Surgery PG University Answers (10 Marks Each)

1. Graft vs Host Reaction (Graft-versus-Host Disease)

Definition

Pathophysiology - The "Three-Step Model"

1. Host tissue damage - The conditioning regimen (chemotherapy/radiotherapy) damages host tissues, releasing danger signals (DAMPs, PAMPs) and pro-inflammatory cytokines (TNF-α, IL-1, IL-6) - the "cytokine storm."
2. Donor T-cell activation - Donor T cells recognize host alloantigens presented by host or donor antigen-presenting cells (APCs) via direct or indirect allorecognition.
3. Effector phase - Activated donor cytotoxic T cells (CTL), NK cells, and macrophages attack host organs, causing tissue injury.

Classification

Organs Affected - Acute GVHD (Clinical Manifestations)

1. Skin - Most common (80% of cases). Erythematous/dusky macules and papules starting on palms, soles, and ears; morbilliform exanthem; perifollicular erythema. In severe cases: bullae, skin sloughing resembling toxic epidermal necrolysis (TEN).
2. Liver - Cholestatic jaundice, elevated bilirubin and alkaline phosphatase; sinusoidal endothelial damage.
3. Gastrointestinal tract - Nausea, vomiting, profuse watery/bloody diarrhea (can be >2L/day), abdominal pain, ileus.
4. Lung (less common) - Bronchiolitis obliterans.

Grading of Acute GVHD (Glucksberg/International Bone Marrow Transplant Registry Criteria)

• Grade I - Mild skin only (rash <25% BSA)
• Grade II - Moderate skin + mild gut/liver
• Grade III - Severe multi-organ
• Grade IV - Life-threatening; generalized erythroderma + severe gut/liver involvement

Chronic GVHD

Risk Factors

• HLA mismatch (donor-recipient)
• Unrelated donor (vs. sibling)
• Older patient age
• Female donor to male recipient (minor histocompatibility Y antigen)
• High-intensity conditioning regimen
• T-cell replete graft

Treatment

• Prophylaxis - Calcineurin inhibitors (cyclosporine/tacrolimus) + methotrexate; T-cell depletion of graft
• Acute GVHD - First-line: systemic corticosteroids (methylprednisolone 2mg/kg/day); steroid-refractory cases: ruxolitinib (JAK1/2 inhibitor, FDA approved), extracorporeal photopheresis (ECP), mycophenolate mofetil
• Chronic GVHD - Prednisone ± cyclosporine; ibrutinib; ECP; hydroxychloroquine for mild disease; belumosudil (ROCK2 inhibitor)

2. Hemangioma

Definition

Classification

• Absent or present as precursor lesion (flat red mark) at birth
• Appears 2 weeks to 2 months after birth
• Female:male ratio 3-4:1; more common in preterm infants and Caucasians
• Most common extracutaneous site: liver

• Fully formed at birth
• Subtypes:
  • RICH - Rapidly Involuting Congenital Hemangioma (involutes in 12-14 months)
  • NICH - Non-Involuting Congenital Hemangioma
  • PICH - Partially Involuting Congenital Hemangioma

• Capillary (most common in GI tract)
• Cavernous (large dilated vascular spaces)
• Mixed

Natural History of Infantile Hemangioma - Three Phases

1. Proliferative phase (birth to 9-12 months) - Rapid growth; bright red, tense cutaneous lesions; subcutaneous lesions appear as deep bluish-purple masses
2. Plateau phase
3. Involution phase - Slow spontaneous regression, usually complete by age 4 years; fibrous septa thicken, endothelial cells replaced by adipocytes

Clinical Features

• Superficial (capillary/strawberry) - Bright red, raised, lobulated; most common on head and neck
• Deep (cavernous) - Soft, compressible, bluish subcutaneous swelling
• Mixed - Combined features

Complications and High-Risk Lesions Requiring Intervention

Investigations

• Clinical diagnosis in most cases
• Doppler ultrasound - Imaging modality of choice; shows high-flow vascular lesion
• MRI - For uncertain cases, deep lesions, or suspected spinal involvement
• CT scan - For visceral lesions

Treatment

• Observation - Most involute spontaneously; majority managed conservatively
• Propranolol (oral) - First-line systemic treatment for complicated/high-risk IH; nonselective beta-blocker causing rapid involution during proliferative phase; multiple RCTs confirm efficacy (Hemangeol approved by FDA)
• Timolol (topical) - For small, superficial lesions
• Corticosteroids - Second-line (systemic or intralesional)
• Interferon-α - Reserved for steroid-resistant, vision-threatening cases
• Laser therapy - Pulsed-dye laser for superficial residual telangiectasias
• Surgical excision - For non-regressing lesions, significant residual fibrofatty tissue, or redundant skin after involution
• Sclerotherapy - For localized deep lesions
• GI/rectal cavernous hemangioma - Small lesions: endoscopic ablation; large/multiple: surgical resection; massive rectal bleeding: may ultimately require proctectomy

3. Role of Colour Doppler in Surgical Conditions

Principle

Key Roles in Surgery

A. Deep Vein Thrombosis (DVT) - Detection and Follow-up

• CDU is the gold standard and first-line investigation for DVT.
• Criteria for DVT on Duplex/Color Doppler:
  • Non-compressibility of the vein (primary criterion) - failure of the vein wall to collapse with probe pressure indicates intraluminal thrombus
  • Absence of color fill (no flow signal) in the vein
  • Absent augmentation of flow on distal compression
  • Loss of phasic flow variation with respiration
• Sensitivity/specificity for proximal DVT: 97%/94%
• Sensitivity for calf vein thrombosis exceeds 90% with color Doppler
• A continuous femoral flow pattern on one side vs. phasic on the other suggests ipsilateral iliac vein obstruction
• Bilateral pulsatile common femoral waveforms suggest tricuspid regurgitation or heart failure
• CDU avoids radiation and contrast, unlike venography

B. Peripheral Arterial Disease (PAD) / Arterial Occlusive Disease

• Detects stenosis or occlusion of lower limb arteries
• Duplex Doppler evaluates waveform morphology (triphasic → biphasic → monophasic with increasing stenosis) and peak systolic velocity
• Resistive Index (RI) = (PSV - EDV) / PSV - assesses peripheral vascular resistance
• Pre-operative mapping before bypass surgery or angioplasty
• Assessment of bypass graft patency (arterial and venous grafts)
• Guides decision for surgical vs. endovascular intervention

C. Carotid Artery Disease

• Screening for carotid artery stenosis in patients with TIA/stroke
• Characterizes plaque morphology (echogenicity), surface, and calcification
• Measures degree of stenosis by peak systolic velocity (PSV >125 cm/s suggests >50% stenosis; >230 cm/s suggests >70% stenosis)
• Pre-operative assessment before carotid endarterectomy (CEA)
• Post-operative surveillance after CEA or carotid stenting

D. Thyroid Surgery

• Pre-operative evaluation of thyroid nodules; "thyroid inferno" (markedly increased vascularity) is characteristic of Graves disease
• In thyroiditis (subacute), decreased color Doppler flow during the toxic phase distinguishes it from Graves disease
• Identifies parathyroid adenomas - peripheral blood supply pattern on color Doppler (vs. lymph nodes which show hilar flow)
• Pre-operative mapping of feeding vessels before thyroid/parathyroid surgery

E. Varicose Veins and Venous Insufficiency

• Identifies sites of saphenofemoral junction (SFJ) incompetence and perforator incompetence
• Detects retrograde flow (reflux) with Valsalva or Trendelenburg maneuver
• Pre-operative mapping of venous anatomy before endovenous laser therapy (EVLT) or surgery (Trendelenburg procedure, stripping, phlebectomy)
• Assessment of short saphenous vein incompetence

F. Renal Vascular Assessment

• Evaluation of renal artery stenosis (RAS): PSV >180-200 cm/s or renal-to-aortic ratio >3.5
• Post-renal transplant: Doppler assessment of transplant renal artery (stenosis, thrombosis), renal vein thrombosis, and parenchymal RI (normal <0.70; elevated RI suggests rejection, obstruction, ATN)
• Resistive index used to monitor graft function

G. Abdominal Aortic Aneurysm (AAA)

• Assesses aortic lumen, mural thrombus, and flow dynamics
• Post-endovascular aneurysm repair (EVAR): surveillance for endoleaks (type II endoleak: color Doppler shows flow within aneurysm sac from collateral vessels)

H. Portal Hypertension and Liver

• Assesses portal vein patency and direction of flow (hepatopetal vs. hepatofugal)
• Detects spontaneous portosystemic shunts (splenorenal, paraumbilical)
• Hepatic artery Doppler post-liver transplantation (hepatic artery thrombosis is an emergency requiring prompt surgical re-exploration)

I. Hemangioma and Vascular Tumors

• High-flow pattern in hemangiomas helps distinguish from lymphatic malformations (low or no flow)
• Imaging modality of choice for infantile hemangiomas

Summary Table

4. Spina Bifida

Definition

Aetiology and Risk Factors

• Folic acid deficiency during early pregnancy (most important preventable cause)
• Genetic predisposition (family history, chromosomal anomalies)
• Valproic acid / carbamazepine use in pregnancy
• Maternal diabetes, hyperthermia
• Recurrence risk after one affected child: ~3-5%

Antenatal Diagnosis

• Maternal serum alpha-fetoprotein (MSAFP) - Elevated (open NTDs leak AFP into amniotic fluid and then maternal serum)
• Amniotic fluid AFP + acetylcholinesterase - Confirmatory
• Antenatal ultrasound - "Lemon sign" (frontal scalloping of skull), "Banana sign" (cerebellar herniation - Arnold-Chiari II malformation), absence of normal posterior fossa structures, visible spinal defect

Classification and Clinical Features

• Bony defect only (posterior vertebral arch fails to fuse) without herniation of meninges or cord
• Skin over the defect is intact and normal
• May have overlying skin markers: tuft of hair, hemangioma, lipoma, dermoid, dermal sinus, or skin dimple - usually in the sacral region
• Often asymptomatic; discovered incidentally on X-ray
• Tethered cord syndrome may develop with progressive neurological deficits

• Herniation of meninges and CSF only through bony defect - no neural tissue in the sac
• Covered by skin or membrane
• Usually presents as a fluctuant midline swelling that transilluminates
• Neurological function generally preserved
• Treatment: surgical closure is indicated

• Most severe open form; accounts for ~90% of symptomatic cases
• Herniation of meninges, CSF, AND neural tissue (spinal cord/nerve roots) through the defect
• Exposed neural tissue (neural placode) visible centrally
• Associated deficits BELOW the level of the lesion:
  • Flaccid paralysis of lower limbs
  • Sensory loss
  • Anal sphincter dysfunction (fecal incontinence)
  • Urinary sphincter dysfunction (neurogenic bladder - dribbling incontinence, UTIs, reflux nephropathy)
• Arnold-Chiari II malformation - Hindbrain herniation through foramen magnum → present in nearly all cases → hydrocephalus (80-90%)
• Most common site: lumbar (L2-L5) and lumbosacral region

• Skin-covered lesion with fatty (lipomatous) tissue tethering the cord
• Associated with tethered cord and progressive neurological deficits

• Complete failure of neural tube closure - open, flat neural plate without any covering
• Most severe form; incompatible with life

Investigations

• Antenatal: MSAFP, amniotic AFP, ultrasound, fetal MRI
• Postnatal: MRI of spine and brain (gold standard), plain X-ray (bony defect), renal ultrasound (for hydronephrosis), urodynamics (neurogenic bladder)

Treatment

• Sterile moist dressing over the defect immediately
• Prone positioning
• Surgical closure within 24 hours of birth to prevent further neurological deterioration and bacterial meningitis (Pye's Surgery)
• Assessment and decision by experienced neonatologist/neurosurgeon
• Exceptions: very severe defects with high-level paralysis where closure is technically impossible

• Treatment of hydrocephalus: ventriculoperitoneal (VP) shunt
• Management of neurogenic bladder: clean intermittent catheterization (CIC), anticholinergics
• Orthopedic management: physiotherapy, splinting, corrective surgery for clubfoot/hip deformities
• Long-term multidisciplinary follow-up

• In-utero repair of myelomeningocele before 26 weeks gestation (MOMS trial): shown to improve neurological outcomes, reduce need for VP shunting, improve hindbrain herniation - though carries maternal and fetal risks.

Prevention

• Periconceptional folic acid 0.4 mg/day (4 mg/day for high-risk women) reduces NTD risk by 50-70%
• Folic acid fortification of food

Prognosis

• Depends on level and extent of lesion
• High lumbar lesions: severe paralysis, wheelchair-bound
• Low sacral lesions: ambulatory with orthotic support
• Major causes of morbidity/mortality: shunt malfunction, UTI and renal failure, pressure sores, latex allergy

Note: Topics 4 (Spina Bifida) and 5 (Role of Colour Doppler) are duplicates of topics 4 and 3 above respectively. The full answers are provided in sections 3 and 4.

Duty of Candour - 10 Mark University Answer (Surgery PG)

Definition

"Any patient harmed by the provision of a healthcare service is informed of the fact and an appropriate remedy offered, regardless of whether a complaint has been made or a question asked about it."

Historical Background and Legislative Origin

Two Distinct Duties

1. Professional Duty of Candour (Individual Obligation)

• Be open and honest when something goes wrong with a patient's treatment
• Offer an apology promptly
• Explain fully what happened and the likely short-term and long-term effects
• Put matters right if possible

2. Statutory (Organisational) Duty of Candour (Institutional Obligation)

Three Core Concepts (Robert Francis Definitions)

1. Openness - Enabling concerns and complaints to be raised freely without fear; questions must be answered honestly
2. Transparency - Sharing accurate information about performance and outcomes with staff, patients, the public, and regulators
3. Candour - Proactively informing any patient harmed by healthcare, and offering an appropriate remedy, whether or not asked

Threshold for Triggering the Duty

Statutory Duty - Notifiable Safety Incidents

• Death (not expected as a result of the underlying condition)
• Severe harm - permanent significant harm
• Moderate harm - significant but not permanent
• Prolonged psychological harm (lasting >28 days)

What is EXCLUDED from the Duty

• Complications of the disease itself (e.g., a patient with rectal cancer developing DVT from the cancer - not a care-related incident)
• Recognised complications that occur as part of the natural course of a patient's illness or underlying condition
• Foreseeable outcomes where no error occurred

The Duty of Candour Process - Step by Step

For Low-Harm Incidents (Professional Duty)

For Notifiable Safety Incidents (Statutory Duty - RCS England Framework)

• Detect the safety incident
• Act immediately to prevent further harm
• Make initial severity assessment and report through local governance processes
• Acknowledge the incident verbally with a factual explanation and verbal apology
• Explain that further information will follow after investigation

• Multidisciplinary team review of the incident
• Establish the facts; involve clinical governance/risk management

• Provide written apology following verbal apology
• Explain fully the short-term and long-term effects
• Offer an appropriate remedy or support
• Explain steps to be taken to prevent recurrence
• Record all details of the discussion in the patient's clinical record

• Formal investigation (Serious Incident review, Root Cause Analysis)
• Maintain all documentation and correspondence in the patient's record
• Provide ongoing support to the patient and family
• Share final investigation findings with the patient

Who Should Have the Conversation?

• Notification and apology are undertaken by one or more representatives of the Trust
• Should be a senior clinician familiar with the patient's care
• As most surgery is multidisciplinary, local candour policy applies to all staff with key roles
• The surgeon directly involved should ideally be present
• Trust medicolegal team or patient safety officer may advise but should not replace the clinical conversation

Practical Aspects for the Surgeon

1. Timing - Should not give an immediate "knee-jerk reaction" before full facts are known; but should inform the patient that an adverse event has occurred and is being investigated without delay
2. Fault is not required - The obligation to be candid persists regardless of whether fault or substandard care has occurred; fault and causation require investigation
3. Apology is not an admission of liability - Under the Compensation Act 2006 (UK), an apology is not of itself an admission of negligence
4. Documentation - Every conversation must be documented in the notes; written apology must follow the verbal one
5. Involve the patient's family/carers - Where appropriate, especially if the patient lacks capacity or has died

Ethical Underpinning

Consequences of Breach

• GMC fitness to practise proceedings - Failure to be candid can lead to regulatory action and erasure
• CQC enforcement action against the organisation
• Increased litigation risk - Patients who discover information was withheld are more likely to sue
• Loss of trust - Undermines the doctor-patient relationship
• Criminal liability - Knowingly providing false information is a criminal offence under the regulations (for organisations)

Duty of Candour vs Apology vs Consent

Summary Points for Examiner

1. Duty of candour = professional (individual) + statutory (organisational) obligation
2. Triggered by harm caused by healthcare delivery - NOT by complications of the disease itself
3. Arose from the Francis Report (Mid Staffordshire scandal, 2013); statutory since 2015 under Regulation 20
4. Key elements: inform, apologise (verbal then written), explain, support, document, prevent recurrence
5. Fault does not need to be established before the duty applies
6. An apology is not an admission of negligence (Compensation Act 2006)
7. Applies even to foreseeable, consented-to complications that materialise
8. Failure to comply: GMC proceedings, CQC enforcement, litigation risk
9. Ethically grounded in patient autonomy, beneficence, non-maleficence, and justice
10. Promotes a culture of safety and learning rather than blame