratory acidosis, which is the most common acid–base
disturbance in the injured child
III. Flail chest and aortic rupture is uncommon in children due to elastic nature of chest
IV. Pulmonary contusions are not evident in the early chest x-ray, but as before, re-evaluation is
necessary for the following 24–48 hours.
Circulation and hemorrhagic control:
I. Hypotension is very late due to physiological adaptations in childrens body
II. IV access should be made first. If it fails, we go for intraosseous access (uninjured proximal tibia
(ideal route) or distal femur) in children younger than 6 years of age

Normal vital signs by age Pulse (bpm)↓ Systolic BP (mm of Hg)↑ Respiratory rate ( breaths per minute )↓

Infant (<1 year) 160 80 40

Preschool (<5 years) 140 90 30

Adolescent (>10 year) 120 100 20

Disability:
I. Head injury is most common cause of death and disability
II. Diffuse axonal injury is more common in children than in adults
Exposure:
surface area to volume ratio make children vulnerable to environmental changes (i.e hypothermia)
I. Txt: rewarming via overhead lamps or heaters, warming blankets and warm IV fluids

PAEDIATRIC SECONDARY SURVEY:

This is essentially similar to the head to toe examination described for adults.
common injuries in children are
• Duodenal hematoma and pancreatic injury secondary to bicycle handlebar striking right
hypochondrium
• Small bowel perforation and mesenteric injury
• Bladder injury due to pelvic shallowness
Urine output by age: (<1 year produces 2 ml/kg/hr, 1-5 year produces 1.5 ml , 6-16 year produces 1
ml)
• Chance fractures of lumbar spine due to restraint from a lap belt.
• Child abuse: non accidental injury (NAI) are considered when there are certain features from both
the history and examination that may point towards NAI, and early identification and alerting of child
protection authorities is essential
o Repeated hospital visits with minor trauma
o Late presentations
o Vague or inconsistent history from guardians
o Child's resistance to examination
o Bite marks, finger marks, belt marks, cigarette burns
o Multiple fractures of different ages
o Perineal injury
o ICH without motor vehicle accident history

2. TRAUMA IN ELDERLY POPULATION:

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 An elderly patient may only be surviving with just enough physiological reserve, and any injury, no matter
how insignificant, may prove fatal (Figure 24.5). Initial assessment and, more importantly, management
has to be even more meticulous in this subgroup of patients.

• Airway and cervical spine control: stiffness in cervical spine cause difficult intubation
• Breathing and ventilation:
I. Patient with COPD may require early intubation but keeping in mind that there might be difficult
extubation
II. Pulmonary complications like pulmonary edema, pneumonia and atelectasis are common
• Circulation:
I. With age above 65 half of population has coronary artery stenosis and heart rate decreases
making it difficult to diagnose ongoing hypovolemic shock
II. Retroperitoneal hemorrhage occurs in minor pelvic injuries
• Disability:
I. Cerebral atrophy is common with increasing age. This leads to increased space within the cranium
and therefore some protects brain from contusions
II. Pre-existing medical conditions may be a cause of confusion in the elderly making assessment of
consciousness difficult after head trauma
III. Osteoporosis increases risk of spinal fracture
IV. Spinal injury may also be more common because of pre-existing stiffness and spinal stenosis. This
rigidity predisposes the patient to central and anterior cord syndromes.
• Exposure: elderly have reduced thermoregulatory abilities. Thus the elderly patient should be protected
from the effects of hypothermia during the initial assessment and management.
SECONDARY SURVEY: (AMPLE)
• Reduced skin fragility of elderly ptnts can result in pressure sores if spinal board is used for too long
• Increase risk of femoral fracture -> humerus -> wrist fracture (Mc to Least common)

3. TRAUMA IN PREGNANCY:
• fundamental principles of ATLS remain same but obstetrician is brought on board for
maternal and fetal care
• During primary survey uterus of 3rd trimester pregnant lady is manually displaced to the left
to reduce compression on IVC this improves cardiac output
• Signs of hypovolemia (due to massive blood loss) are delayed in pregnant ptnts due to inc
intravascular volume in preg.
This is important to understand and recognize since the mother may appear relatively stable
while the fetus is in distress due to a lack of placental perfusion
• Rh negative mothers are given Rh immunoglobins

Chap 25: Emergency Neurosurgery

****PHYSIOLOGY AND PATHOPHYSIOLOGY*****

-----Cerebral blood flow-----

• Ischaemia results when this rate drops below 20 mL/min, and even lower levels will result in infarction unless
promptly corrected
• In the normal brain, variations in vascular tone maintain a constant CBF across a range of MAP between 50
and 150 mmHg, and a corresponding range of CPP, a process termed ‘cerebral autoregulation’.
• The limits of this range are elevated in patients with chronic hypertension.
• Neurosurgical emergencies, especially head injury, lead to brain swelling, bleeding and
hydrocephalus. The common pathophysiological pathway is then elevated ICP and reduced CPP and CBF.

-----ICP & Monro Kellie doctrine----

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• Any expansion in the contents, (haematoma etc) -->
○ initially accommodated by exclusion of fluid components, (venous blood and cerebrospinal fluid (CSF).)-->
○ Further expansion is associated with an exponential rise in ICP -->
○ resulting in hypoperfusion & herniation

*****Head trauma*****

------Initial evaluation and management------

Resuscitation is performed according to Advanced Trauma Life Support (ATLS) guidelines

-----History-----
taken from paramedics if ptnt cant give it

-----Mechanism-----
• Head injuries arising from high energy mechanisms of injury, (such as a fall from a height or a high-speed
road accident.) --> makes multisystem injury (especially to the spine) likely so a full search should be made for
these
• road traffic accidents, extraction time and evidence of hypoxia or haemodynamic instability at the scene is
important information to obtain from the paramedics.
• The possibility that a fall or crash may have resulted from a prior medical problem, such as myocardial
infarction, hypoglycaemia or subarachnoid haemorrhage, should be borne in mind when trying to get a full
history (Summary box 25.2).

------Neurological progression-----
• A specific check should be made for any loss of consciousness at the time of injury, and its duration
• GCS to be taken at the scene & on arrival
It cannot be overemphasised that deterioration in GCS is an important index of developing, and potentially
reversible, secondary injury
• assess extent of amnesia, retrograde or anterograde
• if intubated at the scene , was the ptnt moving all 4 limbs before this?

-----Examination: primary survey-----

• The priority in any resuscitation is to ensure uninterrupted perfusion of the brain with oxygenated
blood. This is especially true after a head injury given the disturbance to intracranial autoregulation and the
sensitivity of the primary injured brain tissue to further insult.
• Bleeding from scalp lacerations may require management as part of the primary survey, as the blood loss can
be substantial and on-going
• Blood glucose level should also be measured as early as possible as hypoglycaemia is very dangerous and
eminently reversible

----Pupils-----
•The pupil size should be recorded in millimetres, and reactivity documented as present, sluggish or absent.
• Uncal herniation (Figure 25.2) can compress the third nerve, compromising the parasympathetic supply to the
pupil, so that unopposed sympathetic activity produces an enlarged and sluggish pupil, which then, if the
compression continues, becomes fixed and dilated
•Direct ocular trauma or nerve injury in association with a skull base fracture can cause mydriasis (dilated
pupil) present from the time of injury.

------Glasgow Coma Score------

• Remember that the score represents the best performance elicited, so a patient flexing in response to a
painful stimulus on the left and localising on the right scores ‘M5’.
• A sternal or supraorbital rub, or trapezius squeeze will usually be an appropriate stimulus.
• Remember that 3/15 is the lowest possible GCS score!

-----Neurological deficit-----

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• Gross focal neurological deficits, such as paraplegia, may be evident at the primary survey, and an
assessment to exclude such deficit should be carried out, especially if the patient is to be intubated so that
subsequent examination will be impossible.
• Detailed neurological examination is included in the secondary survey

*******Examination: secondary survey*******

-----Head------
• Midbrain or brainstem dysfunction may produce
○ gaze paresis (inability of eye to look across beyond the midline),
○ dysconjugate gaze (inability of the eyes to work together),
○ roving eye movements.

• Inspect the eyes (conjunctiva and cornea of the eyes, and the
retina) using an ophthalmoscope, looking for hyphaema (blood in
the anterior chamber of the eye), papilloedema or retinal
detachment.
• Blood in the mouth may be due to tongue-biting at seizure or at
the time of trauma.
The GCS and pupil status, assessed as part of the primary survey,
require re-evaluation at the secondary survey and regularly thereafter (Summary box 25.4).

-----Neck & spine-----

• cervical spine injury must be presumed in the context of head injury until actively excluded
Plain xray & CT does not exclude the dx of cervical injury so ptnt should be ina hard collar until spine is cleared
clinically
• peripheral nerve examination --> early to identify spinal pathology.
This is especially important in patients who may subsequently be intubated and ventilated when this
assessment will no longer be possible. Obtunded (partially conscious) patients should move all four limbs in
response to an appropriate painful stimulus.

• The patient will need to be log-rolled to palpate for thoracic or lumbar deformity, and any cervical collar
should be removed at this stage to allow palpation of the cervical spine, before it is then replaced again.
• If there is associated spinal injury, a thoracic sensory level is
much more easily established by sensory examination on the
back.
• A per rectal examination is also performed at log-roll, assessing
for anal tone, sensation in the awake patient, and anal
wink (sphincter seen to contract in response to a pinprick
stimulus).
• Priapism is a strong predictor of severe cord injury even in
intubated patients

----Pupils-----
•The pupil size should be recorded in millimetres, and reactivity documented as present, sluggish or absent.
• Uncal herniation (Figure 25.2) can compress the third nerve, compromising the parasympathetic supply to the
pupil, so that unopposed sympathetic activity produces an enlarged and sluggish pupil, which then, if the
compression continues, becomes fixed and dilated
•Direct ocular trauma or nerve injury in association with a skull base fracture can cause mydriasis (dilated
pupil) present from the time of injury.

-----Important aspects of injury------

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Classification:
• diffuse (the brain has been shaken),
• blunt (a direct non-penetrating blow) and
• penetrating (the cranium has been breached).
○ low velocity or
○ high velocity (cavitation caused by high velocity injuries is especially damaging to the brain)
• Rapid deceleration often produces shearing of axons (diffuse axonal injury) and coup–contrecoup contusions
(see below under Cerebral contusions).

• Skull fractures can be

○ open or closed.
○ If intracranial air can be seen on the x-ray, then the dura has been breached too.

Fractures may be
○ linear (when they can be difficult to see on x-ray) or
○ comminuted when they may also be depressed.
Fractured base of skull may present with bleeding from the eyes, ears nose or mouth or with rhinorrhoea (CSF
leaking from the nose).

-----Intracranial haematoma-----

• Haemorrhage within the cranium occurs in four main sites:

extradural, subdural, subarachnoid and intraparenchymal.
• A common characteristic is that all cause a rise in intracranial
pressure, which may compromise perfusion of the brain.
Minimising the secondary injury by making sure that the patient
is well oxygenated and that their blood pressure is within normal
limits is important in the early management of these
cases (Summary box 25.6).

****Ongoing management: prevention of secondary injury******

• Following initial resuscitation -> the patient will require on-going management directed at minimizing
secondary brain injury
• This occurs in the minutes, hours and days following primary injury, as a result of factors summarised in
Figure 25.9
Unlike the primary injury which describes the diffuse axonal injury and intracranial bleeding with which the
patient presents, secondary injury is often preventable through avoidance of hypoxia and hypotension,
and control of intracranial pressure.

-----Control of intracranial pressure------

• Intubation and ventilation is required early in the management of severe brain injury for airway control.
• Sedating the patient prevents clinical assessment of intracranial pressure by monitoring of GCS and focal
neurological signs, leaving only pupil responses as a guide.
It is therefore important that intracranial pressure monitoring is instituted as soon as possible to guide
pressure management.
• Coagulation profile & CT ( needs to be done prior to insertion of probe for inc ICP)

-----Initial measures----
Initial measures include
• positioning the head up 20–30° (reverse Trendelenburg positioning by tilt of the whole bed if the spine has
not been cleared).
• The cervical collar should be loose enough so that it does not restrict venous return.
• Ventilation is regulated to achieve normocapnia: hypocapnia may be used to achieve transient ICP control in
the short term, but the cerebral vasoconstriction which results can produce hypoperfusion and eventual
further secondary brain injury.

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• Sedation using a combination of opiates and barbiturates at escalating doses and with boluses to coincide
with turns and suctioning will assist in control (Table 25.4).

-----Intermediate measures-----
• Where initial measures fail adequately to control ICP, sedation may be escalated and supplemented with
paralysis
• External ventricular CSF drainage represents a useful adjunct to physiological compensation.
○ Mannitol can be administered to control ICP temporarily.
○ This is helpful where there is evidence of herniation, such as development of a dilated unresponsive pupil
during transfer.
○ 100 mL of 20 per cent mannitol is a typical bolus
○ Complications: Repeated or excessive use is counterproductive because it is an osmotic diuretic and
produces hypovolaemia and hypotension.
○ This will compromise cerebral perfusion.
○ Administration of mannitol necessitates catheterising the patient to monitor fluid balance
• Pyrexia increases brain oxygen requirements and cell damage, and so should be avoided
Active induction of therapeutic hypothermia is effective in controlling intracranial pressure, but predisposes to
complications including sepsis and coagulopathy

-----Final measures-----
Initial measure: • Decompressive craniectomy (Figure 25.11) involves removal of a portion of the skull vault
and opening of the underlying dura, so that brain swelling can occur without the pressure increases predicted
by the Monro Kellie doctrine
• Generally, a unilateral or bifrontal decompressive craniectomy is
performed, with the bone flap placed subcutaneously in the
abdomen, then replaced (cranioplasty) weeks or months later.

• alternative strategy for managing uncontrolled intracranial

hypertension is induction of thiopentone coma.
• This carries a high risk of complications and results in the loss of
normal EEG activity and pupil responses, compromising ongoing
evaluation of the patient

---Pituitary dysfunction: endocrine and metabolic management----

• All aspects of pituitary function may be compromised in the setting of TBI.

• Routine screening of pituitary hormone levels and liaison with endocrinology is an important aspect of
optimal medical management
•administration of corticosteroids in severe head injury is associated with increased mortality and is not
recommended
• electrolyte imbalance is common in TBI -> leads to brain swelling --> seizures
• Mechanisms:
○ Cerebral salt wasting, a poorly understood form of excretory dysregulation in association with brain insult,
leads to volume depletion and hyponatraemia
○ SIADH --> leads to water retention and hyponatraemia in the context of pituitary damage.
antidiuretic hormone
○ (ADH) secretion may be compromised in the context of trauma, producing diabetes insipidus resulting
in hypernatraemia. This may be managed with boluses of desmopressin in consultation with endocrine
specialists.
----Seizures-----

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• Seizures may occur early (within 7 days) or late.
• Risk factors include
○ injury severity,
○ especially the presence of ICH,
○ depressed skull fractures and
○ tears of the dura.
• Txt: Antiepileptics, typically phenytoin, are administered
prophylactically to patients at high risk of seizures

----Nutrition-----
• Enteral nutrition is preferred to intravenous parenteral nutrition on
grounds of cost and associated complications, and should be
commenced within 72 hours of injury.
• Prokinetics (e.g. metaclopramide, erythromycin) can be administered
to promote absorption

*****SURGICAL ASPECTS OF HEAD INJURY*****

-----Skull fractures-----

•Closed linear fracture --> managed conservatively with primary closure where possible
•Prophylactic antibiotics are not usually required, even in the case of CSF leak, which generally resolves
spontaneously.
Blind nasogastric tube placement is contraindicated in these patients
•Fracture of the air sinuses --> managed as open fractures, using broad spectrum antibiotics with or without
exploration.
• depressed skill fracture -->
○ involve inward displacement of a bone fragment by at least the thickness of the skull (Figures 25.4 and
25.5).
○ They occur when small objects hit the skull at high velocity.
○ They are usually compound (open) fractures,
○ are associated with a high incidence of infection, neurological
deficit and late-onset epilepsy.
• compound fractures will require exploration, debridement and
elevation of the fragment.
Prophylactic treatment with a course of broad spectrum
antibiotics is normal practice (Summary box 25.7).

******Outcomes and sequelae*****

-----Mild injury: concussion, second impact syndrome and postconcussive syndrome-----

• Concussion is defined as alteration of consciousness as a result of closed head injury, but is generally used in
describing mild head injury without imaging abnormalities
• CF:
○ Key features include confusion and amnesia
○ The patient may be easily distractable,forgetful,
○ slow to interact or emotionally labile.
○ Gait disturbance and incoordination may be seen.
• patients may be especially vulnerable to repeat impacts

• Postconcussive syndrome is a loosely defined constellation

of symptoms, persisting for a prolonged period after injury, and
exacerbated in some patients by the potential for secondary gain
(compensation).

89
 • Patients may report somatic features, such as headache, dizziness and disorders of hearing and vision. They
may also suffer a variety of neurocognitive and neuropsychological disturbances, including difficulty with
concentration and recall, insomnia, emotional lability, fatigue, depression and personality change

-----Moderate and severe injury------

• The long-term sequelae of significant brain injury are likely to include many of the somatic and
neurocognitive problems described above, combined with the effect of deficits attributable directly to the
primary and secondary injury sustained
• The Glasgow Outcome Score is used to quantify the degree of recovery achieved after head injury, especially
for research purposes, and is detailed in Table 25.5.
• Good recovery implies independence and potential to return to work rather than a full return to previous
capacity (Summary box 25.14).

*****ANEURYSMAL SUBARACHNOID HAEMORRHAGE*****

• ‘Spontaneous’ aneurysmal subarachnoid haemorrhage (SAH) is due to the rupture of an aneurysm in about
80 per cent of cases.

----Epidemiology----
• Berry aneurysms of the circle of Willis develop at branch points
• Risk factors include age, female sex, hypertension, smoking, cocaine abuse and a family history with two
first-degree relatives affected

----Clinical Features----
• They are then at high risk of succumbing to early complications, especially a rebleed.
• The typical presentation of a subarachnoid haemorrhage includes a ‘thunderclap’ headache, which is both
sudden and severe and is outside the patient’s normal experience.
• Sometimes it is difficult to establish whether SAH has caused a fall, or whether a fall with head injury is
responsible for the SAH.
• Neurological examination may be normal (‘good clinical grade’(WFNS 1-3), see Table 25.6), or the patient
may have focal deficits and an impaired conscious level (‘poor grade’)(WFNS 4 and 5)
• The combination of subarachnoid haemorrhage and vitreous haemorrhage is known as Terson syndrome

----Investigation---
• CT scan is the imaging of first choice, and, when performed within 12 hours of ictus, will confirm bleeding in
more than 98 per cent of cases.
• The sensitivity of CT scan, however, deteriorates to less than 50 per cent at 1 week after a bleed. In light of
this, patients with a suggestive history and negative CT scan will require lumbar puncture, especially where
presentation is delayed
•The CSF supernatant should be analysed by spectrophotometry (visual inspection is not reliable) for the
spectra of haemoglobin breakdown products oxyhaemoglobin and bilirubin. These are clearly detectable in
samples taken at least 6 and preferably 12 hours after subarachnoid haemorrhage, but not in CSF mixed with
fresh blood due to traumatic puncture and analysed immediately
• Failure to exclude subarachnoid haemorrhage with an appropriate delayed lumbar puncture may necessitate
formal cerebral angiography, and the risks this entails

---Management----
• Patients should be placed on bed rest with hourly neurological observations.

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• They require strict input–output monitoring and intravenous fluid replacement with normal saline initially.
• Oral nimodipine at a dose of 60 mg every 4 hours has been shown to reduce the rate of poor outcome
associated with delayed neurological ischaemic deficit due to cerebral vasospasm.
• Analgesics, laxatives, antiemetics, gastric protection and compression stockings are also likely to be
necessary.

• After resuscitation, the priorities in subarachnoid haemorrhage are:

○ to prevent rebleeding by identifying and controlling any underlying lesion;
○ to recognise and manage:
○ neurological complications, especially vasospasm (or delayed ischaemic neurologic deficit) and
hydrocephalus;
○ systemic complications, including electrolyte imbalance, severe hypertension, cardiac infarct and
arrhythmia, and neurogenic pulmonary oedema.
• These goals are best served by early transfer of the patient to a neurosurgical centre.
• In elderly patients with a poor WFNS grade, a decision to offer only supportive management may be
appropriate.

--Prevention--
• CT angiography (CTA) has a high sensitivity for aneurysms
and arteriovenous malformations (AVMs), but digital
subtraction angiography (DSA) remains the gold standard
• Aneurysms demonstrated may be removed from the
circulation
surgically by craniotomy and ‘clipping’, or by endovascular
embolization, also known as ‘coiling’.

---Complications---
• Hyponatraemia is a frequent complication of subarachnoid haemorrhage, attributed to cerebral salt wasting
in the context of fluid depletion

• The approach to a patient who has deteriorated should follow standard

principles of resuscitation, with consideration paid to the high incidence of electrolyte imbalance, cardiac
infarcts and arrhythmias, and neurogenic pulmonary oedema in this group.
• Neurological deterioration should prompt a repeat scan to exclude evidence of rebleeding and of
hydrocephalus
This is typically the communicating type, which is a common sequel of haemorrhage. Where these
complications are not demonstrated, deterioration is often attributable to delayed ischaemic neurological
deficit (DNID), which commonly develops 3–10 days after aneurysmal haemorrhage and can progress rapidly to
infarction. The process is attributed to cerebral vasospasm in response
to, and correlating with, the blood load.
• Dx: This process can be visualised angiographically, and the velocity of
blood flow in the cerebral vasculature, measured using transcranial
Doppler ultrasound (TCDs), provides an indirect assessment of the
degree of stenosis.
• Txt: Outcomes are optimised by the prophylactic administration of
nimodipine and maintenance of fluid volume, typically with 2.5–3 L/day
of normal saline
• In established vasospasm, the goal is to maintain cerebral
perfusion.(Summary box 25.17)

****OTHER SPONTANEOUS INTRACRANIAL HAEMORRHAGE****

• Intracerebral haemorrhage may be spontaneous or traumatic
• The majority occur in the context of hypertension or amyloid angiopathy, or as a complication of ischaemic
stroke.
• Coagulation disorders, especially patients being treated with warfarin, are a major risk factor

Clinical Features:

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• Patients typically present with sudden focal deficit and reduced conscious level.

Management:
• Following initial resuscitation, these patients will require CT scan to establish the diagnosis, and the size and
position of the bleed (Figure 25.16).
• They require reversal of anticoagulation, on-going hourly neurological observations and blood pressure
monitoring.
• High blood pressure may be longstanding and associated with adaptations to autoregulation, so attempts at
lowering it acutely with intravenous antihypertensives should be made only if the values are very high (e.g.
MAP >130 mmHg).
• Craniotomy and evacuation is used to alleviate raised intracranial pressure, just as it can be in a subgroup of
patients with ischaemic strokes in the posterior fossa or in the middle cerebral artery territory.
• Surgery has no role in addressing focal deficits corresponding to direct damage from the bleed itself.

Indications:
• Young patients with haematomas close to the cortical surface, demonstrating progressive neurological
deterioration, represent good surgical candidates.
• Posterior fossa clot is also a strong indication for surgery because of the potential for rapid deterioration due
to brainstem compression and hydrocephalus.
• A substantial minority of intracerebral bleeds are attributable to focal vascular lesions, and this must be
considered when planning any surgery

• Vascular malformations are usually congenital in origin.

•CF: They may present with headaches, pulsatile tinnitus, seizures or focal deficit, or else acutely with rupture
and haemorrhage
• Arteriovenous malformations are responsible for about 10 per cent of subarachnoid haemorrhages.

•Dx: Vessels and calcification may be apparent on CT or magnetic resonance imaging (MRI), and the lesion
is confirmed on angiography (Figure 25.17).

Txt:
• Endovascular embolisation, with tissue glue, is often a useful first-line therapy, but carries significant risks
and rarely achieves complete and permanent obliteration.
• Most patients will therefore ultimately require craniotomy, taking into account the risks of deficit
associated with operation.
• These may be predicted using the Spetzler–Martin grading system, which is based on the size of the lesion,
the eloquence of adjacent brain, and the pattern of venous drainage.
• Vein of Galen malformations are AVMs feeding into an embryological venous remnant dorsal to the
brainstem presenting in childhood. High-flow malformations may cause cardiac failure. They may be treated by
embolisation. Dural arteriovenous fistulae (DAVFs) are shunts between dural arteries and veins or sinuses.
They are proposed to arise as a result of vessel remodelling in response to dural sinus thrombosis and
subsequent recanalisation. They may present with subarachnoid, intracerebral or subdural bleeding, or with
headache and pulsatile tinnitus.
A carotid cavernous fistula is a spontaneous or traumatic DAVF between the internal carotid artery and
surrounding cavernous sinus, typically producing eye pain, ocular muscle palsies and exophthalmos.
Angiography is diagnostic.
• Cavernomas (Figure 25.18) are venous anomalies, demonstrated
on MRI, but not with angiography, which may require operation if they cause progressive deficits, intractable
epilepsy or recurrent bleeding.
• Related lesions, usually clinically silent, include developmental venous anomalies (DVAs) and capillary
telangectasia

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Chap 26: Neck and Spine
Notes made in anki.
Similar to IM,, simply add extra info that’s not present in IM

Chap 27: Maxillofacial trauma

Etiology
social factors, climatic, road traffic

Clinical Features of maxillofacial trauma

•laceration or fracture can lead to respiratory obstruction
•immediate obstruction (due to inhalation of tooth fragment or accumulation of blood etc)
management of this: semi prone position with head supported on bent arm
neck supported until cervical fracture is excluded
intracranial surgery should always be considered
•initial hemm will be dramatic but sustained bleeding is unusual
•delayed edema occurs in cases of facial fracture (60-90min later)
so ptnt can have good airway but then rep obstruction
MC occurs in lefort 3 fractures

Examination:
note pattern and extent of soft tissue injury
then hard tissue injury
examine whole head
note any assymetry and check via gentle palpation
tenderness over known weak sites should be done

•middle third injuries are accompanied by some degree of epistaxis (except isolated zygomatic arch fracture )
• Lefort 2&3 --> CSF leak with CSF rhinorrhea
• fractured zygoma --> subconjunctival hemm (often doesn't have a posterior limit)

then examine intra orally

• not occlusion
• fracture of jaw--> mandible and maxilla dont fit
• fracture of alveolus tears gingivae
• fracture of mandible --> haematoma in floor of mouth
• note alignment and missing teeth
• step defects --> fracture of underlying bone
• test jaw movement : deviation from the midline at rest or on opening suggests a fracture of the side to
which the jaw is deviating.
• maxilla fracture test : If a fracture of the maxilla is suspected, then the maxillary dental arch should be
grasped between the index finger and thumb of one hand in the incisor region, while the other is placed on the
forehead. If the maxilla is fractured, gentle pressure forward and backward, or side to side, will reveal
movement between the examining hands. With the mandible, gentle manipulation across the suspected site of
a fracture will produce

93
‘springing’ if a fracture is present.

• palatal lacerations tend to occur in yound children who fall on to objects held in the oral cavity

Checking for intact nerves

• Paraesthesia suggests a fracture proximally along the course of the nerve.
○ cheek and upper lip --> fracture involving the infraorbital foramen or floor of the orbit,
○ the lower lip --> fracture of the mandibular body.
○ Facial palsy -->
◘ in facial lacerations -> damage to facial nerve. This is common in penetrating wounds of the parotid
gland.
◘ w/o facial lacerations -> a fractured temporal bone.
• Check visual acuity in both eyes. This may be difficult in the oedematous patient with marked periorbital
oedema, but a pen torch shone directly through the lids will confirm gross optic nerve function. Where
possible, pupil size and reflexes to light should be observed and recorded, as should eye movements.
• Check for diplopia by asking the patient to follow the light of a pen torch through a full range.
○ Diplopia --> damage to the thin orbital plates of bone, particularly the floor of the orbit or from damage to
the III, IV or VI cranial nerves.
• All findings should be recorded accurately, preferably with diagrams to include measurements of lacerations,
abrasions and areas of tissue loss. Photographs of the initial injury can be very helpful if litigation is likely to
follow (Summary box 27.2).

FRACTURE OF FACIAL SKELETON AND MANAGEMENT:

FRACTURE OF ZYGOMATICO ORBITAL COMPLEX:
• most important fracture of middle third of face apart from nose
• Fracture occurs through points of weakness: infraorbital margin, frontozygomatic
suture, zygomatic arch, anterior and lateral wall of maxillary sinus (check diagram
from bailey. Figure 26.8. pg.359)
• With exception of isolated zygomatic arch, isolated
infra orbital rim and extensively comminuted
fractures, if ZMC is fractured then all 4 legs of the
stool are fractured. Excluding these 2 fractures all
ZMC fractures also involve the bony orbit, so
careful assessment of ocular position and function
necessary.
• Epistaxis due to tear in antral mucosa
• Paresthesia due to infraorbital nerve damage
• Investigation: occipitomental radiograph, most
fractures displaced in posterior direction. (Role of
plain radiography decreasing) CT scanning is
standard investigation except in the simplest
fractures.
• Management:
• Mainstay of treatment is ORIF with fixation at one of the 4 legs of the stool. Single,
double, triple or 4-point fixation depends on stability of fracture post reduction and
degree of comminution. Uncomplicated→ treated within 10 days of injury
o Most fractures are reduced by Gillies temporal approach
▪ Incision in the hairline superficial to temporal fossa about 15 mm long
at 45° to the vertical
▪ Deepen down to temporalis fascia
▪ Bristow or rowe elevator is inserted beneath zygomatic arch and force
is applied to reduce fracture

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 ▪ After reduction the position is checked by palpation to see if there is
still any limitation in movement by inferior oblique and inferior rectus
muscles
▪ Any restriction shows entrapment of infraorbital soft tissues
o Open reduction internal fixation for unstable fractures
▪ Frontozygomatic suture is exposed by small incision
▪ Displacement may be reduced or fixed by intraosseous wires or bone
plates
o Formal eye observation in postoperative period, size of pupil, response to
light all are checked
o Complications: retrobulbar hematoma, proptosis, loss of vision
NASO-ORBITAL ETHMOIDAL FRACTURES:
• Simple nasal bone fractures or comminuted fracture involving nasal bone, maxilla,
infraorbital rim, frontal bone, impacted into anterior cranial fossa, in region of
cribriform plate. Usually caused by blow to bridge of the nose.
• Severe fracture→ peri-orbital ecchymosis, swelling and nasal bleeding with
depressed bridge of nose, nasal tip rotated upwards, allowing nostril to be seen
straight on (piggy nose).
• Disruption of medial canthal ligament from bony attachment occurs that lead to
traumatic telecanthus (widened intercanthal distance)
• Investigation→ CT scanning
• Treatment delayed for 7-10 days, ORIF and repositioning of fragments with medial
canthi attached
CRANIO-FACIAL FRACTURES:
• Fractures that involve cranial cavity and facial bones in continuity
• Sometimes involve frontal and ethmoidal sinuses, creating communication between
cranial cavity and nasal air sinuses. If combined with dural tear, then CSF rhinorrhea.
Antibiotics not indicated for this. Most common site of injury is posterior wall of frontal
sinus.
• Persistent leak lasting 10 days is treated with surgical intervention, done with open
anterior fossa repair. Sometimes done endoscopically. In most patients, treatment
by canalisation of frontal sinus with obliteration of frontonasal duct. Treatment is
delayed for 7-14 days.
PANFACIAL FRACTURES
• Fractures at all levels of facial skeleton (upper, mid and lower)
• Indicate significant amount of force, hence associated injuries to the brain, cervical
spine and other organs is more common
• Reconstruction difficult as little normal anatomy to guide
• Each component is treated in the same way as an isolated fracture. Sequencing is
difficult. Options include top down, bottom up, inside out (centrally then laterally) or
outside in
DENTAL INJURIES:
• Primary (deciduous) dentition erupted by 2.5 years.
• First permanent teeth (lower incisors) erupt at age 6
• Between 5-13, primary dentition shed and replaced by secondary
• If adult whole tooth is avulsed, cleaned gently in saline and reimplanted (the
sooner, the better) – avulsed deciduous teeth are not implanted. Done under L/A
after irrigation and debridement of socket. Then referred to dentist to splint tooth and
immobilise it, to protect from dental occlusion
• Fractures of teeth involve: enamel, enamel and dentine, enamel, dentine and pulp
• If dentine exposed, fractured tooth is very painful, so dental dressing done (LA
anaesthetic infiltrated in apex of root). If pulp exposed, then LA topically to exposed
pulp.
SOFT TISSUE INJURY:

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 • facial soft tissue has an excellent blood supply and heal well so should be sutured
following injury after careful exploration, debridement and cleaning
• Most lacerations can be closed under local anesthesia
if GA is required initially LA is used to close the wound temporarily
• The muscles beneath tissue should be brought together with absorbable sutures so
the edges lie within 2 mm of final position, then by monofilament suture (5-0 or 6-0)
the edges are brought together
• Broad spectrum antibiotics are given
• Alternate sutures should be removed on 3rd day with remaining removed on 5th day
• Intraoral complications are treated with resorbable sutures
• Failure to close deeper lacerations result in wound dehiscence and thick scars.
Careful cleaning with removal of all dirt minimises chances of wound tattooing.
• Wounds involving eyelid margins and crossing vermillion of lip need careful
approximation of all involved layers
• Small defects (direct closure), larger (local skin flaps). Greater tissue loss (grafts or
free tissue transfer)
SKIN LOSS:
• Etiology: human bite most commonly nose and ear
• Facial bites are closed primarily and not left open. All bites debrided carefully and
closed in usual way, and antibiotics given.
• Small areas of tissue loss treatment: tension free closure of wound
• Large areas of tissue loss treatment: reconstruction with grafts and local flaps
FACIAL NERVE INJURY:
• Primary repair in case of major division of nerve is involved
• Severed nerve ends are approximated using operating microscope
• Secondary repair is generally unsatisfactory
• Injuries that lie behind a line from lateral canthus to the angle of the mouth and
repairable and should be attempted.
PAROTID DUCT INJURY:
• Obvious as saliva leaks into the wound, buccal branch of facial nerve also injured.
• laceration of duct treatment: insert fine cannula in the duct through mouth and pass it
posteriorly until it appears in the wound to find other end and anastomose it
• Cannula is left in the place for several days to prevent post anastomotic stricture
formation
LACRIMAL APPARATUS INJURY:
• nasolacrimal apparatus is involved in eye and facial injuries
• Clinical features: pain, edema, bleeding
• Most surgeons refer to ophthalmic surgeons before proceeding to primary repair
FRONTAL BONE FRACTURE:
• depressed fractures of frontal sinus or posterior wall fracture of frontal sinus requires
neurosurgical collaboration
• Fracture of anterior sinus wall is managed with reduction and fixation using titanium
plate and screws
• Missing bone segment requires bone graft
FRACTURE OF MAXILLA:
• Principle of reducing facial and frontal bone fracture is that surgeon starts from top
and proceeds to bottom
• If no lacerations are present frontal bone, supraorbital ridge and nasal root is
approached by bicoronal incision high in hairline and skin and galea are reflected
forward until supraorbital ridge is exposed
• Reduced and fixed by stainless steel wire or titanium microplates
• Bone deficient: cortical cranial bone graft
• For midface we use blepharoplasty incision exposing lower conjunctival sac and
infraorbital region

96
 • lower part of the maxilla is approached through a {{c5::gingival sulcus}} incision above the maxillary
teeth as far back as the second molar. Fractures are {{c5::fixed with plates or wires.}}

Chap 28: Torso Trauma

Intro same as IM , topics that are missing:

Immediate life threatening injuries

Airway obstruction:
• Early intubation is very important, particularly in cases of neck haematoma or possible airway
oedema.
• Airway distortion can be insidious and progressive and can make delayed intubation more difficult if
not impossible.

Tracheobronchial injury
• Severe subcutaneous emphysema with respiratory compromise can suggest tracheobronchial disruption.
•Inv:
A chest drain placed on the affected side will reveal a large air leak and the collapsed lung may fail to re-
expand.
If after insertion of a second drain the lung fails to re-expand, referral to a trauma centre is advised.
• Bronchoscopy is diagnostic.
• Treatment involves intubation of the unaffected bronchus followed by operative repair.

Blunt myocardial injury:

• Significant blunt cardiac injury that causes haemodynamic instability is rare.

• Blunt myocardial injury should be suspected in any patient sustaining blunt trauma who develops early ECG
abnormalities
Inv:
• Two-dimensional echocardiography may show wall motion abnormalities.
• A transoesophageal echocardiogram may also be helpful. • There is very little evidence
that enzyme estimations have any place in diagnosis.
Management:
All patients with myocardial contusion diagnosed by conduction abnormalities are at risk of developing sudden
dysrhythmias and should be closely monitored.

◘Esophageal injury ◘pulm contusion ◘cont blood loss

INDIVIDUAL ORGAN INJURY

Spleen
• Splenic injury occurs from direct blunt trauma.
Indications
• Indications of nonoperative management:
○ isolated splenic injuries, especially in children,
• Indications of operative management (splenectomy )
○ in adults, especially in the presence of other injury,
○ age >55 years, or
○ physiological instability (unstable patient),

• The spleen can be packed, repaired or placed in a mesh bag. Splenectomy may be a safer option, especially
in the unstable patient with multiple potential sites of bleeding and who is >55 years of age, due to risk of

97
rebleed.
• In certain situations, selective angioembolisation of the spleen can play a role.

Complications:
Following splenectomy, there are significant though transient changes to blood physiology.
The platelet and white count rises and may mimic sepsis.

BILIARY INJURIES:
• isolated traumatic biliary injuries are rare
• It is mainly injured by penetrating trauma in association with injuries to other organs
• Common bile duct is repaired over T-tube or drained and referred for damage control
surgery, or ligated.
STOMACH:
• mostly injured by penetrating trauma
• Presence of blood in NG tube is diagnostic, in absence of bleeding from other
sources
• Surgical repair is the treatment
• Examine carefully as anterior wounds usually have exit elsewhere on the organ
DUODENUM:
• Duodenal injuries are associated with injuries to adjoining pancreas
• Injuries are retroperitoneal so are hidden and only discovered late or on laparotomy
• Investigation: CT (gas or fluid collection in peri duodenal tissue, and leakage of oral
contrast
• Minor injuries repaired with primary repair
• Major with damage control surgeries
• The 1st, 3rd and 4th part of duodenum behave like small bowel and can be repaired in
same fashion. 2nd part is fixed to the head of the pancreas with a common blood
supply and may have a poorer blood supply compared to remainder.
SMALL BOWEL:
• frequently injured by blunt trauma Trapping the loops resulting in high pressure
rupture of loops or tear in mesentery
• Requires urgent repair
• Haemorrhage control takes priority and these wounds can {{c2::be temporarily
controlled with simple sutures.
• In blunt trauma, damage to mesenteric vessels can result in Ischemia requires
resection and end to end anastomosis
• Hematomas requires surgical exploration
• Low velocity trauma requires primary repair After debridement
• Destructive trauma requires resection and anastomosis
• Damage control clip and drop of damaged or resected bowel may be necessary
COLON:
• Penetrating traumas are more common than blunt traumas
• Small injuries with viabilities require primary repair
• In case of extensive contamination and doubtful viability, then bowel can be closed
off (clip and drop. A defunctioning colostomy performed later or bowel
reanastomosed
RECTUM:
• 5% colon injuries involve rectum
• Arise from penetrating trauma
• DRE shows blood in colorectal injuries
• Associated with bladder and proximal urethral injuries
• With intraperitoneal injuries rectum is managed same as colon

98
 o Full thickness extraperitoneal rectal injuries: diverting end colostomy and
closure of distal end (hartmann’s procedure) or a loop colostomy
o Presacral drainage is normally not used
UROLOGICAL INJURIES:
• Stable patient: CT contrast is investigation of choice
• Assessment of bladder injuries: cystogram is performed (minimum 300 ml of contrast
instilled into bladder. Film assessed as:
1)2 views-AP and lateral (and sometimes oblique)
2) 2 occasions-full and post micturition
• Treatment of renal injuries:
o Stable: angioembolise the kidney
o Unstable: operative measures
• Ureteric injury management:
o Diverting ureter and reconstructing it
• Bladder management:
o Intraperitoneal: surgical repair
o Extra peritoneal: heal with adequate urine drainage via transurethral route.
When this not possible, then supra pubic drainage.
THE PELVIS (27th Ed):
• Hidden bleeding source
• Extreme force required to disrupt pelvic ring
• To save these patients, 3 questions are asked? Is patient at high risk of massive
bleeding, where is the source of bleeding, how to stop the bleeding?
ANATOMY:
• Pelvic inlet is circular, very strong. Isolated fractures of anterior or posterior ring
uncommon
• Has a rich collateral supply of blood. Most pelvic hemorrhages are from: venous
injury and fracture sites. In hemodynamically unstable patients with severe pelvic
injury, arterial bleeding
• Extra pelvic peritoneal space can accommodate more than 3000ml blood.
Hematoma may extend upwards into mediastinum
(chimney effect) or downwards into medial thigh in case of
rupture of pelvic floor.
• Disruption of sacroiliac joint: severe hemorrhage and
arterial obstruction of internal iliac artery and sciatic nerve
palsy.
• Shear forces acting on pelvis: avulsion and shearing
injuries
• Inappropriate treatment may lead to severe disability in
acetabulum
CLASSIFICATION:
1. TYPE A:
• Most common fractures and completely stable
• Result from lateral compression, causes compression
fractures of pubic rami or compression fracture of
sacrum posteriorly
2. TYPE B:
• Partially stable
• Disruption of anterior pelvis and partial disruption of posterior pelvis
• Can open and close like a book. Because sacroiliac ligaments are intact, no
vertical displacement
• Internal or external stabilisation required. Blood loss significant
3. TYPE C:

99
 • Completely unstable
• Anterior pelvis and posterior pelvic complexes disrupted. Disrupted pelvic bones
free to displace horizontally and vertically.
• In both B and C, high risk of abdominal injuries and rupture of diaphragm.

CLINICAL EXAMINATION:
• may reveal instability
• any instability indicates presence of major pelvic fracture, and life threatening blood
loss
• inspection of skin: lacerations in groin, perineum or sacral area indicating open pelvic
fracture
• evidence of perineal injury mandates radiological evaluation of urinary tract from
below upwards (retrograde urethrogram followed by cystogram and an excretory
urogram)
• inspection of urethral meatus may reveal drop of blood, showing urethral damage
• inspection of anus: lacerations to sphincter mechanism
• blood in rectum or discontinuity of rectal wall: rectal laceration
• high riding prostate: complete urethral avulsion
• a full neurological examination of perineal area, sphincter mechanism, femoral,
sciatic nerves
DIAGNOSIS:
• FAST is unreliable as does not localise intra abdominal bleeding in these patients
• CT in hemodynamically stable patients
• CT angiography: to provide details of anatomy of fracture and origin of bleeding
• Displacement of anterior pelvis by greater than 2cm indicates partial instability
MANAGEMENT:
• initial management: compression binder or sheet, applied around the true pelvis at
level of the greater trochanters (reduce the pelvic volume)
• 85% bleeding from venous origin, can be controlled by non operative means:
compression either by binding or external fixator or by extra peritoneal packing
(packing the loose space between the bony wall of the pelvis and peritoneum) to
compress pelvic veins.
• If bleeding from arterial origin: interventional angio embolisation
ABDOMINAL COMPARTMENT SYNDROME AND OPEN
ABDOMEN:
• syndrome caused by raised intra abdominal pressure
• Causes morbidity and mortality in critically ill patients
• In case of ACS abdomen is left open and managed as damage control surgery

ORGAN EFFECTS

Renal Increase in renal vascular resistance decreasing GFR

Cardiovascular Decrease in venous return to heart decreasing cardiac output and

preload but increasing after load

Respiratory Increase in ventilation pressure, because of splinting of diaphragm and

decrease in lung compliance increasing airway pressure

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 Visceral Reduction in visceral perfusion
perfusion

Intracranial Rise in ICP

DAMAGE CONTROL:
•
Patient after major surgery are at risk of mortality if surgery is performed in unstable
patient
• Deadly triad at highest risk are
a. Hypothermia
b. Coagulopathy
c. Acidosis
• Such patients are managed by repairing minimal damage while definitive surgeries
are withheld until patient is stable
• 2 goals of damage control surgery are:
d. Stopping any active surgical bleeding
e. Controlling any contamination
DAMAGE CONTROL RESUSCITATION:
• Time in emergency dept is minimised and patient is managed both for resuscitation
and damage control surgery in operation theatre
• Resuscitation is carried out as in individual with testing of Hb, acidosis and assessing
clotting profile
• Resuscitation is carried out in OT using biologically active fluids e.g. blood

DAMAGE CONTROL SURGERY:

• Stages of damage control surgery

I Patient selection

II Control of hemorrhage and control of contamination

III Resuscitation continued in ICU

IV Definitive surgery

V Abdominal closure
• Initial focus is hemorrhage control by ligation of bleeders or packing or stapling of
vessels
• Closure of abdomen by sheet of plastic eg opsite and suction over the bowel, an
intermediate pack to allow suction and a further sheet of adherent plastic drape to the
skin to form watertight and airtight seal. Suction is applied to intermediate pack area
to collect fluid from abdomen. This is called VACPAC or Opsite Sandwich
• After controlling the patient is transferred to ICU
• Next stage of stabilization is definitive surgery. The team must perform definitive
anastomoses or vascular reconstruction within 24-72 hours of surgery
• Abdomen is closed keeping in mind risk of ACS so requires aggressive offloading of
fluid and haemofiltration
• Best is closure of abdominal fascia. If not possible then skin closure only.
Sometimes, mesh closure, with skin grafting over mesh and subsequent abdominal
wall reconstruction.
• Thoracic damage control: aim is minimizing bleeding and air leak

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 • Damage control of extremities: shunting vessels, debridement and fasciotomy
• Indications for damage control surgery:

Anatomical • Inability to achieve hemostasis

• Complex abdominal injuries
• Combined vascular, hollow and solid organ injuries
• Inaccessible major venous injuries
• demand non operative control of other injuries e.g. fractured
pelvis
• Anticipated need of time-consuming procedure

Physiological • Temp < 34°

• PH < 7.2
• Serum lactate > 5 mmol/L
• PT > 16 sec
• PTT > 60 sec
• > 10 units blood transfused
• Systolic BP < 90 for > 60 mins

Environmental • Operating time > 60 mins

• Inability to approximate abdominal incision
• Reassess the intra abdominal content

RADIOLOGICAL INTERVENTION:
• both as diagnostic and therapeutic tool for vascular injury
• Angioembolisation is important procedure for ongoing bleeding
NON-OPERATIVE MANAGEMENT:
• preferred for solid organs in stable children and adults
• CT imaging is prerequisites for this approach
• Failure is uncommon and typically occurs in first 12 hours
• Antibiotics can be given in all penetrating traumas but no recommendation for use in
chest drainage. Until major contamination, single dose is sufficient.

Chap 29: Extremity Trauma

DIAGNOSIS

HISTORY:

• Mechanism of injury and amount of force involved

• Translate mechanism of injury into common anatomical injury patterns e.g. electrocution
leads to posterior dislocation of shoulder
• History of AMPLE
1) Allergies
2) Medication (anticoagulant anti-platelet, corticosteroids or immunosuppressants)
3) Past medical and surgical history (if anaesthesia in past and any complications)
4) Last time-something to eat and drink
5) Events-which led to injury

EXAMINATION:

• Examination of individual extremity begins once life and limb threatening injuries excluded
• A top to toe evaluation by systematic approach:

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1) Look 2) Feel 3) move (active and passive) 4) special tests 5) special investigations
• Examine joint above and joint below the site of injury
1) LOOK
• Look at whole limb back and front, for swelling, bruising, deformity
• Any break in skin or abrasion
• Photograph taken to document injury
• Note colour of limb and general swelling
2) FEEL
• Start examining away from zone of obvious injury
• Feel for bony tenderness and note degree of swelling, and tenseness of compartments
• Sub cutaneous crepitus of air in open fractures, air jet injuries and around chest in
pneumothorax
• Feel for pulses and assess capillary return
3) MOVE
• Active movement- initiated and maintained by patient
• Passive movement- examiner moves the limb
4) SPECIAL TESTS
• Looking for ruptured Achilles tendon by placing patient prone with foot over edge of bed
and squeezing calf, plantar flexion of foot and ankle shows tendon is intact
• In all knee injuries make sure patient can actively straight leg raise and get leg off couch
• To assess triceps function and elbow extension, ensure patient can actively extend against
resistance
• Neurovascular examination-document findings before and after manipulation or cast
application. Document both sensibility and motor function for nerves. Look for vascular
injury. In injuries commonly associated with vascular injury, such as knee dislocations, occult
injury should be excluded with angiogram. If angiogram not performed, repeated thorough
vascular evaluation of limb should be undertaken for first 24-48 hours
5) INVESTIGATIONS
• Hematological investigations: full blood count, serum biochemistry, clotting factor,
creatinine kinase, blood gas including pH, base excess and lactate
• Ultrasound: useful for soft tissue injuries
• Radiography- mainstay of initial evaluation of extremity trauma. Remember rule of 2’s:
i) 2 views-in orthogonal planes to avoid missing a fracture out of plane on 1st radiograph
ii) 2 joints- radiographs of joints above and below fracture
iii) 2 occasions- 2nd series of radiographs undertaken after 10-14 days if suspicion of bone injury
persists
iv) 2 sides-in paediatric injuries radiograph from opposite and uninjured site if doubt
• Computed axial tomography-good for characterising bony anatomy of injuries, allowing for
multi-planar reconstruction of injury anatomy, and 3D info. CT angio may be added for
vascular anatomy. One disadvantage- dose of radiation
• MRI-3D info without radiation involved in CT. useful info about soft tissues, info on blood
supply to bone. Disadvantage- time taken to acquire image, patients suffering from
claustrophobia-traumatic for them. Also, magnetic field may be disrupted by non-ferrous
metal and presence of ferrous metal contraindicates MRI. MRI angiography- info about
vascular anatomy
• Nuclear medicine scans- technetium 99 nuclear medicine scans register osteoblastic activity,
used to show occult fractures

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 DESCRIPTION AND CLASSIFICATION OF INJURY

SOFT TISSUE INJURY:

• First step of soft tissue injury is to decide if an open or closed fracture

• Open fracture: any fracture where the fracture hematoma communicates with a breech
in the epithelial lining, not just skin
• Severe soft tissue injury in presence or absence of fracture may still lead to
compartment syndrome

TYPE

I A low energy open fracture with a wound less than 1cm long and clean

II An open fracture with a laceration more than 1cm long without extensive soft tissue damage,
flaps or avulsion
III High energy injury irrespective of size of wound. Extensive damage to soft tissues including
muscles, skin and neurovascular structures and high degree of contamination.
Multifragmentary and unstable fractures
SUB-GROUPS OF TYPE III

A Adequate soft tissue cover of a fractured bone after stabilisation

B Inadequate soft tissue cover of a fractured bone after stabilisation (i.e. flap coverage
required)
C Open fracture associated with an arterial injury requiring repair

GUSTILO AND ANDERSON CLASSIFICATION FOR OPEN INJURIES

NEUROLOGICAL INJURY

Seddon classification:

• neurapraxia-no loss of nerve sheath continuity of peripheral Wallerian degeneration.

Recovery potential is good, may take months if pressure is removed from the nerve
• axonotmesis- nerve sheath remains intact with internal nerve fibre damage with Wallerian
degeneration. The neural tube (endoneurium) can guide regenerating nerve fibres to their
target. Good potential for recovery. Nerve fibre regrowth is at 1mm/day
• neurotmesis-complete division of the nerve, nerve sheath and nerve fibre. Poor outcome
without surgical intervention to restore continuity of nerve sheath

BONY INJURY

Describing the injury:

• name of bone injured

• region of bone injured
• pattern of fracture line: transverse, oblique, spiral, segmental or multifragmentary (fig 28.4
pg.386, from 27th edition bailey)
• presence of compression

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 • presence of displacement of fracture fragments: undisplaced or displaced
• type and degree of displacement: angulation, translation, rotation, shortening
• presence of pre-existing pathology
• associated joint pathology, dislocation or sub luxation

In children, green stick fractures, where one tension cortex fails due to plastic, less brittle nature of
bones. If compression cortex buckles, called torus or buckle fractures

Classification:

1) AO classification: first number defines bone injured, 2nd- segment of bone injured: proximal
metaphysis, diaphysis, distal metaphysis. The letter and number that follows further defines
nature of injury. (fig 28.7 & 28.8 from pg. 387, 27th edition)
2) Growth plate injury classification:
• In children and adolescents, injuries involving growth plate lead to abnormal growth or
growth arrest, complete or partial. Complete growth arrest causes length abnormalities
and partial growth arrest causes angular deformities
• Salter-Harris classification:
i) Type 1: simple fracture line just involving physis. No affect on growth
ii) Type 2: fracture line through physis exiting through metaphysis, producing
metaphyseal fragment. Seldom affects growth
iii) Type 3: fracture line through physis, exiting through epiphysis (intra-articular)
iv) Type 4: fracture line across epiphysis, cross physis and across metaphysis. Can
cause focal fusion of physis leading to abnormal growth
v) Type 5: crush injury of the physis. Growth disturbance
vi) Type 6: injury to perichondral structures by direct trauma. High chance of
abnormal growth. (Fig 28.9 pg 287 27th edition bailey)

TERMINOLOGY OF BONE HEALING AFTER FRACTURE:

• Union: fracture healed sufficiently to withstand physiological loads, with very little pain and
minimal tenderness. Radiologically: when callus bridges fracture site
• Delayed union: fracture that is slow to heal and has not healed in expected time frame
• Non-union: fracture has not healed and shows no potential to heal without intervention OR
a fracture that fails to demonstrate clinical/radiological improvement over 3 months.
• A fracture isn’t described as a non-union until 6 months after injury
• Factors with regard to non-union: biology of fracture, mechanical environment and
host (smoking/diabetes)
• 3 types of non-union:
i) Atrophic: biological problem (lack of stimulus or blood supply)
ii) Hypertrophic: when too much movement at fracture site
iii) Infected
• Consolidation: follows union and shows bone has returned to normal strength. Radiologically:
return of normal cortical pattern
• Remodelling: mostly in children bone remodels based on forces passing through it.

Indication for surgery in limb trauma:

• Fracture unsuitable for non operative treatment
• Open fracture
• Failed non operative fracture

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 • Multiple injuries
• Pathological or impending fractures
• Displaced intra-articular fractures
• Salter-Harris type 3-5
• Avulsion fracture that compromises functional integrity of a ligament/tendon around
joint
Established non-union and malunion
MANAGEMENT BY TYPE AND REGION:
DIAPHYSEAL FRACTURE:
It is composed of dense cortical bone. If the bone heals with adjacent joints in normal
relation, the anatomical reduction of fracture fragment is of secondary importance
• Restore length, alignment, rotation
• Consider whether primary or secondary bone healing is the objective
• Radius and ulna need precise reduction to function
METAPHYSEAL FRACTURE:
• A type fracture (extra articular):
o Injury is close to joint so more liable to cause joint stiffness
o Bone on either side of fracture is not same i.e. cortical bone in diaphysis and
cancellous bone in metaphysis so fixation is imbalanced
o Fixation is achieved with plates and screw but can also be achieved by
external fixator. In small joints: K-wires
o Joint congruity is not an issue
• B type fracture (partial articular)
o Joint surface is involved so alignment and congruity are important to maintain
o Here congruity is of prime importance so is obtained by light weight fixation
o Treated with screws or screw with plate
• C type fracture (complete articular):
o Joint surface is involved
o Need joint congruity and bone alignment
o Treated with plates and screw or external fixator
o When articular surface separated from metaphysis, articular surface first
anatomically reduced by k-wire or lag screws, then articular block re-attached
to shaft
• Osteoporotic intra articular fractures are a challenge. Rigid fixation devices may cut
out of soft bone. Injectable bone substitutes used to fill bone voids and augment
fixation.
Thumb metacarpophalangeal ulnar collateral ligament:
• Called game keeper's thumb or skier's thumb caused by thumb forced laterally away
from hand
• Tenderness on ulnar aspect of metacarpophalangeal joint
• Assessment with stress test
• Treatment:
o Partial tear: cast immobilisation
o Complete tear with instability: open reduction of ligament to restore bone
contact , with a suture anchor repair of ulnar collateral ligament as ends of
ruptured ligament may become separate by aponeurosis of adductor pollicis
so natural healing cannot take place (Stener lesion)
o Rupture of ulnar collateral ligament suspected when ulnar directed force
directed at MCP joint
Distal radial fracture:
• Common is type A fracture. Volar or dorsal direction.
• Significant initial displacement and comminution: fracture reduced and held with k-
wires, plate and screw fixation or external fixation.

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 • Intra-articular fractures (type B and C) require anatomical reduction. A gap or step of
less than 2mm may be accepted in the radius
• Most common form of treatment: closed reduction and percutaneous k-wire fixation,
and plaster cast for 4-6 weeks
Radius and ulna:
• Both work together coupled at proximal and distal radio ulnar joint for forearm
pronation and supination. Therefore, principles same as intra articular fracture:
anatomic reduction and rigid fixation
• When both radius and ulna involved: open reduction, anatomic alignment and rigid
plate fixation.
• Isolated fractures of ulna: night stick fractures. Treatment depends on patient factors
as non operative management here risks non-union and delayed union
Olecranon fracture:
• displaced or undisplaced
• undisplaced fracture < 2mm gap at articular surface: treated non operatively
• in displaced: fixation with k-wire and figure of 8 tension band wiring or plate fixation
Humeral shaft fracture:
• Majority of fractures are non operatively managed with functional brace and collar
and cuff. Achieves union in 12 weeks. Active shoulder abduction avoided to prevent
varus deformity
• Indication for operative management: open fracture, presence of humeral head
injury, multiple injury, ipsilateral arm fracture
• Operative measure: plating is generally treatment of choice, but intramedullary
nailing can be done (high risk of non-union)
• Radial nerve: most commonly injured nerve in humeral shaft fractures
• If nerve injury at time of original injury: non-operative injury
• If nerve injury after injury (e.g. at time of brace application) then it should be explored
Fractures of proximal humerus:
• Neer classification- 4 individual pieces of proximal humerus (articular head fragment,
lesser tuberosity, greater tuberosity and shaft)
• If a fragment displaced by more than 1cm or angulated by more than 45 degrees in
respect of another fragment, then considered a part
• The greater the number of parts, higher chances of interruption of vascularity of head
• 3 factors used to predict vascularity of humeral head:
1) Fracture through anatomical neck
2) Loss of medial hinge
3) Less than 8mm of bone along medial calcar
• Displaced fractures, avascular head in older patients with osteoporosis and other
comorbidities, requires replacing humeral head (anatomical hemiarthroplasty).
Limitations: involves reliable healing of tuberosities and rotator cuff so now a primary
reverse polarity shoulder prosthesis is used.
• In younger patients: reduction and fixation
Clavicle fractures:
• Diaphyseal fractures of middle third: broad arm and sling
• Mid-third: mostly non operative treatment
• 2cm shortening of clavicle impacts shoulder girdle function. Internal fixation with intra
medullary device or plate and screw construct restores length, alignment and
rotation.
Femoral shaft fracture:
• Traction is applied for 12-16 weeks as first aid to relieve pain and maintain length
(long time in hospital)
• Most femoral shaft fractures: locked intramedullary nail (up and about soon)
Patellar fractures:
• Undisplaced: non-operative treatment

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 • Displaced: anatomical reduction
• Cartilage on patella is very thick, so increased amounts of displacement compared
with other joints is accepted
• Simple displaced: 2 k-wire and figure of 8 tension band wiring
• Multifragmentary: patellar excision (reduces advantage of extensor mechanism)
Tibial plateau fractures:
• Ct scan to see full extent of injury
• Undisplaced: non-operative with hinged knee brace, weight bearing over 8-12 weeks
• Displaced: reduction and stabilisation
Tibial shaft fracture:
• For undisplaced non comminuted fractures (type A fracture): closed reduction and
above knee cast, after 4-6 weeks it is changed to moulded patella tendon bearing
below knee cast to allow knee to move
• For comminuted and complex fractures (unstable B or C type fractures):
intramedullary nail is frequent choice
• Unstable fracture near metaphyseal junction at knee and ankle: plate and screws
• External fixation is also good option for many tibial shaft fractures
Ankle fracture:
• 2 columns: medial and lateral. Each column has bony and soft tissue component
• Lateral side: lateral malleolus, lateral collateral ligament and syndesmotic ligaments
• Medial side: medial malleolus and medial collateral ligament (deltoid ligament)
• If one column injured, then stable injury: treated non operatively with cast or splint
protection for 6-8 weeks
• If both columns involved or talar shift: open reduction and rigid fixation
Calcaneal fractures:
• Os calcis injury by fall from height
• Most involve posterior facet of sub talar joint
• Severity assessed by Ct scans
• Treatment depends on severity of injury, and widening of heal leading to peroneal
impingement
Talus fracture:
• Most common injury: talar neck fracture (caused by forced dorsiflexion of forefoot-
aviator’s astralgus)
• In displaced talar neck fractures: blood supply to body of talus interrupted
Tarsometatarsal (Lisfranc) joint injury:
• Injury follows forced plantar flexion of mid foot, or when foot forced flat by heavy
weight
• Diagnosis: plain radiograph or CT
• Treatment: closed reduction and plaster cast application, k-wire fixation
Achilles tendon rupture:
• 20% injuries are missed at initial presentation
• History: sensation of being kicked at the ankle while playing sports
• Simonds test positive: patient is prone, feet off the edge of the bed, squeezing calf to
produce passive plantar flexion of ankle (no movement)
• D/Ds: intrasubstance tear of gastrocnemius muscle (Simmonds test painful and
negative)
• Diagnosis: ultrasound
• Treatment:
o Small gap: serial plaster
o Wide gap >5 mm gap: percutaneous repair
Managing fracture in skeletally immature:
• Children fracture heal more rapidly than adult fractures
• Nearer the fracture to growth plate, greater remodelling capacity

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 • In extra articular fractures there is remodelling potential, so increased degrees of
deformity may be accepted
• Remodelling is greatest at the ends of bone that contribute most to longitudinal
growth e.g. distal femur, proximal humerus
• Pediatric fractures heal more rapidly so do not need to be held as long as in adults
• Growth plate injuries are reduced anatomically
• Repeated attempts to fix physis result in injury to growth plate leading to growth
arrest
• Internal fixation should not be performed at physis, if absolutely necessary smallest
pins should be used
• Commonest site of growth arrest is distal and proximal tibia, distal radius and distal
femur
• Paediatric periosteum very thick, requiring exaggeration of deformity & pushing
fracture back instead of just longitudinal traction. Periosteal hinge preserved for
better holding
• Complications unique to children: growth arrest, progressive angular or rotational
fracture, overgrowth of long bone (post femoral fracture)
SPECIFIC PEDIATRIC INJURIES:
Distal radius fracture:
• Most common fracture in children
• Fracture proximal to growth plate may be treated symptomatically or by manipulation
under anesthesia
• Physeal fracture: closed manipulation and fracture held in position, with a below
elbow plaster cast. Growth arrest rare after Physeal fracture of distal radius
• Complete metaphyseal fracture of distal radius requires manipulation while ulna is
intact, holding is a challenge as brachioradialis is a continual deforming force
• Secondary redisplacement is common, so weekly radiographs for 3 weeks and if
displaced so require primary K wire
Distal humeral (supracondylar) fracture:
• Associated with two main complications:
o Neurovascular compromise - early complication
o Residual deformity - late complication due to poor initial reduction or loss of
reduction e.g. varus or valgus deformity is common at elbow
• Undisplaced: collar and cuff or back slab for 3 weeks, then progressive mobilisation
• Minimally displaced (dorsal periosteal hinge intact) = above elbow cast for 4-6 weeks
• Displaced (periosteal hinge is broken) = k wire is required plus an above elbow cast
• Complication of paediatric supracondylar fracture: Volkmann’s ischemic contracture.
This is due to excessive swelling and missed compartment syndrome. Don’t put
elbow in deep flexion if lot of swelling. If deep flexion only way to hold then k wires
• White pulseless hand: surgical emergency
• Pink pulseless hand: if satisfactory perfusion, then reduce and stabilise. Pulse
returns in 24-48 hours
Lateral condylar mass fracture at elbow:
• Apparently benign injury which is easily missed but if missed results in significant
morbidity
• Clinical feature shows localised lateral tenderness
• Radiograph: small flake of distal humeral above capitellum as the bulk of fracture lies
within cartilage which has not yet ossified (very deceptive)
• It is intra-articular fracture that crosses the growth plate
• If displaced or unstable: anatomical reduction and fixation
• If stable: non operative treatment
• If late reduction is performed it may develop avascular necrosis of capitellum and
non-union of lateral condyle lead to so called fish deformity
Femoral shaft fracture:
• Reduced with traction

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 • In infants <12-15 kg simple gallows traction is performed i.e. leg suspended vertically
with the buttocks just off the bed
• Toddlers and small children: traction followed by hip spica application. Shortening of
up to 1cm and angulation of 15-20 degrees acceptable
• Children 4-12 years: traction & hip spica OR elastic stable IM nailing (ESIN) OR
external fixation
• Older children and adolescents = operative fixation is performed (ESIN, external
fixation)
• Overweight adolescents: locked IM nailing as titanium elastic nails not strong enough
• Intramedullary nailing should be avoided in < 12 yrs girls and <14 years boys as it
can cause growth arrest
• Adults = intramedullary nail
Tibial shaft fracture:
• Unstable tibial fracture that is not amenable to cast management is: external fixation,
elastic nailing, plating are all reasonable options
• Remodelling in tibia is limited, so less angular deformity accepted
SPECIAL CONSIDERATIONS:
Osteoporotic fracture:
• Fragile fracture = minor accident can cause fracture
• Fixation must allow full weight bearing
• Internal fixation in osteoporotic bone remains a challenge because it leads to backing
out of screws and loss of fracture reduction
• Locking plates and bone void fillers are used to overcome these problems
Intra-articular fracture:
• Long term complications of post traumatic arthritis are relatively less important in
elderly
• Dealing with tibial plateau fracture initially requires examination under anesthesia
o Stable: non operative management
o Unstable: operative management with grafting
Pathological fracture:
• When abnormal bone fails under normal load
• Typical history of fracture with mild trauma
• Investigations: blood tests, radiographs, bone scan
• Primary tumor: treated to prevent dissemination
• Metastatic tumors: treatment to reduce pain and morbidity. If poor life expectancy,
stabilisation with a load bearing device. If isolated metastasis: enbloc excision of
primary and secondary
• If metastatic deposit seen before fracture prophylactic fixation if impending fracture
likely
Open fractures:
• Good stabilisation of bony injury and management of soft tissue injury important for
good outcome with low complication rate
• Aim of management: bony union, optimum function and avoid infection
• Treatment:
1) Pre-surgical phase:
o Photograph to document severity of injury and limit repeated openings
o Assess neurovascular status. If compromised and fracture displaced, quickly
remove macroscopic dirt and reduce fracture/dislocation. Not necessary
anatomical reduction, just remove pressure from soft tissues
o Splint affected limb; treatment of open fracture is treatment of soft tissues
o Apply moist saline dressing
o IV antibiotics (broad-spectrum)
o Obtain tetanus immunisation history and treat accordingly
o Inform senior and make preps for surgical phase
2) Surgical phase:

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 oStable fixation of bony injury important to prevent deterioration
oStabilisation: external fixation, internal fixation
oManagement of soft tissue critical to prevent zone of injury spread
oDebridement
oLose or devitalised bone fragments discarded
osoft tissue reconstruction involves primary or delayed primary closure of
wound, or microvascular free tissue transfer
o continue IV antibiotics 48 hours after definitive wound closure
COMPARTMENT SYNDROME:
• raised pressure in Osseo fascial compartment to a level which compromises
perfusion
• causes: fractures (70%), soft tissue constructions (23%), bleeding disorders, burns,
post ischemic swelling, tight casts/dressings, extravasation of IV infusions
• pathophysiology: increased tissue pressure, reduced micro perfusion, tissue
ischemia, irreversible muscle damage
• pain out of proportion, increasing pain and pain on passive stretch. Late features:
paralysis, paresthesia, pallor
• monitoring useful in diagnostic uncertainty and in altered consciousness
• accepted pressure thresholds: absolute pressure>30 mm Hg or pressure difference
(diastolic pressure-compartment pressure)<30mm Hg
• emergency treatment: splitting casts and/or dressings to skin and elevating extremity
• can occur in open fracturess

Chap 30,31 → add in IM, very similar

Chap 32: Disaster surgery

DISASTER SURGERY
INTRODUCTION:
natural disasters like flood, earthquake, depletion of ozone layer, global warming have
enormous impact on human life.
COMMON FEATURES OF MAJOR DISASTER:
• any event that results in loss of human life is disastrous
• Unnatural events like plane crash and accidents
• Common features are:
o Massive casualties
o Damage to infrastructure
o A large number of people requiring shelter
o Panic and uncertainty among people
o Limited access to area
o Breakdown of communication
FACTORS INFLUENCING RELIEF EFFORTS AND PROVISION OF MEDICAL AID:
• communication: major tool enabling authorities to respond quickly (wireless
technology and satellite imagery have improved communication)
• Location of disaster: rural or urban e.g. terrorist events target to large population.
Natural disasters occurring in remote area are difficult to deal due to geographical
isolation and lack of infrastructure
• Accessibility to location: densely populated areas have better medical services,
but have limited access by road and air
• Time frame in which disaster occurs e.g. earthquakes happen in matter of
seconds, but floods and tsunamis continue for days
• Economic state of development of area

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SEQUENCE OF RELIEF EFFORTS AFTER DISASTER:
1. Establishing a chain of command: for the country it is its organisation that deals with
particular disaster
2. Damage assessment: first objective in disaster is damage assessment and the
number of casualties. 24-hour news services are first on scene
3. Mobilising resources: all modes of transportation are used but helicopter is quickest
4. Rescue operation: must have trained members and also complement local
volunteers who are familiar to that area. First priority is to prevent further damage
(people & infrastructure)
o People with head, thorax and abdominal injuries will either have been treated
or succumbed to death by 24-72 hours
o After 2 weeks (1 in 27th edition) only casualties requiring treatments are those
with complex limb trauma or wound infection
5. Coordination with relief agencies: help from govt and non govt organizations (NGO)
in response to disaster
o Rescue and preparedness in disaster (RAPID) deals with search and rescue
o International committee of red cross (ICRC) and Oxfam deal with general
disaster related relief
o WHO and world food program (WFP) and UN high commissioner for refugee
(UNHCR) deals with medical care, food provision and refugees
6. safety of helper: if help arrives late it is common to encounter mobs looting food and
essentials which result in injuries
7. Dealing with media: media has powerful influence in shaping public opinion. With
careful handling media can become a powerful ally and play constructive role
8. Triage: arise from French word trier meaning to sort and is cornerstone of
management of mass casualties. Its aim is to identify the patients who will benefit the
most by treating earliest. Ensuring ‘greatest good for greatest number’ Triage lessens
the immediate burden on medical facilities by sorting out minor injuries. To keep pace
with changing clinical picture of an injured person, triage is done in field before
evacuation and at the hospital
o Mistake by seniors: they assume that their energies will be better utilized in
actual patient management rather than in triage
o Triage area: injured are brought into undamaged structures like school or
stadium to provide shelter, water, light and treatment to injured and also
decide area of morgue.
o Practical triage: emergency life saving measures should proceed along with
triage helping in decision making. ABC, vital signs, GPE, brief history
o Documentation for triage: contain basic patient data, vital signs with timings,
brief details of injury(preferably on diagram) and treatment given and attach
colour coded tags to patients neck or wrist
o Triage categories: all methods of triage are simple criteria based on vital
signs. Rapid clinical account taking into account patients’ ability to walk,
mental status, ventilation and capillary perfusion. Triage carries serious
consequences especially for patients who are consigned to unsalvageable
category. Rapid clinical account taking into account patients’ ability to walk,
mental status, ventilation and capillary perfusion

Priority Colour Medical need Clinical status Example

First (I) Red Immediate Critical but likely to Tension pneumothorax, severe
survive with early facial trauma, hemothorax, flail
treatment chest, profuse external bleeding,
major intra abdominal bleed, extra
dural hematomas

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 Second Yellow Urgent Critical likely to Compound fracture, degloving
(II) survive if injuries, pelvic fracture and spinal
treatment is given injury, ruptured abdominal viscus
within hours

third (III) Green Non urgent Stable likely to Simple fracture, sprain, minor
survive even if laceration
treatment is
delayed hours to
days

Last (0) Black Unsalvageable No breathing and Severe brain damage, very
pulseless, no extensive burns, loss of chest
medical treatment /abdomen wall structures
can help

9. Evacuation of casualties: a quick retriage is important to find out if travelling is safe

for patient and are definitive surgery facilities available there. Adequate supply of essentials
such as IV fluids, dressings, pain medications and oxygen is arranged. Prevent second
accident during transfer
10. Field hospitals: need of field hospitals depends on patient, no. of casualties and
speed with which evacuation is organised. Two basic field hospitals are
o Traditional tented structure: for initial management
o Modular type housed in containers: even operations are performed
o Which ever the facility is it should be equipped with x-ray plant, operating
rooms, vital signs monitor, blood bank, sterilising equipment, ventilator and
basic lab facilities
11. Management in the field:
o First aid
o Emergency care for life threatening injuries
o Initial care for non life threatening injuries

Condition Examples Further

First aid Suture cuts and lacerations, splinting simple fracture. Review at local
Most sent away with antibiotics and pain relief hospital

Emergency care Endotracheal intubation, tracheostomy, relieving After damage

for life tension pneumothorax, stopping external hemorrhage, control surgery
threatening emergency thoracotomy/laparotomy for internal transfer patient
injuries hemorrhage, amputation of devitalized limb and to base hospital
treatment of gas gangrene, relieving extra dural once stable
hematoma

Initial care for Debridement of contaminated wound, reduction in Transfer patient

non-life- fractures and dislocations, external fixators and to base hospital
threatening vascular repairs for definitive
injuries surgery
Replantation of amputated limbs and other extensive procedures not attempted in field
hospitals as time consuming and divert resources and personnel to treating fewer patients.
• DAMAGE CONTROL SURGERY:
o Life and limb threatening surgery in field hospital
o minimum surgery to allow safe transport

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 o Take actions to prevent deterioration of the patient during
transfer
o Secure airway (intubation, tracheostomy)
o Control bleeding (craniotomy, laparotomy, thoracotomy, repair
major limb vessels)
o Prevent pressure build up (chest drains, fasciotomy, burr
holes)
o Prevent infection by sterile closure (by extensile exposure-27th
ed)
o Remove devitalised tissue, prevent contamination to develop
in infection
• DEBRIDEMENT:
o Wounds sustained in disasters are heavily contaminated,
containing foreign bodies and non-viable tissues
o Laying open of the tissue
o Debridement reduces the chance of anaerobic and necrotising
infections and prevents systemic sepsis
o Principles of debridement for all contaminated wounds:
▪ In sterile environment with good lightening by
surgeons
▪ After anesthesia first step is opening and cleaning of
wound and copious irrigation by normal saline, pulse
lavage is ideal but large syringe is needed, then
remove foreign body with forceps, dirt enmeshed in soft
tissue is removed with excision of wound. Lavage with
pressured system controversial as tissue trauma and
spread of debris
▪ Small opening with large cavitation wound (gunshot)
require longitudinal incision for better access. Done
under tourniquet (helps visualise damaged structures,
and to identify severed ends of major nerves and
tendons)
▪ Excision of all dead and devitalised tissues e.g. skin,
non- viable muscle and crushed bone fragments.
Tourniquet let down to check vascularity of tissues.
Skin: excision minimum, only margins of wound
trimmed. Excision of devitalised muscle done
generously. Must be removed: muscle pale or darker in
color, does not contract on pinching, does not bleed on
cutting when removed. In traumatic amputations: bone
ends are tidied, muscle edges trimmed to lowest level
possible, wound left open
▪ In patient with associated fractures, skeletal
stabilisation should be obtained before repairs. (use ext
fixators)
▪ In major trauma in acute setting only vascular repair is
justified. For lacerated vessels: ends trimmed, and
anastomosis done. Loss of substance of vessel wall:
vein patch or reversed vein graft. Silicone tubing used
as temporary bypass, while vascular repair done in pts
with critically compromised distal circulation.
▪ Nerves and tendons should not be dissected
▪ Wounds in disaster are highly contaminated so do not
go for primary repair. Blood vessels and exposed joint
covered. wound then covered with fluffed gauze and

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 sterile cotton, and splinted with plaster of paris,
elevation of limb to reduce edema
▪ Broad spectrum antibiotic:3rd generation cephalosporin
prophylactically and continued for 5-7 days
▪ Reinspect wound 24-48 hours later for checking
viability of tissue. Wounds closed between 4th to 6th day
if no infection. Tension is avoided
▪ Wound with gross infection require eradication of
infection and then vacuum assisted closure is done.
Once wound is free of infection secondary closure is
undertaken
DEFINITIVE MANAGEMENT:
• Undertaken at major hospitals selected on the basis of facilities and number of
injured patients that they can handle
• Rule of thumb is that only one half the bed strength of a hospital can be utilised to
provide optimum trauma care in an emergency situation
• Hospital reorganisation:
o Transferring patient with non urgent conditions to other facilities
o Reorganise medical wards to surgical care units
o Reorganising specialist rota
o appeal for blood donation is broadcast
SPECIFIC ISSUES:
• destruction of building and explosion can produce whole spectrum of external injuries
from minor cuts to extensive degloving, compound fractures and amputation
• Those near explosion site suffer from lungs, abdominal viscera injuries and burns
• Crush injuries causing gross contamination both favourable for anaerobic and
microaerophilic infections

1. Limb salvage:
1. Mangled extremity severity score (MESS) is useful in making judgement
about limb salvage
2. Indications of amputation (in the past):
1. Extensive tissue loss
2. Neurovascular damage
3. Loss of long fragments of bone
c. Currently wound of any dimension is covered with microvascular flap to heal
d. Vascular repair can salvage acutely ischemic limb
e. Because of advancement in medicine majority of patients reaching tertiary care
facility within 24 hours have limb salvage if early debridement and vascular repair done in a
field medical facility
f. Limb is unlikely to survive if vascular repair is delayed more than 4-6 hours
Facial injuries:
. General principle of management: debridement and delayed closure
a. Due to facial involvement and extensive blood supply high ability to counter infection
b. Because of functional and cosmetic importance, skin and soft tissue excisions kept to
minimum
c. Even in patients who present late with gross contamination, careful debridement,
then delayed primary closure gives good results
Tetanus:
. Fatal condition called lockjaw is caused by clostridium tetani which is gram positive
spores forming bacilli which enters body through wound, thrives on anaerobic condition in
devitalised tissue
a. Pathophysiology: produces tetanospasmin a potent exotoxin that binds with NMJ of
CNS blocking neurotransmitter release which results in failure of motor responses to sensory

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 stimuli and generalized contraction of agonist and antagonist muscles causing tetanic
spasm
b. Incubation period is 7 days (4-14 days)
c. Clinical features:
1. Early symptoms: painful spasm of masseter and facial muscle (risus
sardonicus)
Spasm of paravertebral and extensor limb musculature producing opisthotonus, an arching
of whole body. Laryngeal muscle spasm causes apnea, asphyxia, respiratory arrest
d. Diagnosis: clinical
e. Prevention: active immunization of 0.5 mL tetanus toxoid IM. Gross contaminated
wounds are provided with 250-500 units human anti tetanus globulin (ATG) IM. Full blown
tetanus requires 3000-10000 units ATG. Avoid wound manipulation for 2-3 hours after ATG
administration to minimise tetanospasmin release.
f. Wound care:
o Debridement
o IV penicillin G 10-24×106/day for 10-14 days
o Delayed primary or secondary closure
g. Supportive care for established disease: manage patient in ICU (or in dark quiet
room). Diazepam for spasm is given, but if they become sustained, patient
paralysed, intubated and placed on ventilator. Gradually weaned off ventilator
under cover of anticonvulsants
iv. Necrotising fasciitis:
a. Dangerous and rapidly spreading infection of fascial planes leading to necrosis of
subcutaneous tissues and overlying skin by beta-hemolytic streptococci (most common)
b. Other pathogens: staph aureus, bacteroides, clostridium, proteus, pseudomonas,
klebsiella
c. Fournier's gangrene: its is called Fournier’s gangrene when it affects perineal area
d. Meleney's synergistic gangrene: affecting abdominal wall
e. Clinical features:
1. Inflammatory infiltrate, excessive necrosis, edema, thrombosis
2. Painful, very tender area with dusky blue or black skin due to
thrombosis
3. Bullae progressing to overt cutaneous gangrene with subcutaneous
emphysema producing skip lesions that later coalesce
4. Fever and generalized toxicity
5. Septic shock, renal failure, hypovolaemia, cardiovascular collapse
6. Without aggressive treatment mortality is 70%. Progresses rapidly
f. Diagnosis:
1. Clinical
2. Elevation of CK
3. Biopsy (confirmatory)
g. Treatment:
1. Admit to ICU with aggressive treatment
2. Oxygen therapy (hyperbaric oxygen -HBO) 100% at 2-3 atm pressure
or intubation
3. High dose penicillin G, broad spectrum antibiotics ( 3rd generation
cephalosporin ) and metronidazole given IV until toxicity abates
4. Surgical excision of necrotic tissue (removed generously going
beyond area of induration) and control bleeding by transfusion. Wound
lightly packed with gauze and dressed. This whole process is
repeated daily as necrosis prone to spread beyond edges of excised
wound. This results in large wound, so skin grafting or flap coverage
Gas gangrene:
. Dreadful consequences of inadequately treated missile wound, crush injuries and
high voltage electrical injuries

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 a. Rapid progressive condition characterised by widespread necrosis of muscles and
soft tissue destruction
b. Causative organism: clostridium perfringens gram positive spores forming
saprophyte living in anaerobic environment
c. Non clostridial gas producing organisms are isolated in 60-85% cases of gas
gangrene
d. Pathogenesis:
i. alpha toxin is a lecithinase that destroys rbcs, wbcs, platelets, muscle cells and
fibroblast
ii. Phi toxin causes myocardial suppression
iii. Kappa toxin for destruction of connective tissue and blood vessels
e. Incubation period is <24 hours (1hour-6weeks)
f. Clinical features:
o Necrosis of muscles, thrombosis of blood vessels
o Progressive edema further compromising blood supply
o Production of gas (nitrogen, hydrogen sulphide, carbon dioxide)
o Hypotension, shock, hemolysis, renal failure and ARDS
o Earliest symptom is pain that rapidly increases in severity due to myonecrosis
o Swelling of limbs and serosanguinous discharge
o Brown then blue-black skin (due to muscle necrosis) with hemorrhagic bullae with
sickly sweet odour and crepitus of soft tissues
o Pyrexia, tachycardia, tachypnea, altered mental status
g. Diagnosis: clinical, blood smear showing hemolysis, metabolic acidosis and renal
failure in biochemical profile, CT showing gas in soft tissues
h. Treatment:
1. High dose penicillin G
2. Clindamycin and 3rd generation cephalosporin IV
3. Surgical excision of necrotic tissue is mainstay of treatment
4. Amputation in established gas gangrene with systemic toxicity (shouldn’t be delayed)
5. Amputation stumps are left open, wound lightly packed with saline soaked gauze,
then dressed
Blast injuries:
Mechanism of blast injuries:
o Bombs and shells rupture to produce high velocity fragments which cause
devastating injuries
o Blast waves: cause internal injuries and air fluid interfaces
• Dynamic overpressure: complex blast wave composed of blast pressure
waves
• Blast wind: mass movement of air at supersonic speed
o Injured organs: ear, lungs, heart and to lesser extent GIT
. General management of blast injuries:
• Structures injured by primary blast wave in order of prevalence are middle ear, lungs
and bowel
• Most common urgent clinical problems in survivors are penetrating injuries
• Other injuries: blunt, blast and thermal injuries
• Soft tissue wounds are heavily contaminated
• Management: ATLS protocol
Crush injury and syndrome:
Crush injury: injuries which occur when body part is squeezed between two heavy or
immobile objects. Damage occurs include laceration, fracture, bleeding, bruising,
compartment syndrome and crush syndrome
Crush syndrome:
I. Associated with rhabdomyolysis and renal failure

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 II. Prolong crushing of muscle leads to reperfusion injury which releases myoglobin
and vasoactive mediators, causes myoglobinuria leading to renal failure from
tubular obstruction and also sequesters fluid reducing intravascular volume, renal
vasoconstriction and ischemia
III. Treatment should be given immediately. Late fasciotomy may make situation
worse
IV. Treatment plan:
1. First aid
2. Aggressive volume load i.e. saline infusion of 1000-1500 ml/hour with monitoring
urine output
3. Continued until myoglobin become undetectable in urine
4. Mannitol administration can reduce reperfusion component of injury. Once flow of
urine observed, mannitol alkaline diuresis of upto 8 L/day maintained keeping pH
of urine >6.5
5. Late fasciotomy: causes massive release of myoglobin, so fasciotomy not
performed if entrapment for over 12 hours.
6. Fluid balance and renal dialysis
Compartment syndrome:
2. Pressure within the muscle compartment rises as the result of trauma.
Occurs in muscles enclosed within fascia e.g. calf and forearm
muscles
3. Close bandage, plaster, blunt trauma can lead to rise in pressure
exceeding venous drainage pressure then increase in arterial
pressure decreasing muscle perfusion
4. Distal pulses are still palpable
5. Some people develop early paresthesia
6. Diagnostic: passive stretching of muscle produces extreme pain
7. In early stages fasciotomy is helpful. If not done later signs like distal
numbness and pulselessness will occur
8. Muscle will die and produce fibrosis and shortening producing a
volkmann's ischaemic contracture
9. Diagnosis in unconscious patient: intra-compartmental pressure (not
reliable acc to 27th ed)
10. If suspicion fasciotomy performed
Hypothermia: rectal temp <35°C or 95°F
. Major cause of morbidity and mortality in disaster of cold region
a. Body responds to cold temperature by vasoconstriction due to release of
catecholamine and shivering
b. If temperature continues to fall results in decrease metabolism, hypoventilation,
bradycardia and disturbed clotting function
c. Temp < 28° C /82.4°F leads to ventricular fibrillation
d. Mild hypothermia symptoms: dizziness, lethargy, joint stiffness, nausea and pale
skin
e. Severe hypothermia: hallucination, stupor, coma and cardiac arrest
f. Treatment:
i. Remove wet clothes and move to dry shelter
ii. Warm the room
iii. No fluid should be given oral and passively warm the body
iv. Cover patient with blanket or sleeping bag and rewarmed for 24hrs at room temp (25-
33°C)
v. Blood volume is expanded using crystalloids 300-500 ml
vi. In life threatening cases humidified oxygen is given 10L/min
vii. Even with cardiac arrest resuscitation must be performed and patient should be
rewarmed before labelling dead

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viii. Central venous lines are maintained to give warm fluid and inotropic agents with
defibrillator for arrhythmias
Frost bite and immersion injuries (trench foot):
. The part of body freezes with cells disrupted and tissue dies
a. It is actually a cold burn and categorised according to depth of burn
b. Mechanism: vasoconstriction and reperfusion injury by free radicals on rewarming in
fingers, toes, cheeks, tip of nose and ears
c. When tissue is frozen it gets hard and not be indented
d. Immersion injury occurs due to immersion for long in cold water but do not cause
freezing of tissues hence called trench foot
e. Treatment:
i. Rewarm patient gradually (as heat used may actually cause a burn)
ii. Rehydration swith warm fluid and NSAID like ibuprofen are beneficial
iii. Demarcation between viable and dead tissue occurs naturally
iv. Dead tissue can be left for months before excision as considerable deep recovery
occurs
v. Prevent further injury and infection
HANDING OVER:
• Follow-up and secondary problems:
o Initial treatment is directed to anatomical restoration of damage structure
o Secondary treatment occurs after 3-6 months to deal with nerves, tendon,
bone grafting and osteomyelitis treatment
• Designated centres:
o Initially the casualties are distributed to various hospitals but after first few
weeks only long-term cases are left so they should be advised to certain
designated hospitals to make follow up easier and concentrates expertise and
resources
DISASTER PLAN:
1. Establishment of national level disaster management organisation: 1st step for
management of disaster
2. Anticipating disasters: carry out threat assessment like volcano eruption, flood etc.
and set up early warning system
3. Evacuation planning: evacuation of whole population in the wake of an impending
disaster, clear identification of exit routes must be determined and communicated
with population at risk
4. Organisation of emergency services: fire brigade, police, ambulances must have
definite roles
5. Medical planning: identify and designate hospitals which are able to take large
number of casualties, location of areas that can be used for patient holding and triage

CONFLICT SURGERY(extra chap in 27th

edition)
How is war surgery different?

• Environment of war likely to be austere. Sophisticated diagnostic and therapeutic

techniques may not be available
• War is hostile and potentially dangerous. Medical personnel at increased risk
• War injuries are different than civilian trauma. Modern weapons deliver such amounts
of energy that the tissue destruction and patterns of injury are unlike all but the most
extreme of civilian trauma practice

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 • War is a mass casualty situation. Triage, an important aspect of military surgery. “Do
the best for the most, not everything for everyone.”
• War surgery delivered in stages. Principles of damage control surgery often applied
Ethical and legal considerations

• International humanitarian law (IHL)regulates humanitarian issues during armed

conflict
• It provides medical personnel with rights in times of armed war, also assigns duties to
them surrounding rights of protected personnel under their care
• Medical personnel bound by medical ethics and IHL to treat patients solely based on
need, without regard for nationality, race, class, religious, political beliefs
• Along with medical care to deployed forces, treatment to both home nation and
enemy combatants
• Medical personnel and facilities are protected under IHL and not attacked. Still
security of facilities and personnel is at highest priority
Medical support roles

• The term ‘role’ used to designate tiers of medical support that integrate into modern
military operation
i) Role 1: routine primary health care, specialised first aid, triage, resuscitation and
stabilisation
ii) Role 2: intermediate capability of reception and triage, resuscitation and
treatment of shock at higher level than role 1. Prepared to provide evacuation
from role 1. Capability for DCS, limited holding facility for short term holding of
casualties till return to duty or evacuation
iii) Role 3: deployed hospital care with multi-specialty capability. Variety of
specialties e.g. primary surgery and diagnostic support
iv) Role 4: definitive medical care that cannot be deployed to theatre or is too time
consuming to be conducted there.
These roles highly variable between different nations
Medical evacuation

• refers to movement and en-route care of casualties within conflict zone.

• Aeromedical evacuation using either fixed or rotatory wing aircraft, has had major
prior to and during aeromedical evacuation. Certain considerations prior to and
during aeromedical evacuation:
i) Patient sufficiently stabilised
ii) Airway and breathing adequate for movement
iii) Iv access, surgical drains, urinary catheters and other tubes firmly secured
iv) Pts at high risk for thoracic barotrauma: prophylactic chest tube placement
v) Blankets and/or warmers should cover patient securely to mitigate against
hypothermia
Patterns of modern war surgery

• Head and neck injuries more common in recent conflict while thoracic and extremity
injuries were less so. Due to increased use of body armor and PPE
• Mechanism of injury has also changed. While ballistic injuries are still and imp
contributor to battlefield trauma, injured due to explosions (implosive explosive
devices (IEDs), landmines, mortars, grenades, rockets) are more common

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 • The relative low cost, ease of production and widespread expertise means IEDs will
play significant role in most conflicts
Principles of war surgery:

• Battlefield death occurs early (or immediately) due to CNS injury and hemorrhage, or
late due to infection.
• Some injuries causing immediate death are non-survivable and only managed with
prevention.
• Treatment of hemorrhage is mainstay of military trauma management
• Bleeding should be recognised. Tourniquets for control of catastrophic extremity
bleeding.
• Non-compressible torso hemorrhage carries poor prognosis
• Approach to surgery to stop bleeding, remove necrotic tissue and foreign material
and remove contamination
• Life saving surgery, procedures to salvage limbs, including revascularisation and
fasciotomy
Damage control surgery

• Restore physiology over anatomy

• Phases:
➢ Phase 1: recognition of injury severity, need for damage control principles, both
surgical and resuscitative. Features: rapid sequence induction of anaesthesia
and intubation, early rewarming and prompt movement to OT
➢ Phase 2: immediate laparotomy with rapid control of bleeding and contamination,
abdominal packing and temporary wound closure
➢ Phase 3: movement to ICU for ongoing resuscitation with normalisation of
biochemical and physiological parameters
➢ Phase 4: re-exploration in theatre to provide definitive repair. Multiple procedures
on multiple occasions. If physiology deteriorates, nonessential procedures are
delayed
Multiple trips to theatre increase likelihood of morbidity including abdominal wall hernias,
fistulae and infection. Damage control resuscitation concurrent with DCS. Principle of DCR
include permissive hypotension, avoidance of crystalloid with hemostatic resuscitation, and
recognition and management of acute traumatic coagulopathy (ATC). Application of these
principles to military pts is uncertain because of longer timelines
Massive transfusion

• Degree of injury and massive blood loss, in war injuries necessitates large volume
transfusion
• Use of crystalloids to resuscitate exsanguinating patients is highly discouraged
• Blood transfusion administered in a more forward location (both role 1 & 2) with limited
volumes of blood transported to point of wounding by aeromedical response teams
Decision making within the deployed environment

• In role 3 unit, both DCS and definitive procedures possible

• Decision making crucial in austere environment. Theatre space, intensive care beds,
equipment and blood products are limited.
• Limited resources such as blood divided in 2 patients. In role 1 & 2, immediate
evacuation in preference to more thorough stabilisation

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Weapon effects
Ballistics

• ability to manage conflict injuries relies on understanding of underlying mechanism of

wounding
• ballistic weapons work with the same principles-an explosion is used to propel a
projectile along and out of a straight tube. The explosive force within a modern firearm
comes from a propellant encased within a cartridge.
• Internal ballistics describes characteristics of projectile, while inside the hammer
mechanism of the weapon strikes a primer at the base of the cartridge, which ignites the
propellant. Hot gas produced by the explosion expands and forces bullet away from the
cartridge and along the barrel
• External ballistics describes characteristics of a projectile in free flight. Influenced by
ammunition type and ambient conditions.
• The characteristics of ammunition that determine wound effects are the size or calibre
(which describes internal diameter of weapon barrel) and the material components of the
bullet:
1. full metal jack ammunition has outer coating of harder metal around soft core.
Reduces breakdown of bullet along barrel improving accuracy, reliability, target
penetration
2. soft tip and hollow point ammunition have a degree of exposed lead that flattens
and deforms on impact. Less penetrating injury, but rapid transfer of energy to
impacted tissue and cause large wounds
Ballistic injuries:

• Terminal ballistics (or wound ballistics) describes interaction between projectiles and
target tissue
• This interaction and then transfer of energy leads to trauma
• Kinetic energy of bullet related to mass and velocity of impacting projectile
• Both mass and velocity of military firearms greater than in civilian trauma, so higher
energies and severe wounds
• Determinants of actual wound pattern: weapon and ammunition type, range, angle,
clothing, armour and anatomical variation
• Permanent cavity: localised area of definitive tissue injury caused by contact with the
projectile. This area of cell necrosis due to: direct contact, crushing and laceration of
tissues in path of projectile. Size and trajectory of projectile determines cavity size. This
type of cavity mostly by pistol bullets that have relatively low energy.
• Higher energy projectiles (military rifles and machine gun bullets) , cause more
deformation and tumbling as they travel through tissues. This increases cross sectional
area, leads to larger and less regular permanent cavity
• Temporary cavity: by lateral displacement of tissue not in direct contact with bullet.
Degree of damage depends on amount of energy and the material properties of tissue
• Individual tissues have elastic strength which resists stretching. As energy rises tissue
no longer able to rebound so contusion, laceration and permanent damage
• Skin, muscle, lung and bowel wall tissue have good elastic strength, and rebound well
after stretch with minimum damage
• Liver, brain and spleen have poor elasticity, likely to shatter when stretched
• Incompressibility of fluids within hollow organs (bowel and bladder) means vulnerable to
stretch despite favourable properties of tissue itself

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Management of gun shot wounds

• Extent of injuries not assessed without surgical intervention

• Most penetrating wounds in military setting explored under anaesthetic
• Extent and capacity of recovery of temp wound not seen at 1st operation
• Interval period allows to see permanent wound cavity, with response of surrounding
structures and demarcation of non-viable tissue
Blast

• Predominant mechanism of injury in recent conflict

• Terrorist attacks in urban centres means these injuries also mostly seen in civilian
practice
• Explosive: a substance that can be made to undergo a rapid chemical reaction that will
transform a liquid or solid into gas, liberating a large amount of energy.
• Explosive property depends on: chemical composition and speed at which energy
expelled
• Low explosives react by a process called deflagration where reaction is propagated by
flame passing through material at a rate lower than speed of sound. Made of combustile
material and an oxidant
• Low explosives: gunpowder, gasoline, pyrotechnics (fireworks and flares). Mostly cause
burns rather than typical blast injuries
• High explosives degrade via detonation. Shockwaves passed through material at
supersonic speeds and resultant energy expelled at very high rates e.g. plastic
explosives and TNT
• Input of small amount of energy produces large volume of gas, at high speed and
pressure
• Outward expansion causes wave of compressed air that moves away from point of
detonation, at supersonic speeds at uniform sphere ( in free field)
• The change in surrounding pressure called blast overpressure. Following detonation in
free field, instantaneous pressure rise which falls exponentially, explained by Friedlander
curve
• This pressure peak only seen during truly free (theoretical scenario)
• Enclosure of blast, or reflection of blast waves by people, vehicles, buildings changes
over pressure profile and high pressures sustained for longer periods, so greater injury.
Therefore, blasts in close spaces cause more severe injury
• Detonation of explosives result in expulsion of fragments.
• Blast winds generated by displacement of surrounding air. Direction of winds change as
blast overpressure drops transiently beneath ambient pressure creating partial vacuum
Improvised explosive devices

• Characteristic weapon of modern warfare

• Include road side explosives and blast mines, suicide bombers, and explosive form
projectiles (EFPs)
• EFPS: deformable plate on uppermost surface. The detonation of device and
expansion of explosive products deforms plate into missile shape, while accelerating
upwards at high velocities. Or copper plates may melt to create a high speed molten
jet (a shaped charge)
• Upon contact with target, missile impacts hull of vehicle , penetration dependent on
device and vehicle armour. Huge amount of kinetic energy dispersed through vehicle
and occupants

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 • Injuries caused by direct impact of deforming hull and gross upwards acceleration
followed by downwards deceleration of whole vehicle

BLAST INJURIES
Classification Injury type examples
Primary blast overpressure Tympanic membrane injury, blast lung,
intestinal blast injury
Secondary blast Penetrating/fragmentation All penetrating injuries
Tertiary blast blunt Blunt and crush injuries, traumatic
amputation
Quaternary blast miscellaneous Burns, inhalational injury
Quinary blast Effects of device additions Radiation sickness, infection
Classification of blast injuries
PRIMARY BLAST INJURY:

• Effect of blast overpressure most marked at interface between air and tissue or liquid
• Most common injury: tympanic membrane rupture. Patients are asymptomatic or
transient hearing loss and otorrhea
• Blast lung mechanism: spalling (disruption of tissues at air-liquid interfaces),
implosion (compression and re-expansion of air-filled structures) and rapid
acceleration of tissues of different densities
• Level of injury related to rate of chest wall displacement, rather than maximal depth
of deflection. Severity of injury dependent on strength of blast
• Those working closely with explosives wear personal armour. Torso body armour
provide protection against penetrating injury but not against effects of primary blast
• Pathophysiology of blast lung: immediate and delayed response. Immediate
bradycardia and apnea, a vagally mediated reflex.
• Lung injury itself: alveolar capillary rupture, with intrapulmonary bleeding & edema.
Range from microscopic petechial injury to frank hemorrhage depends on extent of
injury
• Primary blast may leave little external evidence of injury since skin rarely affected
• Clinical features of blast lung: progressive hypoxia
• Other structural lung injuries: pneumothoraces due to pleural rupture without
penetrating injury, injury to larger vessels causes hemothoraces and formation of
alveolar venous or broncho-venous fistulae. Air embolism due to such fistulae→acute
hypoxia with CVS collapse→leading cause of death
• Bat-wing pulmonary infiltrate on chest radiograph, CT discriminates from more
peripheral contusions in blunt trauma
• Treatment: supportive. Mechanical ventilation may be required but consideration to
possibility of air embolism and pneumothorax.
• Primary blast also affects abdomen. The effect of shock wave dispersal more marked
at tissue-air interface. So hollow organs most commonly injured. Caecum most
sensitive to intestinal blast injury. Small bowel and mesentery susceptible to large
shear waves
• Presentation of primary blast injury to the bowel delayed relative to acute onset of
blast lung.
• Abdominal symptoms absent at first then pain and frank peritonitis (if perforation &
contamination). Lack of external injury so indications for operative interventions

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 clinical. Patient assessed anaesthetically, particular importance to effect of
anaesthesia and ventilation on concomitant lung injury
• Mc operative finding: sub serosal haemorrhage. Repeated exposure to lower blast
overpressure-tearing of mucosal surface with bleeding into lumen
• Surgical management: primary repair or resection. Non-perforated but contused
bowel- damage control approach to such injuries, but in physiologically well patient,
resection of segment otherwise, perforation occurs later on
• Solid organs more resistant to primary blast. Injury with bleeding, results from rapid
distractions of organ attachments and mesenteries. This is more likely in closed
conditions
SECONDARY BLAST INJURY:

• Refers to effects of fragments that are accelerated away from device following
detonation. Sources are:
1) Casing of device
2) Purposefully placed fragments in device. Include nails, bolts or ball bearings,
embedded within device or adherent to exterior
3) Nearby objects including glass and stones
4) Biological material such as bone expelled, after suicide bomb or anti-personnel
mine attack
• Shrapnel used to describe explosive fragments
• Energy of primary blast wave disperses quickly in proportion to distance from blast:
inverse cube law. So only people in small radius affected
• Velocity and wounding potential of energised fragment subject to inverse square law.
Secondary blast injuries at long range. Fragments at high velocities
• Irregular surface of fragments: complex patterns of yaw and tumble
• Management: wound debrided. Fragment wounds considered dirty so principles of
septic surgery applied. If possible: serial debridement and delayed primary closure
• Early removal if: fragments easily accessible, in joint space, adjacent to structures
with danger of erosion and further injuries
• Late indications for removal: ongoing sepsis, pain or lack of function
TERTIARY BLAST INJURY

• Result of gross movement of personnel, objects or infrastructure by blast wind

• Wide variety of injuries to all organ systems
• Traumatic amputations included in this
QUATERNARY AND QUINARY INJURY

• Quaternary are misc. injuries not in other categories

• Quinary injuries: injury by intentional addition of biologically or radioactively active
material to explosive device
Environmental effects

• Higher rates of blast lung and TM rupture following enclosed blast (in which both
casualty and blast enclosed)
• In contrast, sec injuries lower as more people protected from energised fragments
• Higher proportion of blunt injuries in enclosed blast (tertiary)
• Underbody blast against military vehicles cause more severely injured

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 • Blunt injury is sustained from displacement within vehicle, shock wave propagates
through solid, upwards deformation of floor, rapid upward acceleration of whole
vehicle, then deceleration following impact with ground.
• Solid blast injury: severe foot and ankle and pelvic injury
• Mortality from underbody blast by head injury, non-compressible torso hemorrhage
(aortic disruption and liver laceration)
• Dismounted IED: lower limb amputation, pelvic fracture and genital, perineal and
rectal injuries
Infection

• Wounding agents are non-sterile and contaminated by bacteria

• Multiple steps in casualty evacuation and delays before treatment causes
progression from contamination to clinically significant infection
• Commonly seen bacteria: gram +ve cocci (staph, strep), gram -ve rods (E. coli,
proteus, klebsiella). Pseudomonas, Enterobacter & Serratia are nosocomial
pathogens expected after long period of hospitalisation. Bacterial dysentery:
salmonella, shigella vibrio
• Candida: malnourishes, immunosuppressed, prolonged hospitalisation, receiving
broad spectrum antibiotics, adrenocortical steroids or parental nutrition
• At points of wounding: sterile dressings applied. Antibiotics if evacuation delayed
• Empirical antibiotic therapy started after movement to medical facility
• Mainstay of treatment: prompt surgical control of infectious cause with adequate
debridement of nonviable tissue and drainage of infective material. Extensive
irrigation to remove dead tissue and foreign bodies.
• High pressure wound lavage increases bacterial propagation into soft tissues so not
done
• Closure of contaminated war wounds not done in first operation (except in facial
wounds). Open wound left with clean, moist dressings. For larger wounds: -ve
pressure wound therapy
• Contaminated war wounds considered tetanus prone, tetanus prophylaxis done
• Adequate exposure, with extension of wound mandated to ensure debridement of all
devitalised tissue. Serial operations may be required. Early consideration to soft
tissue coverage

Unit 5
Chap 34: Sports medicine and sports injuries
Sports medicine and injury
• Stressing body beyond limits leads to injury and science of understanding how they can
be avoided, recognised and treated is sports medicine.
• Injuries are of 3 types:
1. acute extrinsic due to direct external blow such as wounds, fractures and bruises
2. acute intrinsic injury due to failure of patient's anatomical structures because of
excessive loading like tendon rupture, avulsion fractures, ligament injuries
3. chronic injuries: those of unknown onset, involve degeneration or failure secondary to
repetitive loading like tendinosis of Achilles tendon or stress fractures.
Diagnosis of sports injury
1. how the person got injured
2. what type of training are they undertaking: mixed or only one?

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 3. How many hours of training, has it changed recently?
4. Have they had previous injury? When and what rehabilitation given?
5. What is the aim in way of competitions?
6. Do they want to compete again or are they worried about competing?
7. Do they want to retire or not?
Tendon disease
• Become weak or painful because of physical damage or inflammation of tendon sheath
(peri tendonitis)
• Injury due to overload (strength being exceeded by force applied) or overuse (repetitive
load leading to fatigue).
• Overuse can be due to:
1) Internal factors: decrease O2 supply or nutrition, hormonal changes, chronic
inflammation and aging.
2) External factors: worn out equipment (old running shoes) or change in environment
(new running surface)
• Weakest area of tendon in young: apophyseal attachment., musculotendinous junction in
adults, tendon insertions in adolescents. E.g. ASIS (origin of sartorius), anterior inferior
iliac spines (rectus femoris), lesser trochanter of femur (iliopsoas), ischial tuberosity
(hamstrings)
Muscle injury
• sprain, partial tear, complete or re-tear will heal spontaneously
• muscle injuries leave an area of weakness that re-tear in 30% athletes
GRADE DESCRIPTION
0 Normal muscle
1 Subtle muscle abnormality/sprain
2 Definite muscle disruption without muscle retraction
3 Complete muscle tear with retraction

Ligaments
• are acute intrinsic injuries
GRADE DESCRIPTION
0 normal ligament
1 tenderness around injured ligament but no increase in joint laxity
2 partial disruption of ligament with increase joint laxity with soft end point
3 Complete disruption, marked joint laxity, no end point clinically

• difficult to assess clinically in acute phase, use opposite side for comparison. When in
doubt, U/S or MRI
• Grade 1 and 2 treated with pain relief, splinting, gentle mobilisation to avoid stiffness
• grade 3 needs surgical repair (treatment depends on site of ligament & joint stability)
Bursae
• between joint and overlying tissue or muscle and tendons. Are small fluid filled sacks.
decrease frictional forces.
• Can be inflamed commonly the 1st metatarsophalangeal joint(bunion), in front of patella
(housemaids’ knee), behind elbow (olecranon bursitis), behind shoulder (sub-deltoid
subacromial bursitis). When don’t settle with appropriate treatment: surgical excision
Bone fractures and stress fractures
• Sportsmen sustain stress fracture due to repetitive loading. Sites: metatarsals and tibia
• Clinically: poorly localised pain, worse on exercise. More common in runners
Individual sports injury
Golf:
• Most common shoulder and back involvement. Golfer's elbow or medial epicondylitis is
common flexor origin tendonitis

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• Tennis elbow more common in golfer’s than golfer’s elbow
Tennis
• Tendinosis of common extensor origin. Partial rupture of calf muscle called tennis leg.
Rowing
• rib fractures & intercostal muscle tears. Tendon problems: tenosynovitis at wrist &
intersection syndrome (tendinosis where 1st & 2nd extensor tendon compartments of
forearm cross)
Football
• groin injuries, fractures, twisted ankle or knee, turf toe and neuromas to deep peroneal
nerve on dorsum of foot due to repetitive trauma from kicking the ball are specific to it
• goal keepers get wrist and hand injuries including occult scaphoid fractures
Rugby
• high intensity contact sport
• concussion, neck & finger injuries like rugger jersey finger (injury to flexor profundus
tendon)
Javelin
• throwers: injuries due to stress on elbow (similar to seen in baseball). Abnormalities of
ulnar collateral ligament & capitellum
Swimming
• shoulder injury. Impingement syndromes (rotator cuff tendinosis and tears)
Volleyball, netball and basketball
• hand injuries, patellar tendinopathy, internal derangements of ankle & knee
Ballet dancing
• posterior impingement of ankle & tendinopathy of flexor hallucis longus tendon when
working on tiptoe. Stress fractures in females. Back & shoulder injury in males (due to
carrying ballerinas). Young dancers: clicking & pain around hip due to iliopsoas
tendinopathy
Snowboarders and skiers
• high speed sport
• rigid high boots used by skiers protect ankle but increase load up the limb risking tibia
fracture & knee ligament disruption (especially anterior cruciate)
• snowboarders: wrist fractures & acromioclavicular joint injury
Martial arts: judo, karate & taekwondo
• acute extrinsic and intrinsic injury
Weight training
• chronic injury (pectoralis major tears, carpal tunnel syndrome and spine)
Kayaking
• forearm problems including posterior interosseous nerve compression at elbow
Marathon running
• iliotibial band syndrome & stress fractures in feet & shins
Injuries acc to region of symptoms
Pelvis, hip and thigh injuries
1) thigh bruise (charley horse, helmet or corked thigh)
• in all contact sports, large and painful
• require rest as slow to settle and can rebleed. Pseudo-tumor may develop
• surgical drainage should be avoided, as leads to infection of hematoma
• percutaneous aspiration under antibiotic cover
2) quadriceps tears
• in aponeurosis of rectus femoris mostly due to twisting, as weak point where 2 muscles
join
3) complete quadriceps rupture
• while kicking or in old patients
• pt can perform straight leg raise but cannot restraighten raised leg (quadriceps lag)

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• surgical repair only in athletes
4) hamstring injury
• due to twisting mostly in biceps femoris tendon
Groin pain
• difficult to assess as referred pain from: hip (labral tears & OA), adductor tendon injuries,
stress femur fracture, hernia (femoral & obturator), tumors, STDs, gynae and urinary
problems, lumbar spine
• adductor tendon injuries: localised tenderness over adductor region
• labral tear produces impingement sign (clicking & pain in internal rotation & adduction)
Knee injury
Acute (very difficult to examine in acute stage)
• common in contact sports due to studded boots applying loads to knee in rapid turning
• if patient can’t continue playing and knee is swollen immediately then there is blood in
knee, due to anterior cruciate ligament tear, dislocation of patella (relocates immediately)
& intra articular fracture
• If the person continues to play and swelling occurs later so it’s meniscus tear, do fluid
aspiration (it’s clear) and physiotherapy
• Patellar dislocation in hypermobile patients. If not already relocated, straightening knee
will do that
Subsequent diagnosis
• Patellar dislocation: apprehension sign.
• True locking due to loose body in knee or torn meniscus. Person moving normally and
then suddenly cant straighten or bend knee. After period of jiggling, again normal.
Dx: Thessaly’s test specific for this. Imaging is done as clinical assessment difficult
• If meniscal tear is peripheral (where blood supply providing environment for healing),
repair it
• Patellofemoral pain in adolescents when vastus medialis wastes rapidly, and patella
starts to mal track.
CF: difficult to descend stairs &severe pain when moving knee after held still (pseudo-
locking) when descending stairs. Tx: physiotherapy
• Instability due to ant cruciate ligament disruption. Knee gives way on twisting.
Dx: Lachmann test is positive. Tx: physiotherapy if fails, graft may be needed
• If posterolateral corner ligamentous injury & ant cruciate ligament injury: surgery
• Iliotibial band syndrome due to friction over greater trochanter and tibia in long distance
runners (proximally in females and distally in males). If no response to stretch & rest,
steroid injection in adjacent bursae
Ankle injury
• sprains due to inversion. (Lateral ligament complex, fibula & lateral talus injured)
• Ankle x-rayed if Ottawa ankle rules fulfilled i.e. bone tenderness along distal 6 cm of
posterior margin or tip of lateral malleolus or lateral margin or tip of medial malleolus &
inability to weight bear at the time of accident or examination
• Do reduction immediately in ankle dislocation, as necrosis of tented skin & ischemia of
foot
• sprains treated with analgesia & PRICE Then physiotherapy
• In adolescents, peroneal tendon retinaculum can be torn with painful flicking sensation in
lateral malleolus. In young: immobilisation for month.
• Achilles tendon common site for tendinosis because of repetitive trauma
• Tendon rupture in squash and badminton, Thompson's or Simmonds’s test done. Plaster
applied, with foot plantar flexed to bring tendon ends in contact
• If history of kick to calf and Simmonds’s test negative: U/S or MRI as Achilles rupture
may be masked by presence of a plantaris tendon
Foot injuries

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 • turf toe is painful swelling stiffness of 1st metatarsophalangeal joint due to plantar plate
rupture and hyperextension of toe causing injury to joint capsule. Symptomatic treatment
• Stress fractures in marathon runners. Diagnosed by MRI or US. Cause localised pain
over metatarsal on pressure & running.
Shoulder and upper limb injury
• Ant. Shoulder Dislocation in contact sports e.g. rugby. Physiotherapy if first time or
surgery if repetitive or significant anatomical damage
• Shoulder instability from overuse (usually in throwing sports)
• rotator cuff tendinosis from overuse in overhead sports like tennis or bowlers
(overload→impingement→inflammation→tendinosis)
• if supraspinatus tendon tears, repaired surgically
• subacromial subdeltoid bursitis causes pain down arm and wrist worse at night
• acromioclavicular joint injured in wrestlers, rugby and cyclists. Symptomatic treatment. If
OA in joint, clavicle is excised
• biceps injury at long head in weightlifters, wrestlers and gym users on anabolic steroids
or as part of rotator cuff injury
Arms and hand injuries
• medial & lateral epicondylitis: physiotherapy and epicondyle support
• dequervain’s tenosynovitis: in repetitive injuries involving fingers: physiotherapy & steroid
injections
• gamekeepers/skiers’ thumbs when proximal thumb forced radially in a fall. Ulnar
collateral ligament at metacarpophalangeal joint is damaged. If avulsed, Stener lesion
(aponeurosis of abductor pollicis brevis is interposed) so surgery needed.
• mallet/baseball finger due to rupture of distal insertion of extensor tendon into distal
phalanx. Tx: mallet splint
• Disruption of flexor tendon pulleys in climbers, leads to bow stringing of flexor tendons.
Surgery is needed
• All hand injuries assessed by US using dynamic stress, better than MRI
Treatment of injuries
• Acute phase: PRICE (protect, rest, ice, compression, elevation)
• Nsaids slow healing but reduce pain & swelling. Codeine or paracetamol effect less on
injury healing but help with pain
• Be aware of world anti-doping agency (WADA), as some substances banned in training
& contests
• If steroid needed so TUE (temporary use exemption) certificate issued so if spot checked
they are not disqualified, but not use around achilles tendon
• Some patients develop myositis ossificans after muscle hematoma. Increasing swelling
& pain. Tx: indomethacin

Chap 35: The spine

Spine
• 90% acute low backpain resolves in 6 weeks and 70% sciatica in 3 months
• Sciatica is not as common as low back pain
CLINICAL ANATOMY
• Normal cervical lordosis between 35 ͦ and 45 ͦ
• lumbar lordosis between 40 ͦ and 80 ͦ, decreases with age. Most lumbar lordosis between
L4 and S1.
• Thoracic kyphosis between 20 ͦ and 50 ͦ and increases with age.
• For energy efficient posture, cervical & lumbar lordosis balances thoracic kyphosis
• Arteries of spinal cord: anterior spinal artery (supply majority) & 2 posterior spinal arteries
• Radicular artery of Adamkiewicz makes major contribution to ant spinal cord,
• Red flags in backpain:

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 1. Age <20 or >50
2. recent significant trauma
3. hx of malignant disease
4. unexplained weight loss
5. constitutional symptoms (fever, chills)
6. immunosuppression
7. severe or progressive sensory alteration or motor weakness
8. acute difficulty with micturition (painless retention)
9. fecal incontinence and/or numbness in perineum or buttocks
• Non spinal causes of backpain (referred pain)
1. Respiratory (e.g. mesothelioma)
2. Vascular e.g. abdominal aortic aneurysm
3. Renal e.g. pyelonephritis
4. Gastrointestinal e.g. peptic ulcer, pancreatitis
5. Urogenital e.g. prostatic, testicular, ovarian cancer
Physical examination
• Posture evaluated in frontal and sagittal planes while patient is undressed. Shoulder or
waist asymmetry: scoliosis
• Adam's forward bend test accentuates truck asymmetry
• Schober's test for spinal mobility (tape measure used to measure skin mid-way between
posterior superior iliac spines & at points 10 cm proximal & 5cm distal to it when patient
is standing. Patient then asked to bend forward as far as possible, & distance between 2
points is measured in flexed position. Normal: increase of 5 cm between 2 points in erect
& flexed position. Less that this: ankylosing spondylitis
• In kyphosis: forward bending & gaze is assessed
• Myelopathy or UMN lesion: spasticity, motor weakness, hyper reflexia, positive
Hoffmann’s sign (forceful flexion of distal phalanx of middle finger results in flexion of
thumb & index finger), upgoing Babinski response, patellar and ankle clonus.
• Radiculopathy or LMN lesion: sensory loss, motor weakness, flaccid paralysis,
fasciculation, muscle atrophy, loss of reflexes
• Straight leg test (supine patient, leg elevated with knee straight to increase tension along
L5 & S1 nerve roots) positive if provokes radicular pain upon straightening. +ve:
herniated disc
• Lasegue’s sign: radicular pain aggravated by ankle dorsiflexion
• Femoral stretch test positive if pain in anterior thigh (prone, extend hip, flex knee)
creates tension on L2-L4 nerve roots
• Non-organic physical signs in low back pain (for secondary gain) superficial or non-
anatomical tenderness, simulation tests: axial loading or rotation, distraction test:
variable SLR, non anatomical sensory or motor loss, over reacting: grimacing, muscle
tremors
Investigations
X ray
• mostly for scoliosis
CT
• bone anatomy
MRI
• red flag signs or failure of conservative therapy
• SC, thecal sac, epidural space, nerve roots, paraspinal soft tissues, bone marrow
Bone scintigraphy
• Metastatic disease, discitis, vertebral body osteomyelitis, assess activity of bone lesions
Bone densitometry
• Bone density & osteoporosis by DEXA of hip, wrist & spine
Provocative discography

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• Place 24-gauge needle into centre of intervertebral disc in conscious patient. 1-3.5 ml
radio-opaque contrast agent injected into disc. Contrast pattern shows degrees of disc
degeneration. Cotton ball or lobular: normal. Irregular/fissured/ruptured: degenerate
Facet joint injections
• For facet joint arthropathy: x-ray guided local anaesthetic & steroid injection both
diagnostic & therapeutic for 4-6 weeks. Long-term relief by: facet joint rhizolysis
(denervates facet joint by heat)
Foraminal epidural steroid injections
• For radiculopathy due to prolapsed intervertebral disc
Spinal biopsy
• CT guided or open biopsy for tumor and/or infection
Degenerative conditions of spine
Cervical radiculopathy
• neck and arm pain i.e. brachalgia, paresthesia and motor weakness in distribution of
compromised nerve root due to herniation or stenosis. Tx: physiotherapy & medication
for neuropathic pain (gabapentin, amitriptyline, pregabalin) and CT guided foraminal
epidural steroid injection of local anaesthetic & steroid. Surgery for intractable pain or
neurological deficit.
• Surgical options: anterior cervical discectomy & fusion (using a cage packed with bone
graft & plate), cervical total disc replacement, posterior laminoforaminotomy
Cervical myelopathy
• Commonest cause: degenerative changes in cervical spine causing spinal cord
compression. LMN signs at level of lesion and UMN signs below the lesion
• Surgery: anterior or posterior decompression
Thoracic disc herniation
• axial pain, radiculopathy, myelopathy Tx: physiotherapy, NSAIDs, general fitness
improvement initially. Thoracic discectomy via thoracotomy, & for soft disc prolapse,
thoracoscopic approach
Lumbar disc herniation
• risk factors: family history, male gender, age (30-50 years), heavy lifting or twisting,
stressful occupation, lower income, cigarette smoking
• posterolateral disc protrusion affects traversing root, e.g. an L4/5 protrusion affects L5
nerve root
• a far lateral disc protrusion (extra-foraminal) affects exiting nerve root e.g. far lateral
L5/S1 protrusion affects L5 nerve root
• symptoms: back pain, sciatica, paraesthesia, motor weakness, loss of reflexes, reduction
in SLR
• simple sciatica: 6-12 weeks of conservative treatment (pregabalin & foraminal epidural
steroid injection) If fails, microdiscectomy
• microdiscectomy: prone position, 3-5cm incision with unilateral take down of multi-
fundus. Spinal canal entered via removal of ligamentum flavum under lamina. Dura &
nerve root retracted medially; disc prolapse incised via transverse annulotomy. Disc
fragment removed & disc space cleared or remaining nuclear material. wound then
closed
Spinal stenosis
• any type of narrowing of spinal canal, nerve root canal or intervertebral foramen
• resulting nerve root compression leads to ischemia causing back buttock or leg pain
provoked by movement
• 2 types:
1)congenital: achondroplasia
2)acquired: degenerative (50-70 years)
• Spinal claudication difference from vascular claudication: neurological symptoms worse
in extension & presence of pedal pulses
• Tx: surgical decompression
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Discogenic low back pain
• degenerative discs changes, not all are painful
• chronic relapsing episodes of low back pain between 40-60 years
• if conservative measures fail: provocative lumbar discography or lumbar disc
replacement
Spondylolysis
• unilateral or bilateral pars interarticularis defect without vertebral slippage
• incidence higher in young athletic population. In general population 6% by 14 years
• many cases remain asymptomatic
• investigations: reverse gantry CT, MRI & single photon emission computed tomography
• Tx: rest, Nsaids, orthosis. Surgery: repair of pseudo arthrosis by Buck’s fusion
Spondylolisthesis
• forward slippage of vertebral body.
• Classified into 6 types by causation
Type 1 Dysplastic Congenital deficiency of L5-S1 articulation
Type 2 Isthmic Lesion of pars interarticularis
2A: lytic defect of pars
2B: elongated or attenuated pars
2C: acute pars fracture
Type 3 Degenerative Segmental instability due to degeneration
Type 4 Traumatic Acute fracture
Type 5 Pathological Bone disease (metabolic, neoplastic)
Type 6 Postsurgical After decompression of lumbar spine
• Classified by degree of slip
Grade 1 1-25%
Grade 2 26-50%
Grade 3 51-75%
Grade 4 76-100%
• For progressive slips in skeletally immature (<18 years), intractable pain, neurological
symptoms surgery needed
• for low grade slips (grade 1 & 2) fusion in situ
• higher grade slips reduce and then fuse or fuse in situ
Spine infections
Pyogenic
• pyogenic vertebral osteomyelitis is of disc & osseous margins. Most common route by
which organism spreads to spine: hematogenous
• disc always involved in pyogenic vertebral infection, but in granulomatous such as TB,
not involved
• risk factors: advancing age, Iv drug abuse, diabetes, renal failure, recent infection,
trauma
• mostly by staph aureus. Anaerobic organisms in diabetes & penetrating trauma
• operative intervention when: open biopsy (when closed has failed), failure of medical
management, drainage of abscesses, decompression of SC compression, correction of
progressive spinal deformity, stabilisation of progressive spinal instability
Epidural abscess
• in thoracic spine, surgical emergency
Tb
• Potts disease, tenderness over spine, fever, weight loss, backpain & cough, cold
abscess (fluctuant mass), raised ESR & CRP, anemia, CXR, spinal x ray, anti tb drug,
immobilisation
Inflammatory spondyloarthropathy
Rheumatoid arthritis
• atlantoaxial subluxation (AAS) & myelopathy

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• neurological symptoms due to direct compression by bone/soft tissue or from neural
ischemia
• degree of subluxation checked by performing flexion & extension radiographs
• theatre staff esp. anaesthetist warned to take special care in intubation
• indications for surgery to stabilise cervical spine
1) AAS with a PADI of 14 mm or less
2) AAS with at least 5mm of basilar invagination
3) Sub axial subluxation with sagittal canal diameter of 14mm or less
Ankylosing spondylitis
• epidural hematoma with neurological deficit
• patients with significant fixed flexion deformity at cervico-thoracic junction (chin on chest
deformity), limited forward gaze, eating, swallowing difficulties are treated with closing
wedge osteotomies
Spinal deformity
• categorised in coronal plane deformity (scoliosis) or sagittal (kyphosis & lordosis)
• radiograph for scoliosis: full posteroanterior & lateral standing spine
• curve magnitude known as Cobb’s angle. Scoliosis: cobb’s angle greater or equal to 10 ͦ
Idiopathic scoliosis
• classification: 1) early onset (before 8 years) 2) late onset (after 8 years)
• number of alveoli do not increase after 8 years
• severe curves in early onset: cor pulmonale, right ventricular failure
• risk factors for progression: female gender, remaining skeletal growth, curve location &
magnitude
• curves less than 25° are monitored, in growing children with 20-29°: brace and surgery
after 40°, truncal imbalance & unacceptable cosmesis
• to minimise risk of neurological damage, continuous spinal monitoring used in surgery
Neuromuscular scoliosis
• neuropathic disorders like CP, syringomyelia, poliomyelitis or myopathic disorders like
Duchenne muscular dystrophy & myotonic dystrophy
• timely surgery may prolong life
Congenital scoliosis
• due to vertebral anomalies that produce frontal plane growth asymmetry
• close observation of spinal growth until puberty,
• brace treatment ineffective for primary structural curves as short & rigid but used in
compensatory curves
• for progressive curves, surgery: magnetically controlled growing rod procedures, hemi
vertebra excision, correction & fusion
Scheuermann's kyphosis
• wedging of T7-10. Apical & low back pain (due to attempts by lumbar musculature to
compensate for thoracic hyper kyphosis)
• physiotherapy or bracing up to 65° curve
• surgery if pain, deformity greater than 70 ͦ, cosmetic reason, cardio pulmonary
compromise
Developmental abnormalities
Spinal bifida
• failure of fusion of vertebral arches
• spina bifida cystica is associated with hydrocephalus
• 2 basic types (meningocele and myelomeningocele)
• meningocele with skin treated conservatively, meningocele with prominent sac excised
at 3-6 months
• myelomeningocele: if not closed, majority die in first year. Better outocome with
antibiotics, early surgical closure & shunts to prevent hydrocephalus
Arnold Chiari malformation

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• medulla & cerebellar tonsils herniate through foramen magnum: pressure on lower
medulla
• hydrocephalus and impaired neurological function
• symptoms: headache, vomiting, visual disturbances, mental impairment, cerebellar
ataxia
• decompress foramen magnum & posterior arch of atlas to restore normal CSF flow
Spinal dysraphism
• abnormal embryological formation of tissues
• progressive neurological deficit because of SC tethering/ traction or cord compression
• diastemetaomyelia: abnormal bony/cartilaginous spur across mid of vertebral canal,
diving dural tube and SC in 2
Syringomyelia
• sensory disturbance, hand weakness, loss of pain and temp, asymmetrical abdominal
reflexes associated with Arnold Chiari & spinal cord tumors
• syringomyelia +Arnold Chiari +scoliosis: posterior cranial fossa decompression first, then
correct scoliosis
Metabolic bone diseases affecting the spine
Osteoporosis
• painful thoracic fractures tx with orthosis, bed rest, analgesics. If after 6 weeks, still
painful so vertebroplasty or kyphoplasty
• goals of kyphoplasty: spinal stabilisation, pain relief, restoration of vertebral body height
Global issues in spine surgery
• cost implications
• lack of trained spinal surgeons

Chap 36: Upper Limb- pathology, assessment, and management

Chap 37: Hip and knee

HIP AND KNEE
SURGICAL PROCEDURES
Arthroscopy of the hip

• Treatment of symptomatic labral tears, femoroacetabular impingement & removal of

loose bodies
• Allows clear view of femoral & acetabular articular surfaces, labrum, ligamentum teres &
the head-neck junction, synovium & peri trochanteric space
• Advantages: minimally invasive access to these structures, rapid recovery compared to
open surgery
Arthrodesis of the hip

• Uncommon
• For young patients with severe osteoarthritis who have heavy manual jobs & in whom
joint replacements would fail early
• Aim: achieve painless joint by fusing in functional position, which is 30 ͦ of flexion, 15 ͦ of
external rotation, & 5 ͦ of abduction. Done by intra articular dynamic hip screw or by extra
articular plate with screws
• Resulting problems: altered gait, excessive loading of ipsilateral knee, contralateral hip &
spine

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 Osteotomies around the hip

• Goal: redistribute forces evenly along joint, eliminating excessive point loading
• Achieved by osteotomy on femoral or acetabular side.
• Indications for osteotomies:
1. Developmental dysplasias of hip
2. Perthes’ disease
3. OA in young patient
4. Slipped capital femoral epiphysis
5. AVN
• Done in young patient who maintains good range of motion of hip & radiographs show
good amount of joint space
• Pre-operative planning by 3D CT scans
Total hip replacement

• After surgery: pain reduces, mobility increases & sleep & sexual function improved
PRINCIPLES & DESIGN OF HIP REPLACEMENTS

• Biocompatible & made of inert materials

• Well fixed to host tissue, stable & allowing good range of motion
• Bearing surfaces designed to minimise friction
• Material released from bearing should be non-toxic
• Remove minimum amount of bone
• Produce mechanical stability
• Ideally outlive the patient
MATERIALS FOR FEMORAL COMPONENT

• Most implants made from cobalt-chrome alloy. Stainless steel & titanium also used
• Metal implants able to withstand high loads, inert & easily manufactured, but problems in
terms of ion release if used as bearing surfaces
• Corrosion if 2 dissimilar substances used
BEARING SURFACES

TYPE OF BEARING ADVANTAGES DISADVANTAGES

Metal on polythene Proven efficacy, easy to Comparatively high friction, high wear rates, wear
manufacture, cheap particles causes inflammatory response which leads
to osteolysis
Ceramic on polythene Lower wear rate Expensive; ceramic fracture
Metal on metal Lower wear rate Failure requiring early revision, implant recalls,
metal ion release is a problem; expensive
Ceramic on ceramic Lowest wear rate Very expensive; ceramic can fracture; squeaking

FIXATION OF IMPLANTS
METHOD OF FIXATION ADVANTAGES DISADVANTAGES
cemented Implant does not need to fit cavity Cement polymerisation is exothermic, so
exactly, well proven results thermal injury possible, fragments cause 3rd
body wear & stimulate aseptic loosening,
difficult to remove at revision

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uncemented No cement needed; fixation more Risk of fracture, fit must be perfect, osseous
secure; dynamic & biological fixation integration may not be established, expensive

Surgical approaches to the hip, post operative course & complications

• Operation performed via posterior approach, trochanteric osteotomy, an anterolateral or

Hardinge approach, an anterior approach
• Minimally invasive surgery shortens size of incision, lessens soft tissue damage
• Postoperative course: 3-5 day stay in hospital, physiotherapy: mobilise patient safely &
independently, avoiding movements which lead to dislocation
• Before discharge, occupational therapist assesses pt’s home, arranges for modification
e.g. raised toilet seat
• Follow up: 6 weeks and 1 year post surgery
• Reduce risk of DVT by use of regional anesthesia & early post-operative mobilisation,
mechanical devices (thromboembolic deterrent-TED stockings, foot pumps or
intermittent pneumatic calf compression devices) & medication (LMWH, warfarin or oral
anticoagulants) given for 4-6 weeks after surgery
• Intra operative complications: nerve injury (sciatic, femoral & obturator), vascular injury
(femoral vein & artery), femoral fracture, fragments of cement left in joint
• Post-operative complications: DVT & PE, leg length inequality, dislocation, infection,
aseptic loosening, heterotopic ossification
Revision total hip replacement

• Required if patient is symptomatic sec to failure of implant by loosening, recurrent

dislocations, periprosthetic fracture. Loosening by: infection or aseptic osteolysis by
inflammatory response sec to particle wear
• Initial stage of loosening: pain mainly on weight bearing
• Hx of infection in immediate post-op period may be a cause of premature implant
loosening
• If loosening secondary to infection, 2 staged revision. 1st stage: implant removal,
debridement, implantation of antibiotic loaded cement spacer. Specimens sent for
bacteriology to determine organism & its sensitivity. Then given appropriate antibiotic
• 2nd stage: cement spacer is removed & new prosthesis implanted
• Aseptic loosening: revision as single stage procedure
• If significant bone loss: bone grafts or trabecular metal augments
Arthroscopy of knee

• Indications:
1) Torn meniscus resection/ repair
2) Anterior/posterior cruciate ligament reconstruction
3) Loose body removal
4) Cartilage regeneration techniques including microfracture
5) Septic arthritis washout
6) Inflammatory arthritis-synovectomy
7) Diagnosis of unexplained knee pain
8) Tibial plateau fractures- intra operative assessment & reduction of articular surface
Cruciate reconstruction

• Isolated ACL (anterior cruciate ligament) injury: arthroscopic intra articular reconstruction

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• Graft: bone-patella, tendon-bone, four-strand hamstring autograft
• Post-op rehabilitation crucial for good outcome
• Complications: due to incorrect tunnel placement (femoral tunnel too far anteriorly limits
knee flexion) & early surgery. Graft re-rupture rate 1%/ year
Osteotomy

• Most commonly performed operation is high tibial osteotomy (HTO) for a varus knee.
Realignment with opening wedge medial HTO or closing wedge lateral HTO
• In valgus knee with mild deformity (less than 12 )ͦ : varus producing HTO on medial side
• A deformity of 12 ͦ or more: distal femoral varus osteotomy
• Ideal patient: young, active, well-motivated, disease limited to one compartment
Knee arthrodesis

• Most common indication: failed total knee replacement

• Other indications: uncontrollable sepsis, neuropathic joint, post traumatic arthritis in
young patient, disruption of extensor mechanism
• Ideal position: fusion is 7 ͦ & 15 ͦ of flexion
Knee joint replacement

• 3 compartments in knee: medial & lateral tibiofemoral & patellofemoral

• In OA, medial compartment most commonly affected: varus deformity
• Single-compartment disease: unicompartmental replacement
• Tricompartmental disease: total knee replacement (TKR)
• Knee replacement: femoral articular surface replaced with metal, tibial articular surface
by tough polythene insert
• Indications for replacement: pain (mc), deformity, instability. Reserved until quality of life
significantly impaired
• Natural knee motion is complex, translation & rotation about each of the x, y, z axes, so
difficult to reproduce this motion.
• 3 types of TKR: unconstrained, constrained non-hinged, constrained-hinged
• Primary TKR: unconstrained. Revision TKR: constrained
• More constrained the implant, greater force transmitted, increasing risk of loosening
• Aims of TKR: mechanical axis through centre of knee, joint line perpendicular to
mechanical axis & parallel to ground, balance collateral ligaments, ensure patellofemoral
joint tracks normally
• Post-op: physiotherapy for full extension. Length of stay: 3-5 days
• Complications:
Intraoperative:
1) Poor placement of implants leading to instability or stiffness or pain
2) Nerve or vessel injury including tourniquet damage
3) Fracture
4) Patellar tendon avulsion
5) Malalignment
6) Fat embolism
Post operative:
1) Infection 5) osteolysis
2) DVT/ PE 6) component loosening
3) Pain/ stiffness 7) dislocation

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 4) Instability
Unicompartmental knee replacement (UKR)

• Prerequisites: intact ligaments (esp. ACL), disease limited to one compartment, varus/
flexion deformities of not more than 15 ͦ
• Less invasive than TKR so more rapid recovery, shorter stay, preservation of knee
kinematics. Bone preserving procedure, so revision to TKR, rather than to more
constrained implants
• Lateral UKR for lateral compartment & patellofemoral replacement less common
Revision knee replacement

• Main reason: implant loosening sec to infection or polythene induced osteolysis

• Other indications: peri-prosthetic fracture, malalignment, instability, stiffness, patellar
maltracking
• Imp to exclude infection, because then 2 stage procedure needed

Chap 38: Foot and ankle

FOOT AND ANKLE
MIDFOOT
• Cuneiforms, cuboid & related joints
Midfoot arthritis
• Risk factors: micro trauma, rheumatological causes, flat foot, Lisfranc or similar injuries,
Charcot & cavus foot
• Pain but if painless swollen foot then neuropathy
• Tx: is steroids and physiotherapy, orthotics, analgesia fusion of joints (has poor
outcome)
Charcot
• Acute, hot, red swollen foot (may/may not be painful)
• Secondary to diabetes (may not be diagnosed)
• Immediate offloading in plaster & urgent management
Tendinopathy
• Dorsal pain due to tibialis anterior tendinosis at its insertion. Non operative treatment
Ganglions
• Neuralgia over dorsal bosses
• Injection0aspiration
• Surgery, but recurrence is high
THE HINDFOOT & ANKLE
knee deformities must be corrected before tackling foot problems
Ankle arthritis
• Arthrodesis (fusion) via open (more common) or arthroscopic approach (better
outcomes) or total ankle replacement (TAR)
• TARs are 3 component devices, preserve joint mobility, but at expense of larger
incisions
Hindfoot arthritis (excluding ankle)
• affects triple complex (subtalar, calcaneocuboid and talonavicular joints) Tx: fusion
Ankle with other hindfoot arthritis
• surgery: treat one set of joints & see how patient fares. Secondary surgery can then be
performed. Alternative: treat all joints at once
• hindfoot fusion done

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RHEUMATOLOGICAL PRESENTATIONS IN FOOT
• synovitis of lesser MTP joints and small joint disease.
• Classic deformity: hallux valgus
• Joint sparing surgery, with preservation of metatarsal heads if possible. Destruction of
joints treated with proximal phalangeal partial excisions. Usual requirement: fusion of first
MTP joint
• Excision of metatarsal heads-most surgeons avoid scars on plantar aspect of foot when
possible, but this is one procedure where results are good. But such surgery leaves no
room for revision later
Midfoot
• Rheumatological disease outcome: just pain & stiffness
• Tx: injections & fusion surgery
hindfoot and ankle
• require surgery
• rheumatological disease also affects soft tissues
• achilles tendon never injected with steroid as fear of rupture. Same for tibialis anterior &
posterior
TENDON DISORDERS

• Tenosynovitis is due to overuse or sec to inflammatory conditions. Tx: rest, Nsaids,

physiotherapy. Inflammatory conditions: tenosynovectomy
• Mc tendon affected by degeneration is achilles, tibialis posterior & peronei
Ruptured achilles tendon
• Frequent in 40-50-year old, who undertake vigorous sport after long period away from
such activities
• Acute rupture: non-operative if U/S shows closure of gap in plantar flexion. Alternative:
surgical fixation
• Micro tears which lead to rupture: no treatment necessary
• Missed rupture: AFO ankle brace, reconstructive surgery
Achilles tendinosis
• Shock wave therapy
• Steroid injections not used, high-volume saline, dry needling & sclerosant injections used
Peroneal tendon problems
• develop tendinosis or may subluxate
• peroneal tendon subluxation occurs spontaneously or after injury, associated with grove
at back of fibula being too shallow. Tx: surgical repair, deepening of groove
Ankle instability
• Unstable ankle due to ligament disruption: ‘anterior drawer’ sign
Osteochondral lesion of talus
• patients have persistent ankle pain following injury-osteochondral lesion
• CT/MRI for diagnosis
Synovitis
• Ongoing pain after injury due to synovitis, impaction injury, undiagnosed fracture,
prominence of syndesmotic ligament into joints
• steroid given. Persistent symptoms: arthroscopic debridement
TUMORS
• BENIGN are ganglia, giant cell tumor and angioleiomyomas.
• Pigmented villonodular synovitis (PVNS): locally aggressive condition in ankle,
diagnosed by MRI/histology. Surveillance for recurrence mandatory
• Mc tumor in foot: ‘Lederhosens disease’, painful growing lump in sole along plantar
fascia
INFECTION
• Septic arthritis in foot/ankle rare except in diabetes. Surgical emergency

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• Usually after surgical procedure. Also, hematogenous spread
• Tx: immediate surgical drainage & appropriate high dosage antibiotics
• Most common: MRSA
• In diabetics, failure to treat with debridement: amputation
• Radiographs normal in early stages so clinical diagnosis
DIABETES
• Increased risk of infection, ulceration because of: peripheral neuropathy, peripheral
vascular disease, impaired resistance to infection.Trauma can lead to collapse of foot
known as Charcot neuroarthropathy (painless foot)
Ulcers and amputation
• Ulcers treated urgently. Optimal management pathway: urgent admission, radiological &
clinical assessment, debridement, antibiotics. It is a surgical emergency
• Most amputations preceded by ulceration
Charcot
• Neuropathic destruction of joints. Described as painless, but majority have pain
• due to leprosy or diabetes, or any other neurological condition
• hot, swollen red extremity. Often misdiagnosed as gout, cellulitis, fracture, DVT, but is a
surgical emergency
• MRI and biopsy to distinguish from infection
• stage 1 fragmentation, stage 2 coalescence, stage 3 consolidation (all this takes 18
months)
• Require splintage in Charcot retaining orthotic walker (CROW) or total contact case
(TCC), but mostly aggressive early surgical approach. Surgery: early stabilisation to
prevent deformity, or late reconstruction or removal of bony prominences. Failure:
ulceration & amputation
Entrapment neuropathy
• decompression needed. Tarsal tunnel syndrome much rarer than carpal tunnel
Heel Pain

• commonest cause: plantar fasciitis

• pain is inferomedially within heel, worst first thing in morning & after rest
• majority cases settle in 18 months
• non-resolving cases: U/S guided injections

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Chap 39. Musculoskeletal tumors
Do IM then

Summary box 39.3

Malignant bone tumours
Plasmacytoma – solitary form of multiple myeloma
Osteosarcoma – often secondary to Paget’s disease and
radiotherapy
Chondrosarcoma
Ewing’s sarcoma

Bone tumours can also be classified according to their

site (Table 39.2). Epiphyseal tumours are likely to be
benign (Table39.3). Bone tumours are usually staged
using the Enneking staging system. Benign tumours are
staged as:
latent (i.e. osteochondroma);
active (i.e. osteoid osteoma);
aggressive (i.e. giant cell tumour).

For malignant tumours, the Enneking system combines

stage and grade of a tumour (Table 39.4).

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 Then Do bailey pg 536-539

Chap 40. Infection of the bones and joints

Chap 41. Pediatric orthopedics
Paediatric orthopedics
• Immature skeletons heal rapidly, Physeal
injury or muscle imbalance leads to progressive
deformity
• Heuter-Volkmann principle:
o Compressive forces inhibit growth
o Tensile forces stimulate growth
• Wolff’s law: Bone deposition and resorption depends on stresses applied

Development of musculoskeletal system

• Occurs 4-8 weeks after fertilisation (upper limb: 4 weeks after fertilisation, lower limb: 2 weeks
after that)
• Most congenital limb anomalies in 2nd month
• Apical ectodermal ridge (AER) controls proximal to distal differentiation & interdigital necrosis
• zone of polarising activity (ZPA) directs posterior to anterior differentiation
• Wnt influences dorsal to ventral differentiation

Normal variants

• Include intoeing gait, tripping & falling, bowlegs, knock knees & flat feet
• If symmetrical, symptom-free and supple in an otherwise normal child, no intervention needed
• Family history is positive of similar complains
• If child fails to achieve developmental milestones, or if functional problems, further
investigations.

In toeing gait

• Defined as negative foot progression angle

SITE CAUSE

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 Femur/hip Persistent femoral neck anteversion
Tibia Internal tibial torsion
Foot Metatarsus adductus
Common sites & causes of intoeing gait in childhood

• Persistent anteversion of femoral neck presents as excessive internal rotation at hip joint,
measured with patient prone
• All femurs are anteverted at birth, but as it lengthens also rotates, which improves anteversion
• If by 10-12 years, significant deformity with functional difficulties, corrective osteotomy done
• In such cases, child has either lost ability to externally rotate extended hip or developed
compensatory external tibial torsion. In 2nd, foot progression angle is normal but symptoms of
miserable malalignment syndrome (anterior knee pain & feeling of instability)
• Internal tibial torsion assessed by thigh-foot angle. Spontaneous correction by 4 years, as tibia
rotates as it grows
• Metatarsus adductus is flexible, mostly spontaneous correction by 2-4 years. Otherwise,
stretching with or without plaster casts or straight-last shoes

Other abnormalities of gait

• Extoeing: less common than intoeing, results from femoral retroversion, external tibial torsion,
flexible flat feet. Late walking because of poor balance associated with foot posture &
alignment. Improves with time
• Toe-walking: a phase in normal gait development. If does not mature to heel-toe pattern by 3
years, physiotherapy or surgical lengthening of contracted gastrocsoleus complex.
• If toe-walking starts after walking age, then spinal/neuromuscular etiology & in unilateral cases
an orthopaedic cause for a short leg

Knock-knees and bowlegs

• All children start life with bowlegs & internal tibial torsion. By 2-3 years, they develop knock
knees, which regress to normal adult tibiofemoral angle of 7 ͦ by 7 years
• Intercondylar or inter malleolar distance used to quantify the deformity is not very accurate, so
further investigation needed when severe deformity. MC pathological cause: trauma, rickets,
skeletal dysplasia

Flat foot

• Before development of medial longitudinal arch, all children (<3 years) have flat feet, with fat
pad obscuring the arch. Only 15% adults have flat feet so natural hx is of improvement
• Painless, flexible flat foot: no treatment. Orthoses do not alter natural hx but alleviate symptoms
• All flat feet have flattened medial arch with valgus heel, but 2 major types seen:
TYPES CHARECTERISTICS
flexible On tiptoe, arch is restored & heel corrects into varus, subtalar joint movements are full & pain free
rigid On tiptoe, arch fails to return & heel remains in valgus, subtalar joint movements restricted & painful
• Symptomatic rigid flat foot is because of inflammation, requires investigation, then
surgical/medical management.

Postural abnormalities

• Many babies subjected to moulding pressure in utero. At birth they show postural abnormalities
e.g. torticollis, calcaneovalgus feet, plagiocephaly which improve with time & stretching exercises

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 Congenital & developmental abnormalities of the skeleton

CATEGORY EXAMPLE
Failure of formation of parts
transverse Congenital amputation of the forearm/lower limb
longitudinal Fibular hemimelia
Failure of differentiation Radioulnar synostosis; vertebral body fusion
duplication Extra digits
overgrowth Gigantism; macrodactyly
Undergrowth
Congenital constriction band syndrome Often affects hand/feet with poor formation of digits distally
Generalised skeletal abnormalities Skeletal dysplasia e.g. achondroplasia
Classification of congenital limb malformations

Achondroplasia

• Gain of function mutation in FGFR3 (fibroblast growth factor receptor 3), which affects enchondral
bone formation. Autosomal dominant
• Disproportionate short stature where limbs are shorter than trunk
• Underdevelopment of foramen magnum & spinal stenosis causes neurological difficulties
• Correction of limb alignment and limb lengthening techniques

Hereditary multiple exostoses-diaphyseal aclasis

• Autosomal dominant; loss of function mutation in EXT1 or EXT2 gene

• Exostoses consisting of cartilaginous cap on a bony stalk maybe sessile/pedunculated.
• Grow as child grows, cause cosmetic & functional difficulties so excision done
• Differential growth between paired bones of forearm & lower leg lead to joint deformity &
dislocation of radial head, exacerbated by disordered physeal growth, because of altered
mechanical forces
• Continued growth after skeletal maturity: malignant transformation of benign osteochondroma

Enchondromatosis

• Non-hereditary skeletal dysplasia called Ollier’s disease

• Larger lesions: calcification on radiographs, & vertical streaks of lucency (representing cartilage
columns), run the length of metaphysis. Pathological fractures common
• If soft tissue hemangiomas & lymphangiomas, then it is called Maffucci’s syndrome

Fibrous dysplasia

• Chance finding on radiograph in monostotic form

• Localised defect in osteoblastic differentiation & maturation, normal bone replaced by fibrous
stroma
• Polyostotic fibrous dysplasia: limb deformity & pathological fractures
• In pts with precocious puberty & café-au-lait spots, diagnosis: McCune Albright’s syndrome

Metabolic bone disease

Rickets

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 • In all types, primary problem is inadequate mineralisation of growing bones
• Medical tx improves mineralisation. Correction of deformity then occurs with growth
• Then surgery for any residual limb deformity

nutritional Reduced intake of vit D & calcium

environmental Inadequate exposure to sunlight
Gastrointestinal disease Crohn’s disease, gluten-sensitive enteropathy
genetic X-linked hypophosphatemia
Renal disease End-stage renal failure, renal tubular anomalies, changes related to sec hyperparathyroidism
Common causes of rickets

Osteogenesis imperfecta (brittle bone disease)

• Spectrum of conditions, qualitative/quantitative malfunction of collagen 1 production

• Bone breaks easily but heals promptly & well
• All structures containing collagen affected therefore, ligamentous laxity, blue sclerae, & poor
teeth
• Cyclical bisphosphonate decreases bone resorption & turnover which reduces bone pain &
fracture which in turn improves weight bearing mobility & bone strength
• tx options: casting, surgical procedures to correct limb alignment
• intramedullary techniques for reduction & stabilisation of fractures preferred to plate fixation
• immobilisation minimised & prompt rehabilitation

Abnormalities of knee and lower leg

Osteochondritis dissecans

• most commonly affects lateral aspect of medial femoral condyle of distal femur
• osteochondral fragment becomes separated from joint surface
• MRI best imaging test
• Mild cases: osteochondral fragment remains attached, & heals if treated early with rest &
activity modification
• If completely dethatched, mechanical symptoms necessitate treatment to encourage bone
healing via fixation of fragment or to remove lose body
• Better prognosis in children than adults

Discoid meniscus

• Affects lateral meniscus, which is abnormally thick & covers most of tibial plateau
• Painful clunk on knee extension
• MRI is diagnostic
• Surgery for relief of pain & mechanical symptoms

Anterior knee pain

Osgood-Schlatter disease

• Traction apophysitis of patellar tendon insertion

• Pain, tenderness & swelling at tibial tubercle, increased by exercise is diagnostic.
• Tx: rest & analgesia, resolves once apophysis has fused

Patellofemoral pain

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 • Attributed to adolescent growth spurt, symptoms exacerbated by activity or by rest with flexed
knee
• Tx: alterations to activity levels & sitting position, physiotherapy to strengthen hamstrings &
quadriceps

Ant knee pain maybe because of patellar maltracking. Tx: physiotherapy to develop quadriceps
muscle, surgery

Fibular hemimelia

• Congenital failure of formation of lateral column of lower leg

Foot and ankle Absent lateral rays; tarsal coalition; ball & socket ankle joint
Lower leg Absent or deficient fibula; short bowed tibia
Knee Absent tibial spine (no cruciate ligament); deficient lateral femoral condyle
femur Relative hypoplasia
Limb length & alignment Short; external rotation with or without valgus
Classical radiograph features of fibular hemimelia

• Tibial bow has anteromedial apex

• Management according to severity of deficiency
• Options: show raise, multiple episodes of limb equalisation surgery, amputations

Blount’s disease

• Progressive & severe tibia vara with significant intoeing. Sharp proximal tibial angulation
• Tx: surgical

Congenital pseudarthrosis of tibia

• Anterolateral bow of tibia with or without fracture

• 50% associated with neurofibromatosis
• Once fractured, tibia is reluctant to heal
• Long term orthotic treatment, with subsequent surgical procedures

Abnormalities of foot & ankle

Congenital vertical talus

• Associated with neuromuscular conditions

• Stiff rocker bottom foot with dorsal dislocation of navicular on talus
• Tx: surgical, reverse ponseti method

Tarsal coalition

• Failure of segmentation of adjacent tarsal bones

• School going children: hind foot pain & recurrent ankle sprains
• Investigations: radiographs, CT or MRI
• Tx: initially conservative, but if requires surgery then carried out before significant degenerative
changes develop

Curly toes

• Flexed, medially deviated, often familial, rarely need treatment

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 • Flexor tenotomy used when symptoms or cosmetic concern

Other causes of foot pain:

• Freiberg’s osteochondrosis: forefoot pain & avascular change in 2nd metatarsal head.
Symptomatic bony spurs & osteochondral fragments need excision
• Kohler’s disease: dorsal forefoot pain & swelling in young children. Navicular becomes avascular.
Resolves spontaneously
• Sever’s disease: heel pain related to activity. Enthesopathy of calcaneal apophysis

Abnormalities of upper limb

• Function is the most important consideration when managing more extensive upper limb
abnormalities
• treatment is delayed until hand dominance established
• children are very adaptable & cope with disabilities much readily than expected

Radial club hand

• associated with other malformations for e.g. as part of VACTERL syndrome

• clinical problems depend on whether thumb present & functional or not
• tx: physiotherapy, splinting, surgery

Radioulnar synostosis

• failure of proximal separation of radius & ulna so, forearm never develops ability to pronate &
supinate
• hand is in a fixed position somewhere along arc from full pronation-neutral-full supination
• osteotomy of forearm bones, changes fixed position (for e.g. from pronation to neutral), but
doesn’t restore movement
• choice of position post surgery depends on hand dominance, functional demands, cultural
considerations

Congenital radial head dislocation

• usually posterolateral compared to traumatic anterior dislocation

• restriction of elbow joint movement & forearm rotation, discomfort on activity
• radial head excision after skeletal maturity

ANOMALY DEFINITION TREATMENT

Extra/accessory digits Excise/amputate when necessary
Syndactyly Failure of separation of digits Separation with or without skin grafting
Trigger thumb (digit) Release of A1 pulley of flexor tendon sheath
Clinodactyly (usually 5th digit) Abnormal angulation of digit in radioulnar plane Surgical treatment
th
Camptodactyly (usually 5 digit) Fixed flexion deformity of PIP Splinting/physiotherapy. Rarely surgery
Common minor congenital anomalies affecting hand

Spinal deformities & back pain

Congenital deformities

• failures either of formation or segmentation. Result: usually scoliosis. When kyphosis develops,
progressive neurological deficit. Bracing is ineffective for congenital vertebral anomalies

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Scoliosis

• spinal deformity in 3 planes: lateral curvature most obvious. Rotational component apparent in
forward flexion when rib asymmetry creates rib hump
• cause: congenital, neuromuscular, syndromic, idiopathic. Leg length discrepancy causes postural
scoliosis
• earlier the onset more likely to be progressive
• lung development occurs in early childhood, so the management of early onset scoliosis must
preserve growth: casting techniques or use of growth rods
• adolescent idiopathic curve is MC, affecting girls more than boys. Not painful so if pain, tumour
& infection is excluded
• cobb angle defines severity & guides treatment. Curve< 20 :ͦ no treatment, 25-40 :ͦ braced, >40 ͦ
surgery (instrumenting & fusing spine)

TYPE AGE OF ONSET

Early onset <10 years
Adolescent 11-18 years
Adult Onset at maturity
Classification of idiopathic scoliosis

Kyphosis

• when it exceeds the normal 20-50 ͦ cause is postural or structural

• postural secondary to Scheuermann’s disease (≥5 vͦ ertebral wedging at 3 adjacent levels & end-
plate changes)
• tx: physiotherapy, bracing, surgery, depending on severity, progression & symptoms

Spondylolisthesis

• spondylosis is defect in pars interarticularis. 6 types: congenital, isthmic, degenerative, post-

traumatic, pathological, post-surgical
• spondylolisthesis occurs when upper vertebra slips forward on lower
• mild slips: asymptomatic, no treatment
• tx: physio, bracing, surgery (depends on degree of slip)
• mechanical pain responds to conservative tx, neurological involvement: surgery

GRADE PERCENTAGE SLIP

0 No slip
1 <25%
2 26-50%
3 51-75%
4 >75%
spondyloptosis >100%-complete translation
Classification of spondylolisthesis according to severity of slip

Torticollis

• head tilted towards & rotated away from tight sternocleidomastoid muscle
• congenital due to intrauterine moulding, fixed contracture, palpable tumour. Strong correlation
with DDH

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 • most cases resolve with stretching, persistent cases cause facial asymmetry, surgical release of
sternocleidomastoid required
• acquired torticollis: GERD, posterior fossa tumor, inflammation/infection, ocular problems,
atlantoaxial rotatory subluxation

Back pain

• in a child is a red flag for serious spinal pathology. If mild, intermittent or occurring only on
strenuous activity, then self-limiting: suffer posture related discomfort. Tx: physiotherapy
• red flag symptoms for spinal pathology: systemic illness, fever, weight loss, progressive
neurological deficit, unrelenting/night pain, spinal deformity
• red flag signs investigations: CBC, ESR, CRP, plain radiograph, MRI

Neuromuscular conditions

• in children, if initial insult to neuromuscular system is non-progressive, effects of insult change

with growth
• multi-disciplinary approach needed
• primary therapy aims to maintain range of movement & prevent fixed contractures with an
emphasis on managing tone & position
• surgery has limited role in management of neuromuscular conditions

SURGICAL PROCEDURE AIM OF TREATMENT

Lengthening of muscle-tendon unit
Tendon transfer
Release of joint contracture;
correction of bony deformity
Fuse/stabilise/relocate joints
Neurological problems:
• selective dorsal rhizotomy
• intrathecal baclofen pumps
Leg equalisation procedures
Surgical procedures in management of neuromuscular conditions
Restores joint range (results in relative muscle weakness)
Improves functional movement, rebalances muscle forces, after correction of fixed
deformity
Restores mechanical alignment, & allows muscle to work in a more efficient manner
Improves posture/function; reduces pain
Reduce spasticity (not primarily useful in dystonia)
Improve lower limb mechanics

Cerebral palsy

• caused by non-progressive insult to developing brain, prematurity is a risk factor

• effects only become apparent as child grows & fails to reach expected developmental
milestones
• MRI: periventricular leukomalacia

CHARACTERISTICS
1. TONE
Spastic (high) Commonest type of abnormality, due to damage to pyramidal system. Velocity-dependent
increased muscle tone & brisk reflexes
Dyskinetic Increased tone but reduced activity-stiff movements
• Dystonic Low tone but increased activity-uncoordinated jerky movements
• choreoathetoid Due to damage in extra-pyramidal system
Ataxia Generalised low tone, loss of muscle coordination, due to damage in cerebellum
Mixed No one tone/movement disorder predominates, combination of spasticity & dystonia

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Hypotonia Usually a phase (which may last years) before features of spasticity
2.SITE
Unilateral
Hemiplegia Arm more affected than leg
Bilateral diplegia Legs more affected than arms
Total body involvement Often significant intellectual impairment & associated difficulties
Classification of cerebral palsy with respect to muscle tone & site of involvement

• prognosis for walking predicted by evidence of neurological development i.e. gaining motor skills
with loss of primitive reflexes
• age related gross motor classification system (GMFCS) has 5 categories which also relate to
mobility & prognosis (GMFCS 1-near normal vs. GMFCS V-wheelchair based)
• tone reduced with diazepam, baclofen. Botulinum toxin has temporary effect, given window for
physiotherapy. Fixed contractures do not respond to tone management/splinting. Dynamic
contractures do respond
• spastic diplegia: problems at all levels of lower limb. Single event multilevel surgery (SEMLS) &
gait analysis helps select appropriate plan
• in total body involvement (TBI) & high muscle tone, hip subluxation & dislocation are common
• overall, independent mobility & effective communication are 2 most important requirements

Polio

• muscle weakness proportionate to number of motor units destroyed

• pts develop trick movements to cope with muscle weakness, so careful assessment required

Spina bifida

• extent of disability varies with level of lesion

• VP shunt required to drain hydrocephalus, which develops following closure of myelocele

Muscular dystrophy

• Early operating to release joint contractures and facilitate maintenance of walking abilities &
good spinal posture

Brachial plexopathy

• Devastating effect on UL function particularly if antigravity motor activity not recovered by 6

months
• Tx: physiotherapy, neural repair, surgical interventions

Infection

Septic arthritis

• Diagnosis difficult in neonates & immunocompromised

• Pain, fever, reluctance to move joint or weight bear
• Investigations: FBC, ESR, CRP, blood cultures, imaging studies, combined with astute clinical skills
• Pus in a joint can destroy articular cartilage & cause avascular necrosis
• Tx is prompt removal of pus, appropriate antibiotic therapy, pain relief & splintage. If child fails
to improve, reaccumulation of pus

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• 4 clinical predictors differentiate between septic arthritis & transient synovitis: history of
fever>38.5, non-weight bearing, ESR>40mm/hour, WBC>12x10^9/L

Osteomyelitis

• Infection often occurs in metaphysis of long bones where slow blood flow through looped
vessels combined with microtrauma encourages seeding of infection during bacteremia
• Metaphysis may be intracapsular & infection spreads easily into joint once periosteum is
breached
• Tx: drainage of pus if present, antibiotics, analgesia, splintage, treatment of underlying condition
e.g. nutritional deficiency, sickle cell disease

Complications of bone & joint sepsis

• In neonate vascular channels pass through physis & a poor outcome may ensue, if damage to
physis and epiphyseal growth centres

Meningococcal sepsis

• Secondary to endotoxin induced microvascular injury & ischemic physeal damage

Tuberculosis

• Malaise, weight loss, boggy joint swelling, muscle wasting & joint contractures

Chronic relapsing/recurrent multifocal osteomyelitis

• Radiographic features show osteomyelitis but cultures negative

• Inflammatory rather than infective condition

Discitis

• Children who refuse to weight bear & complain of back pain may have discitis
• Maybe infective/inflammatory but if vertebral bodies involved, infection is assumed

Brodie’s abscess

Clinical dilemmas

The limping child

• Limp due to pain, weakness, deformity, to gain attention

• Examination includes all joints & soft tissues, brief neurological examination, leg length
measurement, assessment of pain at rest or on weight bearing
• Plain radiographs AP & frog lateral views of pelvis
• Age at presentation of certain hip conditions: 1-3 years: late presenting DDH, sepsis. 3-10:
transient synovitis, perthe’s disease. 11-15: slipped upper femoral epiphysis

Non-accidental injury (NAI)

• Increased risk: under 3 years, disabilities in a family with socioeconomic deprivation

• Factors that raise concern in clinical assessment of suspected NAI: hx: delay in seeking medical
advice, variable story, mechanism inconsistent with injury pattern. Examination: unexpected
bruising to buttocks/back of legs, finger mark bruises, bruises of various ages, burns deep
scratches etc.

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• Fracture patterns with a high specificity for NAI: multiple fractures at different stages of
healing/old fractures, posterior rib fractures, corner or bucket handle metaphyseal fractures,
scapular fractures, any fracture in a child below walking age

Unit 6
Chap 42: 42. Skin and subcutaneous tissue

SKIN AND SUBCUTANEOUS TISSUE

CONGENITAL/GENETIC DISORDERS
Neurofibromatosis

• 2 distinct syndromes, where Schwann cells form tumours

• 70%: autosomal dominant. 30%: sporadic mutations
• NF 1 (Von Recklinghausen’s disease) is more common
• Skin manifestations in early life, with more than 5 smooth-surfaced café-au-lait spots,
subcutaneous neurofibromata, armpit or groin freckling and Lisch nodules
Nevoid basal cell carcinoma (Gorlin’s) syndrome

• Autosomal dominant
• Abnormal tumor suppressor gene encoding the patched protein
• 90% patients develop multiple basal cell carcinomas (BCCs)
• Phenotypical characteristics: over-developed supra-orbital ridges, broad nasal roots,
hypertelorism, bifid ribs, scoliosis, brachymetacarpalism, palmar pits and molar
odontogenic cysts
Xeroderma pigmentosum

• >2000-fold increase in skin cancer risk, autosomal recessive

• Sufferers intolerant to UVR: premature skin aging, multiple neoplasms
• Die in early adulthood from metastatic disease (60% mortality by 20 years)
Gardner’s syndrome

• Autosomal dominant disease variant of familial adenomatous polyposis

• Multiple epidermoid cysts and lipomata
CUTANEOUS MANIFESTATIONS OF GENERALISED DISEASE
Hyperhidrosis

• Excessive eccrine sweating of palms, soles, axillae, groins causing functional, social
problems
• Treatment: anti perspirants, periodic local injections with botulinum toxin A. Resistant
cases treated with laparoscopic cervical sympathectomy
Lipodystrophy (lipoatrophy)

• Localised or generalised loss of fatty tissue, primary or secondary

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 • Complication of long-term administration of insulin, following treatment of HIV with
protease inhibitors or transplant recipients
• Treatment: autologous fat grafting, injections of poly-L-lactic acid & free tissue transfer
Inflammatory conditions
1) hidradenitis suppurativa
• follicular occlusion followed by folliculitis and secondary infection with skin flora (usually
staph aureus & Propionibacterium acnes) culminates in chronic suppurative, painful, skin
abscesses, sinus tracts and scarring
• in skin containing apocrine glands (axilla, groins). Also scalp, breast, chest and perineum
• genetic with variable penetrance, associated with obesity and smoking
• management: stop smoking, lose weight. Reduce symptoms by antiseptic soaps, tea
tree oil, wearing non-compressive and aerated underwear.
• Medical treatment: topical, oral antibiotics & anti-androgen drugs. Sometimes, radical
excision. Reconstruction after that, avoids contractures and functional impairment
2) Pyoderma gangrenosum
• Cutaneous ulceration with purple undermined edges
• Secondary to heightened immunological reactivity, usually from another disease, such as
IBD, RA, non-Hodgkin’s lymphoma, Wegener’s granulomatosis
• Ulcers respond to steroids
Infections
1) Impetigo, erysipelas and cellulitis from medicine
2) Necrotising fasciitis
• Synergistic, polymicrobial infection
• Most commonly strep (group A beta hemolytic) with staph, E. coli, pseudomonas,
proteus, bacteroides or clostridia
• 80%: history of trauma/infection. 60%: start in lower extremities
• Predisposing conditions: diabetes, smoking, penetrating trauma, pressure sores,
immunosuppression, IV drug abuse, perineal infection (perianal abscess, Bartholin’s
cyst) & skin damage/infection (abrasions, bites, boils)
• Clinical signs: edema beyond visible skin erythema, woody hard texture to subcutaneous
tissues, inability to distinguish fascial planes and muscle groups on palpation,
disproportionate pain, skin vesicles, soft tissue crepitus
• Early: pts are febrile and tachycardic, with rapid progression to septic shock
• Radiographs show air in tissues (shouldn’t delay treatment)
• Management: early fluid resuscitation, monitoring of hemodynamic status, high dose IV
broad spectrum antibiotics
• Surgical emergency, diseased area debrided ASAP until viable, healthy, bleeding tissue
is reached
• Early surgical review, further debridement, & vacuum assisted dressings. Early skin
grafting minimises protein and fluid losses
• Mortality of 30 to 50%, even with prompt operative intervention
Purpura fulminans

• Rare condition, intravascular thrombosis produces skin necrosis & haemorrhagic infarction,
progresses rapidly to septic shock and DIC. Usually in children
• 3 types: i) acute infectious ii) neonatal iii) idiopathic (based on aetiological mechanism

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• Mc is acute infectious. Mortality of 40-50%, from multi organ failure. Is secondary to acute
bacterial (Neisseria meningitidis) or viral (varicella) infection. Occurs in children<7 years
after URT infection or asplenia
• Endotoxins produce imbalance in procoagulant and anticoagulant activity, protein C
deficiency occurs. Petechial rash, then ecchymoses and hemorrhagic bullae, necrosis,
then hard eschars. Extensive tissue loss results in amputation
SKIN AND SOFT TISSUE CYSTS
Milia

• small, hard keratin retention cysts in babies and after chronic sun exposure in elderly
Epidermal cysts

• lined with true, stratified squamous epithelium, derived from hair follicle infundibula or
traumatic inclusion. Can occur anywhere, fixed to skin, with central punctum (sebaceous
cysts)
• treatment: if inflamed/infected: initially incision and drainage, removed after inflammation
subsides. If not excised completely, recurrence
• meibomian cysts: epidermal cysts on free edge of eyelid. Tricholemmal
(pilar/pilosebaceous) cysts from epidermis of external root sheath of hair follicle. 90% in
scalp, 70% multiple
SKIN TUMOURS
Benign lesions
Basal cell papilloma (seborrheic keratosis, senile keratosis, verruca senilis)

• from macular to soft, excrescent, warty lesions, pigmented and hyperkeratotic. Formed
from basal layer and contain melanocytes
Papillary wart (verruca vulgaris)

• from infection with HPV, which also causes plantar warts and condylomata acuminata
freckle (ephelis)

• area of skin, contains normal number of melanocytes, producing abnormally large

melanin granules
lentigo

• small, pigmented macules, stem from sun damage and some systemic syndromes. Solar
lentigos common in fair skin
moles/naevi

• melanocytes migrate from neural crest to basal epidermis during embryogenesis

• when melanocytes aggregate in dermis or dermo-epidermal junction, called as naevus
cells
junctional naevus

• dermo-epidermal proliferation of naevus cells, visible as deeply pigmented

macules/papules in childhood/adolescence. Progress to form compound/intradermal
naevi with age. Benign mucosal lesions are junctional naevi

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compound naevus

• maculopapular, pigmented lesion, becomes prominent during adolescence

• junctional proliferation of naevus cells, with nests and columns in dermis
intradermal naevus

• faintly pigmented papules, no junctional proliferation, cluster of dermal melanocytes

spitz naevus

• reddish brown nodules, previously called juvenile melanoma

• most common on face and legs, growing rapidly initially then static or regress
spindle cell naevus

• dense black lesions contain spindle cells and atypical melanocytes at dermo-epidermal
junction. Occur on thigh, more common in women. Have malignant potential
halo naevus

• halo of depigmentation around any benign naevus shows antibody response to

melanocytes. Depigmentation also a feature of malignant melanoma. Halo naevi
associated with vitiligo
café-au-lait spots

• coffee colored macules of variable size (a few mm to 10cm)

• multiple lesions associated with NF1 and McCune-Albright syndrome. More common in
dark skinned
Naevus-spilus (speckled lentiginous naevus)

• similar in appearance to café-au-lait spots, but with hyper pigmented speckles

• can be confused with malignant change because of appearance
• management: observation and serial photography (as malignant change rare)
Mongolian spot

• congenital blue grey macule on sacral skin. Pigmentation deepens initially then
regresses completely by 7 years
Blue Naevus

• 4 times more common in children, affecting extremities and face

Naevi of Ota and Ito

• Naevus of Ota: dermal melanocytic hamartoma as a blue/grey macule in trigeminal V1

and V2 dermatomes. More common in women
• Naevus of Ito: dermal melanocytosis in shoulder region and can occur with naevus of
Ota
HAIR FOLLICLES
Trichoepithelioma

• Skin colored nodules in nasolabial folds, Clinically and histologically similar to BCC

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Pilomatrixoma (calcifying epithelioma of Malherbe)

• Benign hair matrix cell tumors which calcify. 40% under age 10
Tricholemmoma (naevus sebaceous of Jadassohn)

• Congenital hamartoma, appearance of linear verrucous naevus. 10% form BCC

Adenoma sebaceum (tuberous sclerosis, Bourneville disease)

• Red facial papules (angiofibromas), on nasolabial folds, cheek and chin

• In children before 10 years of age, increase in size and number until adolescence
• Cosmetic removal by argon or pulse dye lasers or scalpel
Rhinophyma

• End stage sequelae of nasal acne rosacea

• Nasal sebaceous gland hypertrophy and hyperplasia, effects elderly men
• Occult BCCs in 3%. Treatment: dermabrasion or laser
SWEAT GLANDS
Cystadenoma (hydro cystadenomas, hidradenomas)

• 1-3 cm translucent blue cystic nodules

Eccrine poroma (papillary syringoma)

• Single, raised or pedicled lesions on palm or sole

Cylindroma (turban tumor)

• Variant of eccrine spiradenoma, coalesce when multiple on the scalp, forming a turban
tumor
PREMALIGNANT LESIONS
Extra mammary Paget’s disease (intra epidermal adenocarcinoma)

• In cutaneous sites rich in apocrine glands (axillae, genital & perianal regions)
• 25% associated with underlying in situ or invasive adenocarcinoma
• Early skin changes: eczematous lesion or intertrigo
• Treatment: surgical excision, 20% show invasive disease after pathology assessment
Giant congenital pigmented naevus (GCPN) or giant hairy naevus

• Hamartoma of naevo-melanocytes, tendency to dermal distribution

• Similar histo to compound naevi, but naevus cells distributed from epidermis throughout
all layers and in subdermal fat and muscle
• Precursors of melanoma (3-5% lifetime risk), risk decreases with age
• Initial investigations for neurocutaneous melanosis, as maybe leptomeningeal
involvement
• Removal done for both aesthetic and oncological reasons
Atypical (dysplastic) naevus

• 3 of the following characteristics: variegated pigmentation, ill-defined borders, undulating

irregular surfaces, or measure > 5mm

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• Histo= irregular proliferation of melanocytes at basal layer of epidermis
• Sporadic or familial (familial atypical multiple mole melanoma [FAMMM] syndrome)
• Having greater than 5 confers risk of melanoma 6 times greater
• Within FAMMM syndrome, life-long risk of 10%
WOUNDS
Congenital
Cutis aplasia congenita

• Congenital absence of epidermis, dermis and sometimes subcutaneous tissues, with

underlying bony defects in 20%
• Treatment depends on severity but is usually plastic surgery
Parry-Romberg disease

• Progressive hemi facial atrophy of skin, soft tissue and bone

• Affects women more, starts in late 20’s. Can present in childhood, when resulting
deformity is worse because it is magnified by differential growth elsewhere
• Self-limiting, by 5-10 years after onset
• Once stable, plastic surgery
Spina bifida

• Failure of closure of caudal neuropore during 4th week in utero results in incomplete
development of some or all structural elements posterior to spinal cord
• Commonest in lumbar vertebrae. Presents as gross variants, spina bifida occulta: bony
defect without neural protrusion, spina bifida cystica: herniation of meninges, spinal cord
or most commonly both therefore asymptomatic
• Management: protect spinal cord, prevent CSF contamination, and secondary
hydrocephalus and meningitis
Acquired
Pressure sores

• Begin with tissue necrosis at a pressure point, develop in cone shaped volume of
necrotic loss
• Pathogenesis: increase in local tissue pressure greater than perfusion pressure,
produces ischemic necrosis, directly proportional to duration & degree of pressure,
inversely proportional to area over which it is applied
• Muscle and fat more susceptible to pressure than skin
• No predisposing factor: debridement and repair (no recurrence once normal function
and sensibility returns)
• Paraplegic: relieving pressure (special mattress, nursing care, relief of muscle spasm
and contractures), optimise nutrition, correct anemia, prevent infection and dressings.
Surgery: thorough debridement for healing and plastic surgery to reconstruct de

Unit 7
Chap 43: Elective neurosurgery

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 PAEDIATRIC NEUROSURGERY
CYSTS
• Benign fluid filled intracranial lesions
• Arachnoid cyst=middle fossa, CSF in an envelope of arachnoid matter
• Colloid cyst=roof of 3rd ventricle
• Dermoid and epidermoid cyst=posterior fossa (midline) & cerebellopontine angle
respectively
• Porencephalic cyst=brain cavities lined with gliotic white matter, containing CSF
communicating with ventricles or sub-arachnoid space
• Tx: excision, endoscopic fenestration into a cistern or ventricle, or shunting for
hydrocephalus
NEURAL TUBE DEFECTS
• Failure of closure due to folate deficiency, anticonvulsants, family hx
• Prenatal diagnosis by serum alpha protein levels & amniocentesis
Spina bifida occulta
• congenital absence of spinous process, without exposure of meninges & neural tissue
• shallow hair covered hollow at the spine base. Common & not significant
• when associated with tethered cord syndrome (thickening of filum terminale), causes
traction on cord. Presentation: progressive deficits, spasticity, bladder dysfunction,
scoliosis. Tx is surgical exploration & untethering of cord
Meningocele
• sac of meninges covered with skin & contain only CSF. Herniates through ant/post bony
defect
Myelomeningocele
• herniating sac of meninges without skin covering contains spinal cord or nerves or both
• always associated with Chiari 2 malformation
• high infection risk so early surgical repair done
Lipomyelomeningocoele
• adipose tissue adherent to spinal cord herniates through bony defect to Sacro lumbar
soft tissue, associated with bladder dysfunction. Tx: surgical release of tethered cord

• Failure of anterior neuropore closure produces anencephaly (fatal)

• Cranium bifidum is failure of fusion in occipital region. Associated with meningocele and
encephalocele
POSTERIOR FOSSA MALFORMATIONS
Chiari malformations involve cerebellar herniation through foramen magnum:
• Normal: up to 5mm descent
• Chiari 1 is >5mm of tonsillar descent. Presents in young adults with cough headaches &
neurological disturbance (brainstem compression or formation of syrinx). Tx: shunting &
foramen magnum decompression
• Chiari 2 is tonsil and vermis descent in infancy with poor feeding, stridor and apnea
Dandy Walker malformation in infancy with macrocephaly, hydrocephalus and
developmental delay. Imaging: hypoplastic cerebellar vermis and large cyst in post fossa.
Tx: shunt placement
CRANIOSYNOSTOSIS
• Normal fusion of sutures between 6-12 months of age. Frontal fuses later
• premature fusion of one(simple) or more(complex) cranial sutures preventing growth
perpendicular to suture. Causes skull deformities & hydrocephalus
TYPE SUTURE INVOLVED CLINICAL FEATURES
scaphocephaly Sagittal suture Narrow boat-shaped head
brachycephaly Coronal suture Shortened/broad forehead
microcephaly All sutures Small head
plagiocephaly Unilateral coronal/lambdoid suture Asymmetric skull

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 trigonocephaly Metopic suture Pointed narrow forehead
Types of craniosynostosis
FUNCTIONAL NEUROSURGERY
EPILEPSY
• if primary lesion such as tumour, AVM or cavernoma lesionectomy. In other cases,
clinical picture including seizure type, focal features & investigation results used to
identify focus.
• Dual pathology: extrahippocampal lesion plus hippocampal atrophy, removal of both
needed for seizure control
Investigation
• Mainstay is MRI
• Nuclear medicine modalities including single photon emission CT & positron emission
tomography for ictal & interictal metabolic abnormalities
• Electroencephalogram combined with video telemetry
• Neuropsychological evaluation to evaluate patients pre-operative function using Wada
test
• Wada test: sodium amytal injected into each internal carotid artery, with simultaneous
speech & memory testing to localise function. Aim is to confirm language laterality that
resection on side of lesion will not impair verbal memory functions
Surgical management
• Surgical focus resection or disconnection
• Mesial temporal epilepsy: amygdalohippocampectomy
• Specific epilepsy syndromes such as infantile hemiplegia syndrome: hemispherectomy
• Disconnection procedures including corpus callosotomy, for pts suffering drop attacks
• Vagal nerve stimulators implanted in severe drug refractory epilepsy; electrodes applied
to vagus nerve in carotid sheath in neck
MOVEMENT DISORDERS
• levodopa or deep brain stimulation with electrodes
PAIN SYNDROMES
• neurosurgical approaches address underlying etiology or interrupt transmission
responsible for pain
• trigeminal neuralgia: impingement on nerve by sup cerebellar artery. Bilateral in young
suggests MS. Surgical options are:
1) Craniotomy and microvascular decompression: apply material between nerve &
adjacent vessel to prevent direct contact & stimulation. Risk: cranial nerve deficit
2) Peripheral nerve injections: short term relief of pain restricted to small areas
3) Percutaneous Gasserian rhizolysis: needle placement at Gasserian ganglion in
Meckel’s cave. Permits lesioning of ganglion by glycerol injection, radiofrequency
thermocoagulation or balloon compression. This disrupts pain transmission. Similar
effect with stereotactic radiosurgery. Risks: facial numbness & late recurrence of pain
• treating pain elsewhere: lesioning of nerve tracts. Risk: occurrence of deafferentation
(phantom limb)
• electrical stimulation used to modulate pain syndromes
OCCLUSIVE VASCULAR DISORDER
• MOYA MOYA DISEASE is progressive obliteration of one or both internal carotid
arteries, autoimmune process, puff of smoke appearance, causes ischemia or
hemorrhage
COMPRESSIVE NEUROPATHIES
• CARPAL TUNNEL risk factors: pregnancy, obesity, DM, thyroid, acromegaly,
paresthesia in hand worse at night. Wasting of thenar, tinels and Phalen test. Tx;
steroids, splints, decompression
• Ulnar nerve entrapment at elbow affects little finger and ulnar aspect of ring finger and
hypothenar wasting, froment's sign +

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• Meralgia paresthetica is compression of lateral cutaneous thigh nerve producing sensory
disturbance in lateral thigh
CREUTZFELT JAKOB DISEASE
• rapidly progressive dementia, uniformly fatal
• pre-operative check to exclude risk factors for CJD infection. Risk factors: family hx,
receipt of pituitary derived human GH, cadaveric dura matter grafts, previous brain or
spinal surgery. If risk factors, instruments quarantined/destroyed pre-operatively
RISK OF CRANIOTOMY
• infection (5%) & wound breakdown
• Intracerebral hemorrhage
• CSF leak, permanent neurological deficit
• Seizures, death (1%)
BRAINSTEM DEATH
• irreversible loss of cerebral & brainstem function. Legally equivalent to death,
precondition for harvesting organs for transplant from heart-beating donors
• diagnosis requires
1) identification of cause of irreversible coma
2) exclusion of reversible causes of coma
3) clinical demonstration of absence of brainstem function
should be done twice, by 2 clinicians to show absence of:
• response to pain
• respiratory drive (apnea despite a pCO2>6.7kPa)
• pupillary light reflex
• corneal reflex
• vestibulo-ocular reflex
• oculo-cephalic reflex
• gag reflex

Chap 44: The eye and the orbit (not to be done)

Chap 45: Cleft lip & palate: developmental abnormalities of the face, mouth and jaws
Chap 46: The nose and sinuses (not to be done)
Chap 47: The ear (not to be done)
Chap 48: Pharynx, larynx, and neck (not to be done)
Chap 49: Oropharyngeal cancer

OROPHARYNGEAL CANCER
ETIOLOGY
• tobacco and alcohol, HPV, pan, reverse smoking, EBV, Plummer Vinson, poor nutrition,
inherited conditions (Fanconi anemia, Li-Fraumeni syndrome)
INCIDENCE
• Greater in men, mostly affects people of age>65 years
ANATOMY
• frequently involved sites are floor of the mouth, lateral border of anterior tongue, buccal
sulcus, retromolar trigone (attached mucosa overlying ascending ramus of mandible
posteriorly to last molar tooth
HISTOLOGY
• Squamous cell carcinoma is the predominant histology
• Lymphomas, salivary glands tumor
PREMALIGNANT LESIONS

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 • High risk lesions: Erythroplakia (homogenous or speckled), proliferative verrucous
leukoplakia, chronic hyperplastic candidiasis
• Medium risk: oral submucous fibrosis, syphilitic glossitis, sideropenic dysphagia
• Low risk: oral lichen planus, discoid lupus erythematosus, discoid keratosis congenita
Leukoplakia
• White patch or plaque which cannot be rubbed off
• Purely a descriptive term with no histological correlation
• Smooth, wrinkled, fissured, vary in white colour depending on thickness of lesion
Speckled leukoplakia
• Leukoplakia arising on erythematous base. Highest rate of malignant transformation
Erythroplakia
• Less frequent than leukoplakia
• bright red velvety plaque can’t be characterized clinically or pathologically as any other
recognisable condition
• biopsy essential, after which surgical ablation
FIELD CHANGE & SECOND PRIMARY TUMORS
• consequence of diffuse exposure to carcinogenic substances is development of separate
tumors at different anatomical sites. May present simultaneously within 6 months
(synchronous) or maybe delayed (metachronous)
• pts who develop a first tumor in the oral cavity & oropharynx, are more likely to develop a
2nd primary tumor, 80% of which are metachronous
POTENTIAL FOR MALIGNANT CHANGE
potential risk includes:
• severity/grade of dysplasia
• increases with age of patient
• increases with size of lesion
• higher in smokers, people who drink alcohol
• depends on anatomical site (high for lesions on floor of mouth and lateral/ventral surface
of tongue in particularly in young women
PREMALIGNANT CONDITIONS
Chronic hyperplastic candidiasis
• dense plaques of leukoplakia around mouth commissures. Sometimes extend to vermillion &
facial skin
• result of invasion of lesion by Candida Albicans
• tx is 6 weeks topical antifungal or 2 weeks systemic antifungal. If persists, surgical excision
Oral submucous fibrosis
• progressive disease, fibrous bands form beneath oral mucosa. Scarring causes
contractures; limited mouth opening & restricted tongue movement
• pathology: epithelial fibrosis with atrophy & hyperplasia of overlying epithelium
• tx of restricted mouth opening: intralesional steroids
• surgical excision leads to short term benefits only as fibrous bands recur at same site
• strong association with pan masala areca nut. Cessation of use: halts but does not
improve
Proliferative verrucous leukoplakia
• exophytic variant of leukoplakia
• arises in absence of traditional risk factors for oral malignancy
Sideropenic dysphagia (Plummer-Vinson & Paterson Kelly syndrome
• sideropenia (iron deficiency in absence of anemia), leads to epithelial atrophy, renders
oral mucosa vulnerable to infection from carcinogens. Tx: iron supplements (reduces risk
of malignant change)
CLASSIFICATION AND STAGING
TNM
PRIMARY TUMOR (T) REGIONAL LYMPH NODES(N) Distant metastasis

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TX=primary tumor cant be assessed NX=regional node cant be assessed MO=no evidence of distant metastasis
TO=no evidence of primary tumor NO=no node metastasis M1=evidence of distant metastasis
Tis=carcinoma in situ N1=ipsilateral single node <3cm
T1=<2cm N2a=single ipsilateral 3-6cm
T2=2-4 cm N2b=multiple ipsilateral node>6cm
T3=4-6cm N2c=bilateral >6cm
T4=invades adjacent structures N3=any node >6cm
STAGE:
0 Tis N0 M0
I T1 N0 M0
II T2 N0 M0
III T3 N0 M0
T1, T2, T3 N1 M0
IV T4 N0 M0
Any T N2 M0
Any T N3 M0
Any T Any N M1
PATTERN OF LYMPH NODE METASTASIS
• five levels (submandibular, upper, middle and lower jugular, posterior triangle)
• SCC in oral cavity spreads to I, II, III
• SCC of oral tongue to III, IV (without involvement of higher levels)
• Tumors in oropharynx to II, III, IV, retropharyngeal & contralateral nodal groups
• Distant metastases are uncommon
CLINICAL FEATURES
• 25-50% patients present late
LIP CANCER
• Presents early as readily visible, ulcer on vermillion border, mostly in lower lip
• Reflects etiological influence of UV radiation on more exposed lower lip
ORAL CAVITY
• Mucosal ulceration with rolled margins, exophytic & endophytic neoplastic tissue, contact
or spontaneous bleeding. Where involving tooth bearing areas, loss of periodontal/bone
support & mobility
• Nutritional impairment due to pain & restricted oral intake
• Oropharynx: presents much later, lump in neck, painful swallowing, tonsillar
enlargement, otalgia
• Clinical features of oral cancer that warrant investigation: persistent oral swelling for>3
weeks, mouth ulceration for >3 weeks, sore tongue, difficulty swallowing, jaw or facial
swelling, painless neck lump, unexplained tooth mobility, trismus
INVESTIGATIONS
• Incisional biopsy in all cases, examination under anaesthesia
• Biopsy is generous, areas of infection avoided.
• Percutaneous endoscopic gastrostomy for feeding
Radiography
• for dental assessment
MRI
• ideal for oral and oropharynx cancer
• performed before biopsy as biopsy distorts image of primary tumor
CT
• if bony invasion suspected
• CT of thorax done for all patients
Radioisotope bone scan
• little value
Positron emission tomography combined with CT (PET-CT)

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• Work up of patients with malignant cervical lymphadenopathy with unknown primary
Ultrasound
• For evaluation of undiagnosed neck lumps or presumed cervical metastasis
FNAC
• for enlarged nodes. Uses 21 or 23G needle and 10 ml syringe. Aspiration when needle
enters swelling
TREATMENT
General principles
• surgery is primary treatment modality. Used for oral cavity, tumor invading bone, bulky
advanced disease or when multiple tumors are present
• Post-operative radio/chemo
• reconstruction is often needed
• node-positive neck: therapeutic neck dissection
• Malignant tumor of salivary require surgery while lymphoma needed radiotherapy
• 2nd course of radiotherapy to previously irradiated site is contraindicated
Patient factors
• advancing age not a contraindication to major head & neck cancer surgery, but
influences extent of adjuvant treatment
• young pts should not be denied a radiotherapy for fear of inducing 2nd malignancy later
MANAGEMENT OF PREMALIGNANT LESION
• stop risk factors, photographic record of lesion for long term follow up
• incisional biopsy for Erythroplakia and speckled leukoplakia.
• Severe epithelial dysplasia & carcinoma in situ ablated by surgical excision. Laser
vaporisation can be sued but doesn’t provide specimen for histological examination
• Small lesions: surgical excision & primary closure or left to granulate
• Larger defects: laser excision & allowed to epithelise spontaneously
LIP CANCER
• surgery and external beam radiotherapy. Cure rate:90%
• premalignant changes on lower lip: lower lip shave (vermillion defect closed by
advancement of lower labial mucosa
Small tumors(<2cm)
with V or W shaped excision. Defect is no larger than 1/3rd of total lip size. Closed in 3
layers: mucosa, muscle & skin
Intermediate tumors
• defects between 1/3rds & 2/3rds need local flaps using Johansen step technique. Allows
closure of defect by symmetrical advancement of soft-tissue flaps using excess skin in
labiomental grooves. If V or W incision used, microstomia
Total lip reconstruction
• Extensive tumors, which invade adjacent tissues, (t4) need surgery with neck dissection,
7 total excision of lower lip & chin, with or without adjacent mandibular resection. Lower
lip defect closed by free flaps e.g. radial forearm flap, perforator flaps such as
anterolateral thigh flap (ALT) or medial sural artery perforator flap. If bone removed, then
composite (bone-including) flaps used. Scapula free flap is best
TONGUE CANCER
• T1 require 2cm wide complete excision plus neck dissection and radiotherapy. T3 and 4
require major excision i.e. tongue & floor of the mouth. If T4 tumour cross midline, (sub)
total glossectomy
Access
• Important to allow accurate assessment & clear visualisation to enable tumour
clearance. Techniques used are: 1) transoral-small-moderate sized ant oral tumours. 2)
lip-split technique & paramedian /median mandibulotomy 3) visor incision with or without
drop down
Reconstruction

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• The more anterior the defect in oral cavity, greater the impact on speech. The more
posterior the defect, greater the impact on swallowing
• Small defects of lateral tongue: primary closure of healing by secondary intention
• T2,3,4 require reconstruction for good speech & swallowing e.g. ALT or forearm flap
• Large volume defects (total glossectomy) require bulky flaps e.g. rectus abdominus free
flap or ALT. preservation of one/both hypoglossal nerves encourage floor of mouth
function to relearn swallowing
FLOOR OF MOUTH
• partial anterior glossectomy & anterior mandibular resection. Small tumors by simple
excision.
Reconstruction
• anterior floor of mouth reconstruction by radial artery forearm flap. If unfit for
microvascular free flap surgery or bilateral nasolabial flaps
• larger defects with resection of anterior mandible only; soft-tissue reconstruction
• full thickness resection of anterior mandible requires immediate reconstruction to prevent
functional defects. If mandibular & floor of mouth defects: fibula flap/vascularised iliac
crest graft
BUCCAL MUCOSA
• widely excised with underlying buccinator muscle & selective supraomohyoid neck
dissection or sentinel lymph node biopsy
• reconstruction prevents scarring & trismus, radial artery forearm flap or temporalis flap
LOWER ALVEOLUS
• surgery for tumors involving mandibular alveolus
• Ipsilateral neck dissection if lateral tumors and bilateral if anterior tumors. Bone invasion
requires segmental resection of mandible.
• Pri/immediate reconstruction better as better outcome
• Reconstruction via iliac crest or fibula flap
METHOD TECHNIQUE
No reconstruction Primary closure
Soft tissue only Pectoralis major myocutaneous flap
Alloplastic material 2.4mm reconstruction plate alone
Combination alloplastic/soft tissue 2.4mm reconstruction plate & pectoralis major flap
Non-vascularised bone grafts Titanium tray & cancellous chips (iliac crest)
Vascularised bone grafts Fibula (edentulous & dentate); iliac crest (dentate);
scapula (concomitant large soft tissue defect)
Mandibular reconstruction (reconstructive ladder)
RETROMOLAR PAD
• Frequently invade ascending ramus of mandible, soft palate & tonsillar fossa
• Small defects: microvascular free flap (radial artery forearm flap, temporalis muscle flap)
• Segmental mandibular reconstruction: vascularised bone required
HARD PALATE AND MAXILLARY ALVEOLUS
• Maxillary alveolus & hard palate are uncommon sites for SCC. Tumor in this area arises
from oral mucosa, or maxillary antrum penetrating oral cavity.
• small tumors of maxillary alveolus tx with transoral partial maxillectomy, extensive
tumors require Weber-Fergusson incision
• graft needed is iliac crest or fibula
RECONSTRUCTIVE FLAPS USED IN OROPHARYNGEAL CANCER
• Floor of mouth: RFFF (radial forearm free flap)
• Lateral tongue: RFFF/ALT
• Glossectomy: ALT/Rectus abdominus
• Buccal mucosa: RFFF
• Mandible: dentate- iliac crest, edentulous: fibula

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 • Maxilla: low level/hard palate-obturation, RFFF/ALT, high-iliac crest/scapula, soft
palate/tonsil-forearm/MSAP, tongue base: RFFF
• Microvascular free tissue transfer: method of choice for management of defects in
oropharynx
OROPHARYNX
• tx with chemoradiotherapy
• CHEMOTHERAPY: platinum agents and 5 fluorouracil
MANAGEMENT OF NECK
CLINICALLY NODE NEGATIVE NECK
• carcinoma of lateral tongue, floor of mouth, mandibular alveolus managed by
supraomohyoid neck dissection
• Carcinoma of tongue with extended supraomohyoid neck dissection
CLINICALLY NODE POSITIVE NECK
• selective supraomohyoid neck dissection if <3cm ipsilateral node
• Radical or modified radical for N2a and b
• Bilateral neck dissection for N2c
• Radical neck dissection for N3
TYPES OF NECK DISSECTION
1.SELECTIVE SUPRAOMOHYID=remove level I, II, III for No, N1
EXTENTED SUORAOMOHYOID NECK DISSECTION=remove level I, II, III, IV for oral
tongue
cancer with NO nodes
2.RADICAL
FULL=I-IV for N2,3
MODIFIED RADICAL NECK=I-IV with preservation of internal jugular vein, CN XI,
sternomastoid for neck involvement
COMPLICATIONS
• SURGICAL: accessory nerve palsy, soft tissue edema, phrenic nerve injury, thoracic
duct
injury, cranial nerve injury, carotid artery rupture
• RADIOTHERAPY: osteoradionecrosis of mandible, hypothyroidism, carotid artery
atherosclerosis, neck shoulder dysfunction, trismus, xerostomia, visual impairment, radiation
neuritis
• CHEMOTHERAPY: nausea, vomiting, diarrhoea, stomatitis, GIT upset, renal toxicity,
leukopenia and thrombocytopenia
POST TREATMENT MANAGEMENT
• recurrence occur in first 12 months thus follow up needed
prognosis depends on staging, but the most important factor is cervical

Chap 50: Disorders of salivary gland

Unit 8
Chap 51: thyroid and parathyroid glands
Chap 52: the adrenals and other abdominal endocrine disorders
Chap 53: breast

Unit 9
Only pneumothorax to be done from this unit. No one made notes for this.

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Chap 54. Cardiac surgery
Chap 55. The thorax

Unit 10
Chap 56: arterial disorders
ARTERIAL DISORDERS
ARTERIAL STENOSIS AND OCCLUSION:
Narrowing or complete blockage of artery leads to various symptoms depending upon the
site it supplies
OPERATION FOR ARTERIAL STENOSIS OR OCCLUSION:
Site of disease and type of operation:
• This option is reserved for patients having severe symptoms where angioplasty has
failed or is not possible
• Aortoiliac occlusion respond to aortofemoral bypass using a Dacron graft (high
mortality 5%) or for unfit patients axillofemoral bypass is alternative
• If one iliac system is occluded iliofemoral or femorofemoral crossover graft may be
performed
• Superficial femoral artery disease = femoropopliteal bypass
Graft patency depends on:
o quality of inflow outflow
o Graft length
o Conduit used for bypass
• Autologous long saphenous vein (LSV) gives the best result can be used reserved or
in situ after valve disruption
o If long saphenous not available short saphenous or arm veins are used
o If no vein available polytetrafluoroethylene (PTFE) graft may be employed
o Many surgeons construct lower anastomosis using a small collar of vein
(miller cuff) between PTFE and recipient artery to improve patency
• Isolated femoral artery or profunda disease can be treated with endarterectomy and
patch (vein or prosthesis) or a short bypass in groin
• Occlusion of tibial artery = limb salvage may be attempted with femorodistal bypass.
Risk of early graft failure with limb loss is high. These long bypasses are appropriate
for limb salvage
Technical details:
• For aortofemoral bypass = approach through midline abdominal incision; transverse
abdominal incision should not be used as it divides inferior epigastric vessels
(important collateral vessels in occluded aorta)
o Common femoral arteries are exposed through vertical groin incision
o Small bowel is retracted to right and posterior peritoneum is opened
o Retroperitoneal tunnels are made from aorta to groin
o Heparin 5000 IU given IV and vessel is clamped
o Vertical incision is given to anterior aspect of aorta to which an oblique cut bifurcated
Dacron graft is sutured end to end. Graft limbs are then anastomosed down to
common femoral artery
o Posterior peritoneum is closed over the Dacron to prevent adhesion of graft to bowel
and abdomen and groin wounds are closed
• For femoropopliteal bypass = popliteal artery above or below knee is exposed
through a medial incision
o Common femoral artery is exposed at groin level
o Long saphenous vein is used in 2 ways:

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 1. Vein excised, its tributaries tied, and vein used in reversed fashion, so
its valves do not obstruct the flow of blood
2. It may be left in situ and valves disrupted with a valvulotome.
o Graft is sutured to femoral artery proximally and popliteal artery distally
• Femorodistal bypass = fashioning distal anastomosis to a tibial vessel
o If no suitable vein is available prosthetic material (PTFE) may be used with or
without small vein collar (Miller cuff)
• Femorofemoral crossover = tunnelling a prosthetic graft subcutaneously above the
pubis between the groins
• Axillofemoral graft = tunnelled subcutaneously between the axillary artery proximally
to reach one or both of femoral arteries
o Patency of axillobifemoral bypass is better than axillounifemoral bypass
Results of operation:
• Long term results of aortoiliac reconstructive surgery are good
• Femoropopliteal surgery is less successful (can be used for limb salvage in
debilitated pts with short life span)
• Immediate post operative success of vein bypass exceeds 90% but 5 years patency
is 60%
• PTFE yields poorer result than veins bypass (5-year success is less than 50%)
Other sites of atheromatous occlusive disease:
• Carotid stenosis (at bifurcation) can cause TIA. Clinical features include
o Recurrent short duration <24 hrs
o Unilateral motor or sensory loss of arm, leg or face
o Transient blindness (amaurosis fugax)
o Speech impairment
o Etiology: distal embolization of platelet thrombi into cerebral circulation
o Patient should be assessed with duplex scan
o Indications for carotid endarterectomy in symptomatic patients:
70% or more stenosis and:
▪ Ipsilateral amaurosis fugax or monocular blindness
▪ Contralateral facial paralysis or paresthesia
▪ Arm/leg paralysis or paresthesia
▪ Hemianopia
▪ Dysphasia (if dominant hemisphere)
▪ Sensory or visual neglect
• Renal artery stenosis:
o Cause hypertension and renal failure
o Mainstay of treatment is drug to control hypertension and diabetes
o 2nd line = surgery or PTA
ACUTE ARTERIAL OCCLUSION:
compartment syndrome:
• Sudden ischemia followed by revascularisation causes edema. Muscles swell within
the fixed fascial compartment producing ischemia leading to muscle necrosis and
nerve damage due to pressure
• Renal failure due to liberation of muscle breakdown products
• Severe pain out of proportion to clinical findings, worsens with time despite
analgesia. Numbness/paresthesia in distribution of nerves running in compartment
(non-myelinated type C sensory fibres are most sensitive to hypoxia). Presence of
palpable pulses does not rule out compartment syndrome
• Treatment include fasciotomy
• Usual site of fasciotomy is calf (especially anterior tibial compartment)
• Compartment syndrome occasionally affects thigh and arm
Acute mesenteric ischemia :
• May be thrombotic (atheromatous narrowing) or embolic (cardiac cause)

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 • Embolic occlusion causes sudden severe abdominal pain, bowel emptying (vomiting,
diarrhea) & a source of emboli present (usually cardiac)
• Diagnosis: laparotomy showing widespread infarction of small & large bowel. If so,
then fatal usually
• If infarction is limited, Tx: resection of dead bowel , embolectomy or bypass surgery
• 2nd look laparotomy after 24 hours to check viability of gut
Other form of embolization:
• Infective emboli or clot may cause mycotic aneurysms, septicaemia, infected infarcts
• Parasitic emboli: by ova of taenia echinococcus and filaria sanguinis hominis
• Tumor cells (hypernephroma and cardiac myxoma) form rare emboli
• Venous emboli travel to lung causing ARDS
• Fat emboli after major bony fracture
Air embolism:
• Air may accidently enter into venous circulation during surgery of head and neck or
cut throat or may be following fallopian tube insufflation and illegal abortion or
accidentally injected into venous circulation
• Large volume of air if reaches right side of heart may occlude pulmonary artery
causing acute right heart failure
• Treatment: put patient in head down (Trendelenburg) position to encourage air to
enter the veins in the lower part of the body. Patient is placed on left side to help air
to float to ventricular apex, away from ostium of pulmonary artery.
• In severe cases air is aspirated from heart through needle below left costal margin
Therapeutic embolization:
• Used to arrest hemorrhage from GIT, urogenital tract, respiratory tract or treat AVM
• Arterial embolization requires accurate selection of catheter by Seldinger technique
• Materials used: gelfoam sponge, balloons, plastic microsphere, ethyl alcohol, plastic
and metal coils
AMPUTATION:
General:
• Amputation is considered when part of limb is dead, deadly or a dead loss
• Limb is dead when arterial occlusive disease is severe enough to cause infarction of
macroscopic portion of tissue i.e. gangrene
• If occlusion is irreversible then amputation is indicated
• Limb is deadly when putrefaction and infection of moist gangrene spreads to
surrounding viable tissue resulting in cellulitis and severe toxaemia
• Amputation is also indicated for deadly limb:
o gas gangrene or wet gangrene
o osteogenic sarcoma
o AVF
o Spreading cellulitis
• Limb is deemed a dead loss in following situations:
o Severe rest pain with unreconstructable critical leg ischemia (amputation will
improve quality of life)
o Paralysis and contracture (make limb impossible to use & renders it a
hinderance)
o Trauma (unrecoverable damage)
Distal and trans metatarsal amputation:
• Etiology: small vessel disease e.g. diabetes, gangrene of toes occurs with good
blood supply to surrounding tissue. In such situations local amputation of digits can
result in healing
• If metatarsophalangeal joint is involved = ray excision i.e. taking part of metatarsal
and cutting tendons back
• In less extensive gangrene cartilage is removed front joint surface following
amputation to improve recovery

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 • Trans metatarsal amputation is required when several toes are affected but proximal
circulation is intact. Wound is closed with viable long plantar flap or left open
Major amputation:
Choice of operation:
• Major choice is between an above knee or below knee operation
• Below knee preserves knee and allow walking using prosthesis
• Above knee is more likely to heal and may be appropriate if patient has no prospect
of walking again
• If femoral pulse is absent or failure of below knee procedure amputation should be
above knee
Stump should be of sufficient length to give required leverage i.e.
o Not less than 8 cm below knee (preferably 10-12 cm)
o Not less than 20 cm above the knee
Below knee amputation:
• Flap length should be 1.5 times diameter of leg at the point of bone section
• Two types of flaps are
1. Long posterior flap: old, simple and popular method
▪ Anterior incision is deepened to bone
▪ Posterior and lateral incision is given in such a way to leave bulk of
gastrocnemius muscle attached to the flap
▪ If bleeding is inadequate, amputation is refashioned at a higher level
▪ Blood vessels are ligated
▪ Nerves are brought down gently and transected as high as possible
▪ Fibula is divided 2 cm proximal to level of tibial division
▪ The long muscle/skin flap is tapered after removing bulk of the soleus
muscle (much of gastrocnemius left unless it is very bulky)
▪ Area is washed with saline to remove bone fragment and muscles and
fascia are sutured with absorbable material to bring flap over bone
ends
▪ Suction drainage is placed deep to the muscle and brought out
through stab incision in skin
▪ Gauze, wool and crepe bandage is used for dressing
2. Skew flap: requires anatomical knowledge of skin blood supply
▪ Long flap joins anterior aspect 2.5 cm from tibial crest & posteriorly at
the exact opposite point on the circumference of the leg
▪ Gastrocnemius is sutured to cut end of bone to anterior tibial
periosteum with absorbable suture
Above knee amputation:
• Site must be higher if bleeding is poor on incision of skin
• Equal curved anterior and posterior flaps are made
• Skin, deep fascia and muscles are transected at same line cleanly as high as
possible, accompanying artery is ligated
• Muscles are united over bone by absorbable sutures
• Suction drain deep to the muscle brought out through skin clear of the wound
• Fascia and subcutaneous tissues are further brought together so skin can be
apposed by interrupted sutures
• Dressing with wool, gauze and crepe bandage
Through knee amputation:
• Alternative to above knee amputation if soft-tissue viability permits
• It preserves full length of femur & patella, providing a long mechanical lever
controlled by stronger muscles as the line of muscle transection is distal & occurs
through fascial tissue, as opposed to thick muscular bellies as is the case with an
above-knee amputation

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 • Bulbous amputation end allows for a self-suspending prosthetic, that is less likely to
rotate compared to an above knee amputation prosthetic
• For pts unlikely to mobilise with prosthetic e.g. elderly or bilateral amputations,
increased length of stump provides better counterweight to torso, enabling better
core stability
• Equal ant & post semicircular flaps are constructed. Ant incision carried down to tibia
& patellar tendon insertion into tibial tuberosity identified & released.
• Cruciate ligaments released from tibial insertions
• Tibial & peroneal nerves are sharply divided. Popliteal artery & vein ligated
• Hamstring muscles are sutured to posterior capsule. Residual head of gastrocnemius
sutured to the knee capsule to provide a covering of the femur & reduce synovial fluid
drainage
• Suction drain is applied to muscle bed & skin flaps closed with skin clips/ sutures

Post operative care of an amputee:

• Opiate for pain relief
• Good hygiene and care of ulcers (pressure ulcer on remaining foot delays
mobilisation)
• Exercise and mobilisation (prevent flexion deformity)
• Addition of stairs, rails, furniture for support
• Use of inflatable artificial limb (allows weight bearing to be started before temp
artificial limb is ready)
Complications:
• Early complications:
o Haemorrhage (require return to operation theatre for hemostasis)
o Hematoma (requires evacuation)
o Infection (antibiotic)
o Abscess (incision and drainage & antibiotics)
o Gas gangrene in mid thigh stump from fecal contamination
o Wound dehiscence & gangrene of flaps caused by ischemia (higher
amputation is necessary)
o DVT and PE (prophylaxis given with S/C heparin)
• Late complications:
o Infections (sinus, osteitis, sequestrum)
o Scar adhesion
o Bone spur
o Amputation neuroma
o Phantom limb (firm reassurance given that this sensation will disappear,
gabapentin or amitriptyline)
o Ulceration of stump
PERIPHERAL ANEURYSM:
Popliteal aneurysm:
• Accounts for 70% of peripheral aneurysm, usually diagnosed in males in 7th decade
• ⅔rd are bilateral cases
• ⅓rd are associated with abdominal aortic dilatation
• Clinical features: swelling behind the knee, severe ischemia
• Diagnosis: duplex (confirmatory), other investigations (CT, MRI or DSA) are
important prior to repair if foot pulses are absent
• Treatment:
o Elective repair of asymptomatic if exceeds >25 mm or if thrombi is there (to
prevent embolism)
o All symptomatic popliteal aneurysms considered for repair
o Surgery (exclusion repair) is through medial approach to ligate popliteal artery
and restore flow to foot through saphenous vein bypass graft (preferred)

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 o Alternative is posterior approach with inlay graft. Benefit: free ligation of
feeding branches as well as aneurysmectomy in cases with neurovascular
compression. It limits exposure of superficial femoral & crural arteries, only
used when popliteal aneurysm is confined to popliteal fossa
o In acute cases (thrombosed aneurysm & ischemic foot, popliteal aneurysms
rupture very rarely) surgery is often unsuccessful, Fogarty catheter & intra
arterial thrombosis, is used and limb loss rate is up to 50%
Femoral aneurysm:
• True aneurysm of femoral artery is uncommon
• Complications occur only in 3% cases
• Generally conservative management is indicated
• Half are associated with abdominal or popliteal aneurysms
• Cause of false aneurysm:
o 2% cases due to arterial surgery (tx =reanastomosis of bypass in the groin
under antibiotic cover)
o Infection (tx =excision of infected graft & insertion of a further bypass routed
around infected area)
o Femoral artery puncture & <3cm (tx =thrombin injection) if >3cm (open
surgical arterial repair with suturing of puncture site)
Iliac aneurysm:
• Associated with aortic aneurysm
• Tx: open surgery with inlay graft or endovascular repair
ARTERITIS AND VASOSPASTIC CONDITIONS:
Arteritis occurs in association with various connective tissue disorder
• SLE
• RA
• Polyarteritis nodosa
Temporal arteritis:
• Localise infiltration of inflammatory and giant cells leading to arterial occlusion of
temporal artery or sometimes ophthalmic artery
• Clinical features:
o Ischaemic headache
o Tender palpable and thrombosed vessels of scalp
o Irreversible blindness (occasionally)
o Diagnosis: temporal artery biopsy
o Treatment: steroid
Takayasu arteritis:
• Arteritis that damage major arteries arising from aortic arch
Cystic myxomatous degeneration:
• Accumulation of clear jelly (like synovial ganglion) in the outer layers of main artery
especially popliteal
• Narrowing of vessel causes claudication. Investigation of choice: Duplex scan
• Treatment:
o Decompression by removal of myxomatous material
o If ganglion recurs, excision of part of artery with interposition vein graft
Acrocyanosis:
• May be confused with Raynaud’s disease but is painless and not episodic
• Affects young women
• Mottled cyanosis of fingers and/or toes with paresthesia and chilblains
Cervical sympathectomy:
• Previously open sympathectomy was done for vasospastic condition of hand and
palmar hyperhidrosis
• This procedure is now obsolete and replaced with endoscopic transthoracic
sympathectomy

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 • Vasospastic conditions do not respond to it so endoscopic procedure is solely for
hyperhidrosis
Lumbar sympathectomy:
• For treatment of chronic lower limb ischemia
• Open sympathectomy is now obsolete
• Chemical sympathectomy requires small quantity of sclerosant into lumbar
sympathetic chain

Chap 57: venous disorders

VENOUS DISORDERS
VENOUS PATHOPHYSIOLOGY:
• Venous system contains 60% of total blood volume, average pressure: 5-10mmg Hg
• To enable blood to be returned against gravity in the standing position a pressure
gradient must exist between the veins in the leg & the chest. This gradient is created in 2
ways:
1) Increase in thoracic volume during inspiration decreases intrathoracic pressure
2) The pressure in the veins of the legs is increased by compression by the surrounding
muscles (the calf muscle pump) & to a lesser extent the tone of the venous wall
• As the calf muscles contract, veins are compressed & the valves only allow blood to
pass in the direction of the heart
• The net reduction in the pressure of the superficial system is dependent on the presence
of a pressure gradient between leg & the thorax & a patent & compliant venous system
containing competent valves
• An absence of one or more of these results in venous hypertension
• This leads to further vein wall damage including loss of compliance, thickening, dilatation
& valvular dysfunction. All this reduces the function of the affected veins, worsening
venous HTN.
• Chronic high venous & capillary pressures: soft tissues of legs will be damaged
• Factors causing venous hypertension:
1) Pressure gradient dysfunction
• Increased abdominal or thoracic pressure:
COPD, pregnancy, obesity, large tumour, constipation
• Decreased calf muscle pump function:
immobility, ankle joint fusion, paralysis
2) Dysfunction of the venous system
• Venous structural deficit:
valvular agenesis, incompetence, dilation, tortuosity, loss of vein wall
compliance, loss of venous tone, AVF
• Venous occlusion:
Agenesis, thrombosis, iatrogenic/trauma
• Venous compression:
May-Thurner syndrome, pelvic/abdominal tumor or radiotherapy
Clinical features of venous hypertension of the leg
• Varicose vein
• Telangiectasia (thread or spider veins, hyphen webs): tiny intradermal venules <1mm in
diameter
• Reticular veins: small dilated bluish sub dermal vein 1-2.9mm in diameter, usually
tortuous
• Saphena varix: a usually painless groin swelling apparent on standing

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• Corona phlebectomies (malleolar flare): fan shaped pattern of telangiectasia on
ankle/foot. Early sign of advanced venous disease
• Oedema: usually pitting. Starts distally & moves more proximally
• Eczema: itching & discomfort. Extreme cases: blistering & weeping
• Pigmentation (hemosiderosis): brownish discoloration, usually permanent. Around ankle
or close to varicose veins
• Lipodermatosclerosis: chronic inflammation & fibrosis of skin & S/C tissues, causing a
tight contracted woody leg on examination. Causes significant contracture of Achilles
tendon. Sign of severe chronic venous disease
• Atrophic blanche: localised areas of atrophic, white skin surrounded by telangiectasia &
pigmentation. Sign of severe chronic venous disease
• Venous ulcer: full thickness skin loss, usually around ankle, fails to heal spontaneously
CLASSIFICATION SYSTEM:
Clinical classification;
• C0: no sign of venous disease
• C1: telangiectasia & reticular veins
• C2: varicose veins
• C3: oedema
• C4a: pigmentation or eczema (some include malleolar flare)
• C4b: lipodermatosclerosis or atrophic blanche
• C5: healed venous ulcer
• C6: active venous ulcer
Each clinical class further divided depending on symptomatic (S) or asymptomatic (A) e.g.
C2S
Etiological classification:
• Ec: congenital
• Ep: primary
• Es: secondary (post-thrombotic)
• En: no venous cause identified
Anatomical classification:
• As: superficial veins
• Ap: perforator veins
• Ad: deep veins
• An: no venous location identified
Pathophysiological classification:
• Pr: reflux
• Po: obstruction
• Pr,o: reflux & obstruction
• Pn: no venous pathophysiology identified
VARICOSE VEINS:
Management:
i) Compression
ii) Endothermal ablation
1) Laser ablation (EVLA)
2) Radiofrequency ablation (RFA)
• Advantages in favour of EVLA over RFA include:
o EVLA can ablate any vein that can take a guidewire successfully, with low rate of
recanalization. RFA catheter does not advance through very tortuous veins
o Standard EVLA fibre used to treat perforators, a specific additional device is needed
for RFA (increased cost)
o Laser fibres are relatively inexpensive to produce
o In a catheter-based system, catheter is used to deliver targeted foam sclerotherapy
(for e.g. in areas of neovascularisation) prior to actual laser fibre being inserted

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• Advantages in favor of RFA over EVLA include:
o RFA: standardised tx protocol which is automated (minimises uncertainty, learning
curve & possibility of making a mistake with the energy delivery)
o RFA does not require continuous pullback, reducing the learning curve. This also
frees surgeon’s focus allowing better communication with patient & concurrent tx
o RFA does not require laser safety precautions
o RFA associated with a marginal reduction in pain & bruising
Endothermal ablation treats only junctional & truncal incompetence. Varicosities managed
concomitantly or sequentially with phlebectomy/sclerotherapy
iii) Non-endothermal, non-tumescent ablation
Endothermal ablation requires injection of tumescent LA solution, can be uncomfortable
for the patient. Techniques which avoid injection are being developed
1) Ultrasound guided foam sclerotherapy
o Some points are in IM
o Procedure: pt stands, sites of venous cannulation marked using U/S
o Pt supine: major venous trunks & superficial varicosities to be treated, cannulated
using U/S
o Foam is prepared. Most widely used method is of Tessari (2 syringes connected
using 3-way tap)
o A 1:3 or 1:4 mixture of sclerosant & air drawn in a syringe, then oscillated between
the 2 syringes 10 or 20 times
o Foam produced is stable for 2 mins so injected ASAP
o Leg is elevated to empty veins of blood; injection of foam starts with superficial
varicosities & end with injection of GSV or SSV
o 1 or 2ml of foam injected at a time, distribution monitored using U/S probe
o Max volume injected in single session not more than 10-12mL, incidence of
complications directly related to volume of foam injected
o Compression is then applied
o Advantages: avoids tumescent anaesthetic, so less painful, no axial or tributary
veins are too tortuous, allows treatment of calf veins with overlying skin
damage/ulceration without need to pierce through damaged skin, consumable tx
costs are very low
2) Catheter directed sclerotherapy & mechanochemical ablation
o Efficacy of sclerotherapy relies on endothelial contact with fresh undiluted
sclerosant
o So, catheter delivered sclerotherapy used rather than trying to milk sclerosant
down the vein lumen
o Mechanicochemical ablation: a tx device deploys an angled wire from the end
which attaches to a motorised handle
o Catheter placed in vein lumen, trigger on handle is depressed, spinning wire
around & liquid sclerosant infiltrated via catheter as catheter is being withdrawn
o Spinning wire causes physical damage to endothelium, allowing deeper
penetration of sclerosant into vein wall
o Some pts find it uncomfortable, as device can snag on vein, tearing or rarely
stripping it
o Treating longer veins difficult due to limitations in catheter length & safe dose of
sclerosant
3) Endovenous glue
o Endoluminal application of cyanoacrylate glue
o Involves treatment catheter placed in vein lumen
o A handle is used to infiltrate adhesive via catheters
o Vein is compressed, sealing the lumen closed
surgical interventions (comparison of interventions):
• Endovenous and traditional surgeries appear equally beneficial

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 • In early post op period traditional surgery is associated with higher pain score and
analgesic requirement and more severe disability
• Endovenous intervention minimise post op impairment result in more rapid return to
work
Recurrent varicose veins:
• 10-20% patient presenting with varicose veins have had previous interventions
• Recurrence rate
o Significant cases = 10-35%
o Minor duplex detected cases = 70%
• Causes of recurrence:
o Neo-revascularisation
o Reflux in residual axial vein
o Inadequate initial surgery
o New junctional reflux
o More common in SSV than LSV in patient with high BMI
o Stripping of incompetent axial vein reduces recurrence
o Surgery has more recurrence than endovascular approach
• Surgery with recurrent varicose vein is associated with high (40%) complication rates i.e
lymph leak and wound infection thus endovascular approach is a better alternative
Pelvic congestion syndrome:
• PCS is considered among DDs in females presenting with chronic pelvic pain
• Risk:
o Premenopausal (20-45 years of age)
o Young multiparous women
• Clinical features:
o Severe dull aching pelvic pain (due to ovarian & pelvic varicosities)
o Noncyclical pain precipitated by prolong standing
o Dysmenorrhoea
o Menorrhagia
o Rectal discomfort or urinary frequency
o Tenderness over uterus or ovarian or vulval varicosities and haemorrhoids
o Vulval or thigh varicosities
• Diagnosis:
o Abdominal, pelvic, transvaginal duplex scan (initial investigation of choice)
o MR venography or diagnostic venography (more sensitive)
• Medical treatment:
o Psychotherapy
o Progestin
o Danazol
o GnRH and HRT
o NSAID
o Percutaneous pelvic vein embolization has replaced surgical extraperitoneal
resection of ovarian veins
CONGENITAL VENOUS ANOMALIES:
there are 4 types of anomalies:
• Aplasia: most commonly seen in IVC and has similar presentation to post thrombotic limb
o May Thurner cockett syndrome: membranous occlusion of left common iliac vein
often develop where vein passes through the right common iliac artery (iliac vein
compression syndrome). This lead to iliac vein thrombosis
o Commonly affects left iliac and external iliac vein
o Membranes may also narrow the hepatic veins leading to Budd-Chiari syndrome
• Hypoplasia: narrowing of vein
• Duplication: common in vena cava, femoral vein and renal veins found incidentally
• Persistence of vestigial vessels
Klippel Trenaunay syndrome:

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 • This is combined anomaly of cutaneous naevus, persistent vestigial veins with
varicose veins and soft tissue and bone hypertrophy
• Mesodermal abnormality that is not familial
• Segments of deep veins are hypoplastic or aplastic with associated lymphatic
obstruction
• Condition must be differentiated from Parkes Weber syndrome which has multiple
AVF causing venous HTN, ulceration and high output cardiac failure
• Treatment:
o Elastic compression hosiery (treatment for all patients)
o Laser ablation of naevus
o Stapling of bones to avoid leg length discrepancy
o Occasionally removal of superficial varicose veins, provided deep veins are
patent
o LMWH to prevent DVT
ENTRAPMENT OF VEINS:
• most commonly compressed veins:
o Axillary vein: compressed at thoracic outlet between the first rib and clavicle
resulting in axillary vein thrombosis
o Popliteal vein: due to abnormal insertion of gastrocnemius muscle
• Causes discomfort & swelling of limb during exercise before development of
thrombosis
• Treatment: surgical decompression, excising first rib or dividing abnormal
musculature of gastrocnemius insertion
Axillary vein thrombosis (Paget-Schrotter disease):
• Cause: excessive exercise in patient with anatomically abnormal thoracic outlet OR
associated with excessive muscle bulk in weightlifters
• Vein may be compressed by cervical rib if present
• Clinical finding: painful swollen arm
• Treatment:
o Thrombolysis: to remove thrombus
o Vein is imaged to see if compression on elevation of arm. If so, surgical
resection of first rib or cervical rib
VENOUS INJURY:
• Blunt or penetrating trauma damages small and medium sized vessels which can be
ignored or ligated
• Large vessels if damaged should be repaired to reduce morbidity and limb loss
• Many venous injuries remain undiagnosed at the time of injury (e.g. crural vein
damage with tibial fracture) later presents with post thrombotic complications
• 40-50% arterial injuries are associated with venous injuries especially in popliteal
fossa
Classification (Mechanism):
1. Incision
2. Laceration
3. Transection
4. Avulsion
5. Catheter insertion and puncture causing iatrogenic injuries
Complications:
• Thrombosis
• Hemorrhage leading to shock and death (IVC)
• Embolization
• AVF due to penetrating trauma
Clinical findings: hematoma, cyanosis and swelling
Investigations:
• Rarely required. Usually rapid exploration is needed in unstable pelvic fractures with
external fixation improving outcome

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Treatment:
• ABC
• Venous injuries can cause massive bleeding, & pts require circulatory support
• Venous pressures are low & so where access to site of injury, pressure will control
bleeding & in most cases is the definitive management
• Where pressure cannot be applied or when loss of venous function threatens life or
limb intervention is needed
• Interventions: reduction & stabilisation of fracture (e.g. Pelvis) endovenous
embolisation, stent grafting
• Wound exploration with lateral sutures and vein patches are ideal methods of repair
• Autogenous vein replacement (from LSV or IJV) or artificial PTFE (risk of infection) is
used
• Fasciotomy is considered for concomitant arterial or venous injuries
• Contaminated wounds: tetanus toxoid and antibiotics are given
Prognosis:
• Repair has 70-80% success rate
VENOUS TUMOURS:
• cystic degeneration of vein wall is an uncommon cause of venous occlusion detected
by ultrasound
• Treatment is deroofing or excision of venous segment
Venous malformation cavernous angioma/haemangioma:
• Malformation is common affecting skin but also extending into deep tissues including
bones and joints
• Present with variable dilated and swollen veins beneath skin. Sometimes only
complain: pain
• Hemorrhage and thrombophlebitis may exacerbate the pain
• Soft compression mass is present beneath skin
• Dark blue tinge appears even if malformation deeply situated
• Nodules within mass represent previous episodes of thrombosis
• Size and extent of haemangioma are best visualised by nuclear magnetic resonance
with a short tau inversion recovery (STIR) sequence or CT scan with contrast
• Venography rarely show abnormality
• Treatment: surgical excision is rarely done as then embolisation & sclerotherapy is
difficult
Leiomyomas and leiomyosarcoma of vein wall:
• Extremely rare tumours that are slow growing
• Clinical features:
o Pain
o Mass with signs of venous obstruction i.e. edema and veins distended
• Investigations: duplex, CT and MRI show filling defect in vein wall
• Treatment: resection with replacement by autogenous vein
• If tumour affects vena cava resection with replaced prosthetic graft is used
Cystic degeneration:

• Cystic degeneration of vein wall is an uncommon cause of vein occlusion

• Detected by ultrasound
• Cyst is deroofed or venous segment is excised

Chap 58: lymphatic disorders

LYMPHATIC DISORDERS

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ANATOMY AND PHYSIOLOGY OF LYMPHATIC SYSTEM:
Functions:
• Principle function of lymphatics is to return protein rich fluid to the circulation through
lymphaticovenous junctions in the jugular area
• Water, electrolytes, low molecular weight moieties (polypeptides, cytokines, GF) and
macromolecules (fibrinogen, albumin, globulin, fibrinolytic and coagulation factors)
from interstitial fluid return to circulation via lymphatics
• Intestinal lymph (chyle) transports cholesterol and long chain fatty acids and fat-
soluble vitamins directly to the circulation bypassing the liver
• Lymphocytes and immune cells are also transported
Development and macro-anatomy:
• In human embryo lymph sac develops at 6-7 week of gestation as 4 cystic spaces, 1
on either side of neck and one in groin
• These cisterns enlarges and allow lower limb and abdomen to drain via cisterna chyli
into thoracic duct that drains into left IJV at the confluence with left sub-clavian vein
• Head and right arm drains via right lymphatic duct into right IJV
• Lymphatics accompany veins everywhere except CNS and cortical bones whereas
brain has CSF and retina has aqueous humor instead
• Lymphatic system comprises of following components:
o Lymphatic channels
o Lymphoid organs (lymph nodes, spleen, Peyer’s patches, thymus, tonsils)
o Circulating elements (lymphocytes and mononuclear immune cells)
• Lymphatic endothelium is derived from embryonic vein in jugular or peri mesonephric
areas (prox1 and VEGF-C are essential for development)
Microanatomy and physiology:
1) LYMPHATIC CAPILLARIES: Lymphatics originate from ISF space from specialised
endothelial capillaries (initial lymphatics) or non endothelial channels such as space of
Disse in liver. Unlike arteriovenous capillaries in that:
• They are blind ended
• They are much larger (50 micrometer)
• Allow the entry of molecules up to 1000kDa as BM is fenestrated, tenuous or absent
• Anchored to interstitial matrix by filaments. In resting state, they are collapsed
2) TERMINAL LYMPHATICS: Initial lymphatics drain into terminal collecting lymphatics that
possess bicuspid valves and endothelial cells rich in contractile protein actin
• larger lymphatics are surrounded by smooth muscles
• valve partition the lymphatics into segments (lymphangions)
3) LYMPH TRUNK: terminal lymphatics lead to lymph trunk which has single layer of
endothelial cells lying over basement membrane with media comprising of smooth
muscles innervated by sympathetic, parasympathetic and sensory nerve endings
• 10% lymph from limb is drained into deep lymphatic trunks along neurovascular
bundles
• Majority is conducted against venous flow from deep to sup in epifascial lymph trunks
4) STARLING’S FORCES: the distribution of protein and fluid between vascular system and
ISF depends on hydrostatic and oncotic pressure between two compartments together
with blood capillary membrane being impermeable to molecules larger than 70kDa
5) TRANSPORT OF PARTICLES: particles enter the initial lymphatics through
interendothelial openings and vesicular transport through interendothelial pores
• Large particles are actively phagocytosed by macrophages and transported through
lymphatic system intracellularly
6) MECHANISM OF LYMPH TRANSPORT: Resting interstitial pressure is (-2 to -6 mm of
water) but lymphatic pressure is positive showing that lymph flow against a pressure
gradient. This flow depends on following mechanisms:
• Transient increase in interstitial pressure secondary to muscular contractions and
external compressions
• Sequential contraction and relaxation of lymphangions

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 o Contractility is enhanced by noradrenaline, serotonin, prostaglandins,
thromboxanes and endothelin 1
o Pressure up to 50 mm hg is recorded in normal lymph trunk and 200 mmHg in
severe lymphedema
• Prevention of reflux due to valves
• Lymphatics modulate their own contractility through production of NO
• Transport in right thoracic and left lymphatic ducts also depends upon intrathoracic
(respiration) and central venous (cardiac cycle) pressure. So cardiorespiratory
disease has an adverse effect on lymphatic function
ACUTE INFLAMMATION OF LYMPHATICS:
• Acute lymphangitis is an infection caused by staph aureus and streptococcus
pyogenes
• It spread to lymph nodes (lymphadenitis) forming an abscess later
• May progress to septicaemia and bacteraemia
• Clinical features: rubor, calor, dolor and red streak beneath skin along the line of
inflamed lymphatics
• Management:
o Resting the inflamed part (to reduce lymphatic drainage)
o Elevation to reduce swelling
o IV antibiotics
• Failure of treatment after 48 hours of antibiotic indicates:
o Inappropriate antibiotic treatment
o Undrained pus
o Malignancies or immunodeficiency
• Leads to recurrent attacks of infection and lymphedema. Pts with lymphedema prone
to acute inflammatory episodes
LYMPHANGIOMA:
• Dilated dermal lymphatics that blister onto the skin surface
• Fluid is usually clear but may be blood stained
• Long term complications: thrombosis and fibrosis forming hard nodules
• Lymphangioma circumscriptum: lymphangioma <5 cm
• Lymphangioma diffusum: lymphangioma <5 cm but are widespread throughout the
body
• Lymphedema ab igne: lymphangioma forming reticulate pattern of ridges
• Lymphangiomas frequently weep (lymphorrhoea, chylorrhoea) causing skin
maceration and portal of infection
• Lymphangiectasia: protein losing diarrhea, chylous ascites, chylothorax, chyluria and
discharge from lymphangioma
CHYLOUS ASCITES AND CHYLOTHORAX:
• It is associated with mega lymphatics
• Diagnosis is obvious if accompanied with lymphedema and lymphangioma
• Some people develop chylous ascites or chylothorax in isolation, in such cases
diagnosis is made with aspiration and identification of chylomicrons in aspirate
• Further investigations:
o Cytology for malignant cells
o CT for lymph nodes enlargement
o CT with guided biopsy
o Laparoscopy or laparotomy for lymphoma or malignancies
o Lymphangiography may show site of fistula and help in surgical ligation
• Treatment:
o Surgical correction
o Control of leakage at laparotomy or remove segment of affected bowel, even
if no localised lesion is found
o Peritoneal venous shunt in cases of diffuse disease not corrected with
surgery

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 o Medical treatment:
▪ Avoidance of fat in diet
▪ Medium chain fatty acids given to reduce swelling (they are absorbed
directly into blood rather than via lymphatics)
o Chylothorax is best treated with pleurodesis (may lead to death from lymph
clogged lungs as excess lymph has nowhere to drain)
CHYLURIA:
• Filariasis is the most common cause of chyluria occurring in 1-2% cases after 10-20
years of initial infestation
• Other aetiologies: ascariasis, malaria, tumour, tuberculosis
• Clinical features:
o Painless passage of white urine
o Particularly after fatty meal
o Renal colic and hypoproteinemia due to clotting of chyle
• Investigations: IV urography and lymphangiography shows lymphourinary fistula
• Treatment: low fat & high protein diet, increased oral fluids to prevent clotting,
laparotomy & ligation of dilated lymphatics
LYMPHOCELE:
• Localised collection of lymph without distinct epithelial lining
• Cause: leakage of lymph into soft tissues or body cavities secondary to surgical
disruption of lymphatic vessels (postoperative complication after groin lymph node
dissection, radical prostatectomy, vascular reconstructive tumors, renal transplant &
body contouring surgery after massive weight loss)
• Clinical signs: non-tender, non-pulsatile mobile lump, differentiated from seroma or
localised postoperative edema by presence of lymph rich fluid
• Can deform adjacent soft tissues or cause pressure symptoms
• Complications: infection, chronic drainage, (lymph fistula) & prolonged morbidity
• Treatment: i) early stage- repeated needle aspiration & compression.
ii) insertion of drainage catheters, packing/compression or surgical excision
iii) surgery: pre-operative lymphoscintigraphy with on-table isosulfan blue dye
injection
after resecting a large lymphocele, residual dead space needs muscle transposition
to reduce recurrence

SECONDARY LYMPHOEDEMA:
Filariasis:
• Most common cause of lymphedema worldwide, caused by viviparous nematode
Wucheria bancrofti whose only host is man and is spread by mosquito
• Disease is associated with poor sanitation
• Pathogenesis: enter through blood in lymphatics & resides in lymph nodes and cause
obstruction and damage to lymph drainage
• Proximal lymphatics become grossly dilated with adult parasites
• Elephantiasis: massive degree of edema when occurs
• Clinical features:
o Acute:
▪ Fever
▪ Headache
▪ Malaise
▪ Inguinal and axillary lymphadenitis
▪ Lymphangitis
▪ Cellulitis, abscess formation and ulceration
▪ Funiculo epididymo-orchitis
o Chronic:
▪ Lymphedema of leg (arm, breast)

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 ▪ Hydrocoele
▪ Abdominal lymphatic varices (chyluria, lymphuria)
• Investigations:
o Immature parasites (microfilariae) enter the blood at night & can be identified
on a blood smear, centrifuged specimen of urine or in lymph itself
o Complement fixation is positive in past and present infection
o Eosinophilia
• Treatment:
o Diethylcarbamazine destroys parasites but does not reverse lymphatic
changes
o Once infection is clear then treatment is as for primary lymphedema
o Prevention=reduce mosquitoes, protective clothing and netting is used
Endemic Elephantiasis (podoconiosis):
• Common in tropics and affects more than 500000 people in Africa.
• The barefoot cultivation of soil composed of volcanic rock leads to destruction of
peripheral lymphatics by particles of silica which can be seen in macrophages in
draining lymph nodes
• Plantar edema develops in childhood and rapidly spreads proximally
• Condition is prevented and its spread is slowed by wearing of shoes
Bacterial infection:
• Lymphangitis and lymphadenitis causes lymphatic destruction which leads to
lymphoedema further causing acute inflammatory episode
• Lymphangiography may reveal abnormalities in contralateral unaffected limb showing
underlying inherited susceptibility
• TB infection is common in developing countries, causes lymphatic & lymph node
destruction→lymphedema
Malignancies:
• Treatment (surgery and radiotherapy) of breast carcinoma is leading cause of
lymphedema in developed countries (decreasing as surgery becoming conservative)
• Other causes: lymphoma, Kaposi’s sarcoma in HIV
Trauma:
• Etiology is multifactorial and includes disuse, venous thrombosis, lymphatic injury or
destruction; degloving injuries and burns disrupt dermal lymphatics
• Tenosynovitis is associated with localised subcutaneous lymphoedema
Chronic venous insufficiency:
• CVI and lymphedema commonly coexist in same patient
• Both SVT and DVT lead to lymphatic destruction and secondary lymphedema
• Lymphedema contributes to swelling in post thrombotic syndrome
• Lymphedema can also cause DVT & SVT through immobility & acute inflammation
• Duplex ultrasound and plethysmography both are abnormal in patients with
lymphedema
Miscellaneous conditions:
• Rheumatoid and psoriatic arthritis (chronic inflammation & lymph node fibrosis)
• Contact dermatitis
• Snake and insect bites
• Retroperitoneal fibrosis
• Pretibial myxoedema is due to obliteration of initial lymphatics by mucin
Conditions that mimic lymphedema:
1. Factitious lymphoedema: this is caused by application of tourniquet (a ‘rut’ & sharp
cut off seen) or hysterical disuse in patient with psychological and psychiatric
problems
2. Immobility: generalized or localized immobility can lead to chronic limb swelling e.g.
in elderly, hemiplegic stroke patient, young pt with multiple sclerosis
3. Lipoedema: exclusively in women due to abnormal deposition of fat. Bilateral
symmetrical enlargement of legs & sometimes lower half of body.

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DIFFERENTIAL DIAGNOSIS OF SWOLLEN LIMB:
Nonvascular or lymphatic causes:

General disease state • Cardiac failure

• Liver failure
• Hypoproteinemia
• Hypothyroidism (myxedema)
• Angioedema (allergic disorders)

Local disease process • Ruptured baker’s cyst

• Arthritis
• Hemarthrosis
• Calf muscle hematoma
• Achilles tendon rupture

Retroperitoneal fibrosis and • Arterial, venous and lymphatic abnormalities

gigantism

Drug • Corticosteroid
• Estrogen
• Progesterone
• MOA inhibitors

Obesity • Lipodystrophy
• Lipoidosis

Trauma • Painful swelling due to reflux sympathetic

dystrophy
Venous

DVT • Classical sign of pain and redness are absent

Post thrombotic syndrome • Swelling, venous skin changes

• Venous claudication

Varicose vein • Rare cause of limb swelling

Klippel Trenaunay syndrome • Rare cause

External venous compression • Pelvic or abdominal tumour

• Retroperitoneal fibrosis

Ischemia reperfusion • Following revascularisation

Arterial:

Arteriovenous malformation • Local or generalised swelling

Aneurysm • Femoral
• Popliteal
• Iatrogenic leading to false aneurysm

MANAGEMENT OF LYMPHOEDEMA:
4. Skin care:

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1. Protect hands when washing up or gardening; wear a thimble when sewing
2. Never walk barefoot & wear protective footwear outside
3. Use an electrical razor to depilate
4. Never let skin become macerated
5. Treat cuts & grazes promptly (wash, dry, antiseptic & plaster)
6. Use insect repellent sprays & treat bites promptly with antiseptics & antihistamine
7. Do not allow blood to be taken from, or injections given into affected arm (and avoid
bp measurement)
8. Protect affected skin from sun (shade, high factor sunblock)
9. Take antibiotics if going on holiday
10. Wash daily with use of bath oil e.g. balneum and carefully dried with low heat hair
drier
11. If skin is in a good condition: daily application of a bland emollient e.g. aqueous
cream to keep skin hydrated
12. If skin is dry and flaky: apply bland ointment e.g. 50:50 white soft paraffin /liquid
paraffin (WSP/LP) twice daily
13. If there is marked hyperkeratosis: keratolytic e.g. 5% salicylic acid is added to
WSP/LP
14. Commercially available soaps, creams & lotions e.g. Lanolin E45 is best avoided in
patient with lymphoedema as they are susceptible to contact dermatitis (eczema)
15. Fungal infection occurs commonly but chronic use of antifungal leads to maceration
and its better to use powder in shoes or socks
16. Athletes foot is prevented by ointment containing 3% benzoic acid (can be used for
a long time)
17. Lymphorrhoea: managed with emollients, elevation, compression or cautery under
anesthesia
18. Acute inflammatory episode: rapid onset of severe complication that requires
hospital admission
1. Tingling, pain, redness occur suddenly. Fever, rigors, headache,
vomiting & delirium
2. Etiology: group A beta hemolytic strep or staphylococci
3. D/ds: DVT, dermatitis, thrombophlebitis
4. Treatment:
1. Amoxycillin is treatment of choice with erythromycin or clarithromycin in those
with penicillin allergy
2. Flucloxacillin for staph aureus (folliculitis, crusted dermatitis)
3. Oral clindamycin is 2nd line agent given if 1st line treatment fails
4. Hospital admission for patients having signs of septicaemia, deterioration of
condition after 48 hours of antibiotic therapy
1. IV amoxycillin or benzylpenicillin is given with
clindamycin in penicillin allergy
2. Bed rest to reduce lymphatic drainage and spread of
infection
3. Elevation to reduce edema
4. Heparin prophylaxis to reduce risk of DVT
5. Analgesia is given but NSAIDs avoided as they lead to
necrotising fasciitis
6. Any lymphatic massage is stopped during active
infection
5. Prevention:
1. Penicillin V 500 mg daily for those having 2 or more attacks per year
2. Physical therapy and skin care
5. Manual lymphatic drainage:

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 1. Aim: evacuate fluid and proteins from interstitial space and stimulate lymphangion
contraction with decongestion of impaired lymphatic pathway and development of
collateral routes
2. Therapist should perform MLD daily
3. Train patient to perform simple massage for lymphatic drainage termed as simple
lymphatic drainage (SLD)
4. In intensive phase SLD supplements MLD while in maintenance phase SLD is
sufficient
6. Multilayer lymphedema bandaging and compression garments:
1. Elastic bandage that provide compression produce a sustained high resting
pressure and ‘follow in’ as limb swelling reduces but do not change with movement
and posture
2. Short stretch bandages exert support through production of semi rigid casing where
the resting pressure is low but changes in response to movement and posture. This
produces massaging effect within limb & stimulates lymph flow
3. Pressure provided must be graduated:
6. Ankle or foot = 100%
7. Knee = 70%
8. Mid thigh = 50%
9. Groin = 40%
o Non-invasive assessment of ABPI using hand held doppler prior to
compression therapy is done as it is rarely possible to feel pulses in
lymphoedema
o Standard MLLB is commenced in patient with ABPI ≥ 0.8
o Modified techniques with lower pressures in moderate arterial disease: APBI
0.5-0.8
o MLLB is contraindicated in severe arterial insufficiency (ABPI < 0.5),
uncontrolled heart failure and severe peripheral neuropathy
o MLLB:
i) Severe swelling = non elastic MLLB is preferred
ii) Mild cases and maintenance phase = compression (hosiery, sleeves)
o Compression garments are mainstay of management in most of the clinics. It
is extremely labour intensive, changed daily. To control lymphedema requires
higher pressure than CVI:
1. Arm = 30-40 mmHg
2. Leg = 40-60 mmHg
o Patient should put stocking as first thing in the morning before rising
o British classification:
i) Class I = 14-17 mmHg
ii) Class II = 18-24 mmHg
iii) Class III = 25-35 mmHg
o International classification:
i) I= 20-30 mmHg
ii) II= 30-40 mmHg
iii) III= 40-50 mmHg
iv) IV= 50-60 mmHg
o Effects of MLLB:
i) Reduces edema
ii) Restores shape of affected area
iii) Reduces skin changes (hyperkeratosis and papillomatosis)
iv) Eliminates lymphorrhoea
v) Supports inelastic skin
vi) Softens subcutaneous tissue
Difficult to persuade pts to comply, as putting stockings on/off is difficult and very
uncomfortable to wear in warm climates.

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 7. Exercise:
1. Lymph formation is directly proportional to arterial inflow and 40 % of lymph is
formed within skeletal muscle
2. Vigorous exercise (anaerobic and isometric) increases lymphedema. Patients
advised to avoid prolonged static activities for e.g. carrying heavy shopping bags/
prolonged standing
3. Slow, rhythmic isotonic movements e.g. swimming and massage will increase
venous and lymphatic return through the production of movement between skin &
underlying tissues (essential to filling of initial lymphatics) & augmentation of muscle
pumps
4. Exercise also helps to maintain joint mobility
5. Pts unable to move their limbs: passive exercise
6. Elevation of limb at night to reduce swelling
7. Pillow under mattress or blocks under bottom of bed encourages swelling to go
down
9.Surgery:
1. Bypass procedures:
2. Indication: rare case of patient having proximal ilioinguinal lymphatic
obstruction and normal distal lymphatics have benefit from bypass
3. Methods used:
1. Skin bridge (gillies)
2. Anastomosing lymph nodes to veins (Neilubowicz)
3. Ileal mucosal patch (Kinmonth)
4. Lymphaticovenular anastomosis (LVA) most recent one carried out on
vessels of 0.3-0.8 mm of diameter using super microsurgical technique. (Good
outcome with earlier stage treatment)
These procedures more often attempted in UL after lymph node resection or
radiotherapy after breast cancer.
2. Liposuction:
i. Treatment of choice in chronic lymphedema
ii. Reserved for patients who have progressed to non pitting edema
iii. Appears to be safe
3) Limb reduction procedures: are considered when limb is so swollen, it interferes
with mobility and livelihood. Not cosmetic: do not create normally shaped leg,
associated with significant scarring

extre

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