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  • NeuroSurg
    A admin

    Spinal Stenosis

    Doctor Instruction:

    Your next patient is a 51-year-old woman called Rebecca, presenting with lower back pain. Please take a history and perform an appropriate examination.

    Patient History:

    Rebecca, a 51-year-old female, nurse

    You have always been having lower back pain for the past few years, but this has been getting gradually worse. The pain is dull and intermittent. Very often, the pain can diffuse and radiate towards the buttocks, back of the thighs, and feet - when this happens, the pain feels like a burning or cramping sensation. It can be associated with weakness in both legs. The symptoms can be triggered or worsened by sitting down, standing straight and walking downhill. It goes away after a few minutes after being at rest. Bending forward improves symptoms. You tried paracetamol, which only helped a little with pain.

    If you walk for more than 50 yards, you will start noticing numbness and weakness in your legs.

    No previous injury/trauma. Waterworks normal. The bowels are working normally. No other abnormal sensations or weaknesses. No incontinence. No stiffness. No fever. No weight loss. No night sweats.

    Ideas, Concerns, Expectations:

    You think because you often have to bend your back due to work, the pain may be caused by poor posture. You are concerned because it is starting to affect your ability to work in the hospital as a nurse. You would like to see if you can get stronger painkillers and possibly have a scan of your back.

    Past Medical History:

    Obesity, hypercholesterolemia, acromegaly, T2DM.

    No past relevant surgical history.

    Drug History:

    Atorvastatin, metformin NKDA.

    Family History:

    Father has ankylosing spondylitis.

    Social History:

    You work as a senior nurse in a local hospital.

    You smoke around ten cigarettes daily for over ten years but don't drink alcohol.

    Live with husband in a semi-detached house.

    Independent.

    Examination Findings:

    Lower spinal tenderness on palpation at L4-5 region.

    Complete motor and sensory neurological examinations are normal.

    Features of acromegaly e.g. enlarged hands, feet and facial features.

    Lower limb vascular examination is normal.

    No cervical tenderness or restricted movement. Gait normal.

    No cauda equina syndrome features.

    Peripheral pulses and ABPI normal.

    Differentials:

    Lumbar spinal stenosis - likely to be due to degenerative changes

    Osteoarthritis of the spine

    To rule out cauda equina syndrome

    Ankylosing spondylitis/spondylolisthesis

    Rule out peripheral arterial diseases

    Other causes of back pain: spinal tumour, disc herniation, trauma, fracture, and epidural abscess.

    Investigations:

    Imaging:

    XR Lumbar spine (may show degenerative changes/spondylolisthesis)

    MRI Spine. Alternatively, CT myelography/spine when MRI is not available or unsuitable.

    Consider ABPI / CT angiogram to exclude peripheral arterial disease where intermittent claudications are present.

    Special tests:

    Consider electromyographic (EMG) walking test - increased F latency values in lumbar spinal stenosis

    Consider electromyographic paraspinal mapping

    Management:

    Conservative:

    Exercise

    Weight loss if overweight

    Physiotherapy e.g. exercises that minimally stress the back, such as walking, swimming, or bicycling. Exercise may also strengthen the paraspinal muscles.

    NSAIDSs e.g. naproxen, celecoxib +/- PPI cover / antacids

    Paracetamol

    Medication for neuropathic pain e.g. amitriptyline, gabapentin, pregabalin.

    Consider oral steroids for acute exacerbation of painful symptoms.

    Activity modification e.g. limit heavy lifting/prolonged sitting/repetitive bending/twisting of the back.

    Consider deep heat therapy with massage to relieve spasms associated with back pain

    Surgical:

    Consider decompression surgery +/- fusion e.g. laminectomy ( removal of the lamina from affected vertebra) followed by physiotherapy

    Consider interspinous distraction procedure to reduce backward movement of the spine.

    Consider epidural injections with local anaesthetic and corticosteroids under specialist guidance for short/long-term pain relief.

    Viva Questions:

    Explain the pathophysiology of spinal stenosis.

    Spinal stenosis is the narrowing of the spinal canal, which holds the spinal cord and nerves. It's often due to age-related disc degeneration, arthritis, and thickened ligaments. This narrowing can compress the spinal cord and nerves, leading to pain, numbness, and weakness. Factors like herniated discs and inflammation worsen the compression. Treatment involves pain management, physical therapy, and sometimes surgery to relieve pressure on the nerves and spinal cord.

    At what level of the spine does spinal stenosis occur most commonly?

    Spinal stenosis most commonly occurs in the lumbar (lower back) region of the spine. This is because the lumbar spine bears the most weight and undergoes significant movement, which can contribute to degenerative changes over time. Lumbar spinal stenosis can result in compression of the spinal cord and nerve roots, leading to symptoms such as lower back pain, leg pain, numbness, and weakness. However, spinal stenosis can also occur in the cervical (neck) and thoracic (mid-back) regions of the spine, albeit less frequently.

    What are the causes of spinal stenosis?

    Degeneration of spinal structures due to aging.

    Disc degeneration and herniation.

    Osteoarthritis and bone spurs.

    Thickened ligaments.

    Congenital factors and genetics.

    Injuries and trauma.

    Tumors or abnormal growths.

    These factors narrow the spinal canal, compressing nerves and causing stenosis symptoms.

    What are the risk factors of spinal stenosis?

    Age: Risk increases with aging.

    Genetics: Family history matters.

    Congenital: Narrow canal from birth.

    Injuries: Past spine trauma or surgery.

    Lifestyle: Heavy lifting, certain jobs.

    Obesity: Excess weight strains spine.

    Diseases: Arthritis, diabetes, etc.

    Scoliosis: Abnormal spine curvature.

    What are the red flag symptoms/signs of back pain?

    Neurological Issues: Weakness, numbness, or tingling.

    Bladder/Bowel Problems: Loss of control.

    Severe Pain: Unbearable or unrelenting.

    Fever: Along with back pain.

    Unexplained Weight Loss: Rapid and unintended.

    Cancer History: Especially if pain is new.

    Night Pain: Worse at night.

    Trauma: After injury or accident.

    Age Over 50: New-onset pain.

    Steroid Use: Especially long-term.

    B Stations

  • NeuroSurg
    A admin

    Stroke

    Doctor Instruction:

    Your patient is Charlie, a 63-year-old man presenting with problems with speech. Please take a history and carry out a relevant examination.

    Patient History:

    Charlie, 63y/o M, Engineer.

    Your partner noticed a few hours ago that you were difficult to understand while speaking during dinner. Your speech has been slurred, according to your partner, and it happened very suddenly. Your partner was really worried about this and therefore called an ambulance.

    You have noticed you cannot see things on your left which is “kinda weird” – you have never experienced this before in the past – you have to constantly rotate your neck to the side to see more. You also feel tired and not “really yourself”. You noticed you could not pick up your fork with your left hand or lift your left leg up when you tried to walk. These symptoms have not settled since then.

    You are unsure whether you have swallowing difficulties, but you ate fine before slurred speech kicked in. No dizziness/ unsteadiness/ numbness/ headache/ confusion/ loss of consciousness/fever.

    Ideas, Concerns, Expectations:

    You think this might be another "ministroke". You had this last year which quickly resolved. You think you are likely to get better because of this. You have no concerns – you don't know why your partner was so concerned about this. You just want to go home and don't want to miss out on watching your favourite TV show.

    Past Medical History:

    Hypertension, atrial fibrillation, obesity, hypercholesteremia, previous “ministroke” x1 last year. Had a hernia operation in 2014.

    Drug History:

    Atorvastatin, aspirin, amlodipine, ramipril, apixaban.

    NDKA

    Family History:

    Father had a heart attack when he was 50

    Social History:

    You live with your partner in a semi-detached house.

    You work as an engineer.

    You smoke 10 cigarettes a day since when you were a teenager (can't remember for how long exactly).

    you drink a pint of beer every weekend.

    Examination Findings:

    Slurred speech

    Left-sided weakness for arm and leg

    Left homonymous hemianopia

    No higher cerebral dysfunction (dysphasia, visuospatial disorder)

    Differentials:

    Stroke – likely ischaemic PACS ( Ischaemic stroke (87%) vs Haemorrhagic stroke (13%) )

    Stroke – other forms

    TIA

    Investigations:

    Observations + neuro observations

    ECG / Echo – to rule out cardiac cause

    Bloods: glucose (exclude hypoglycaemia), U&Es (neurological signs + exclude renal failure), FBC (r/o anaemia or infection), coagulation screen with INR

    USS doppler carotids – rule out aortic stenosis

    Non-contrast CT Scan (immediate) – to determine management: ischaemia vs haemorrhage

    For further investigations: MRI Scan/CTA/MRA

    Management:

    Conservative:

    Smoking cessation

    Dietary changes

    Lose weight

    Exercise

    Alcohol Control

    Manage risk factors/co-morbidities: hypertension, hypercholesteremia, diabetes, AF, obesity, high cholesterol level…etc.

    Rehabilitation (MDT: PT + OT + SALT + Nurses+ Dietician + social services + Optometry/Opthalmology + psychology + Orthotics)

    Neuro observations + monitor with supportive care.

    Maintain target oxygen saturation

    Medical:

    Referral to hyperacute/acute stroke unit.

    Ischaemia:

    Thrombolysis (<4.5 hours from onset) – alteplase if ischaemic and intracranial haemorrhage has been excluded (repeat CT scan needed post-thrombolysis to rule out haemorrhage complication).

    Alternative: mechanical thrombectomy (6-24 hours of onset)

    Antiplatelet therapy with PPI (e.g. STAT aspirin 300mg after CT and continued for 2 weeks – to be switched to clopidogrel 75mg lifelong for secondary prevention of stroke)

    Statin e.g. atorvastatin 80mg life-long for secondary prevention

    Haemorrhagic:

    Withhold blood thinners

    Urgent referral for neurosurgical assessment

    Control blood pressure.

    Consider reversal of anticoagulation.

    Viva Questions:

    What are the risk factors for stroke?

    High blood pressure (hypertension)

    Smoking

    Diabetes

    High cholesterol levels

    Heart disease

    Obesity and lack of physical activity

    Poor diet

    Excessive alcohol consumption

    Age and gender (risk increases with age and is higher in men)

    Family history and genetics

    Previous stroke or transient ischemic attack (TIA)

    Certain medical conditions (e.g., sickle cell disease)

    Sleep apnea

    Certain medications (e.g., hormone-based contraceptives)

    What is the ROSIER scale?

    The ROSIER (Recognition of Stroke in the Emergency Room) scale is a clinical tool used to aid in the early recognition and diagnosis of stroke, particularly within the emergency room setting. It's designed to help healthcare professionals quickly assess the possibility of a patient experiencing a stroke and facilitate prompt intervention. The scale evaluates specific signs and symptoms commonly associated with stroke.

    The ROSIER scale typically considers various criteria, including facial weakness, arm weakness, speech disturbance, and age, to determine the likelihood of a patient having a stroke.

    What are the indications for immediate CT Head?

    Acute Head Trauma: Significant head injury.

    Stroke or TIA: Focal neurological deficits or suspected stroke.

    Subarachnoid Hemorrhage: Sudden severe headache.

    Intracerebral Hemorrhage: Sudden severe neurological symptoms.

    Mass Lesion or Tumor: New-onset or worsening neurological symptoms.

    Infections or Abscesses: Suspected intracranial infections.

    Hydrocephalus: Symptoms of increased intracranial pressure.

    Vascular Abnormalities: Suspected aneurysms or AVMs.

    Altered Mental Status: Sudden mental status changes.

    Seizures: Prolonged or atypical seizures.

    Severe Headaches: Sudden severe or atypical headaches.

    Ophthalmologic Symptoms: Acute visual disturbances.

    Post-Operative Patients: Recent neurosurgery with acute symptoms.

    What are the key cerebellum defect signs?

    Ataxia: Uncoordinated movements and balance issues.

    Dysmetria: Difficulty judging distances accurately.

    Intention Tremor: Shaking during purposeful movements.

    Speech Disturbances: Slurred or abnormal speech rhythm.

    Nystagmus: Involuntary rhythmic eye movements.

    Vertigo or Dizziness: Sensation of spinning or unsteadiness.

    Wide-Based Gait: Feet spaced apart for stability.

    Incoordination of Movements: Difficulty with precise motions.

    Tremor: Rhythmic shaking or quivering movements.

    Reflex Abnormalities: Altered reflex responses (reduced or increased).

    Tell me about the Bamford classification of ischaemic stroke.

    The Bamford classification categorizes ischemic strokes into four types based on their clinical presentation:

    Total Anterior Circulation Infarct (TACI): Severe deficits involving at least two areas (leg, arm, face, higher cortical functions).

    Partial Anterior Circulation Infarct (PACI): Moderate deficits that don't meet TACI criteria.

    Posterior Circulation Infarct (POCI): Involves brainstem and/or cerebellum, causing specific symptoms.

    Lacunar Infarct (LACI): Small, deep infarcts causing motor or sensory deficits.

    B Stations

  • Orthopedic
    A admin

    Cauda Equina Syndrome

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 45-year-old gentleman, Adam, who presents back pain after being hit by a slow-moving car yesterday. Please take a history and perform an appropriate examination.

    Patient History:

    Adam, a 45-year-old gentleman, banker

    You came in today following a small car collision towards your back while walking across the road last night. You brushed this off – thinking it was no big idea. However, you started noticing lower back pain with weakness in your lower limbs.

    Back pain is located centrally in the lower back – can sometimes radiate down both legs. You describe the pain as sharp, rating it 10/10. You tried many things to ease the pain without success e.g. paracetamol and ibuprofen. Back pain can be triggered by simple back movement but not worsened by coughing or straining. You have numbness and tingling sensation running down both of your legs.

    Also, while wiping yourself afterwards in the toilet, you couldn’t feel the sensation around your bottom as well as your genitals– it was very strange, and at that point, you knew you needed to go and seek medical attention. You developed incontinence for passing urine and faeces. You no longer have the urge to go the toilet, and they can come out involuntarily, which is very concerning for you—no other previous back injuries.

    Idea, Concern, Expectation:

    You have no idea what is going on, but you think it is related to yesterday's injury. You are very concerned and don’t want to be paralysed – you are still very young! You would like to find out what is going on. You are very scared if you need any surgery for this.

    Past Medical History:

    Hypertension, obesity

    Drug History:

    Ramipril, Atorvastatin

    NKDA

    Family History:

    Ankylosing Spondylitis

    Social History:

    Smoke 10 cigarettes/day for over 20 years

    Drink around 2-3 pints of beer every weekend

    Work as a banker

    Live with a wife and two kids in a semi-detached house

    Examination Findings:

    Both lower limbs power 4/5 with reduced sensations, tone, and reflexes.

    Lower back spinal tenderness at L3/4 region.

    PR Examination: Reduced anal tone and sensation.

    No upper motor neurone signs

    Differentials:

    Caudal Equina Syndrome caused by trauma

    Prolapsed lumbar disc

    Conus medullaris syndrome

    Mechanical back pain

    Peripheral neuropathy

    Spinal tumour

    Investigations:

    Basic observations

    Routine bloods for baseline and pre-assessment e.g. FBC, U&Es, LFT, Bone Profile, CRP

    Consider blood culture if suspected infection.

    Emergency MRI to confirm and exclude cauda equina syndrome

    Consider CT myelography/spine

    Consider XR spine

    Consider Urodynamic studies -to monitor bladder function

    Management (Cauda Equina Syndrome):

    Hospital Admission

    VTE prophylaxis

    Prevention of further damage e.g. Immobilise spine if CES is due to trauma

    Neurosurgical input for consideration of lumbar decompression surgery – the earlier this is performed, the higher the chance of regaining functions.

    Surgery may involve removing bone fragments, tumour, herniated disc, blood, debulking for SOL e.g. tumour abscess…etc.

    Anti-inflammatories such as steroids, if due to inflammatory cause

    For infectious causes, patients should be treated with antibiotics

    Postoperative care includes physiotherapy, occupational therapy, and addressing lifestyle issues e.g. obesity.

    Treatment for metastatic spinal cord compression includes analgesia, high-dose dexamethasone, surgery, radiotherapy, and chemotherapy. Investigations include biopsy, staging CT, PET scan…etc.

    Viva Questions:

    Explain the pathophysiology of cauda equina syndrome.

    Cauda equina syndrome is caused by compression of nerve roots at the base of the spine. This pressure leads to severe back pain, leg pain, numbness, weakness, and bladder/bowel dysfunction.

    Why is cauda equina syndrome a surgical emergency?

    Cauda equina syndrome is a surgical emergency because the compression of nerve roots can cause permanent and severe neurological damage. Prompt surgery is essential to prevent irreversible loss of sensation, muscle function, and bladder/bowel control. The urgency is to minimize lasting deficits and improve patient outcomes.

    Where does the spinal cord terminate (at what level)?

    The spinal cord typically terminates around the level of the first or second lumbar vertebra (L1-L2) in most adults. Below this point, the spinal cord transitions into a bundle of nerve roots known as the cauda equina, which continues down the vertebral canal and provides innervation to the lower extremities and pelvic organs

    What is conus medullaris?

    The conus medullaris is the tapering, lower end of the spinal cord. It is located at the termination of the spinal cord, usually around the level of the first or second lumbar vertebra (L1-L2). Below the conus medullaris, the spinal cord transitions into the cauda equina, a bundle of nerve roots that extend further down the spinal canal. The conus medullaris is an important anatomical landmark and holds significance in medical imaging, surgical procedures, and discussions related to spinal cord and neurological health.

    What are the causes of cauda equina syndrome?

    Cauda equina syndrome is caused by conditions that compress or damage the nerve roots at the base of the spinal cord. Common causes include herniated discs, spinal tumors, spinal stenosis, trauma, infections, inflammatory conditions, and postoperative complications. Immediate medical attention is crucial to prevent permanent nerve damage.

    Does cauda equina syndrome show lower or upper motor neurone signs or both?

    Cauda equina syndrome leads to signs and symptoms characteristic of lower motor neuron involvement. These include bilateral reduction in sensation of the lower limbs, impaired bladder and bowel function, weakness in the lower limb muscles, intense back pain, and potential issues with sexual function.

    B Stations

  • Orthopedic
    A admin

    Adhesive Capsulitis (Frozen Shoulder)

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is called Bob, a 41-year-old gentleman presenting with shoulder stiffness. Please take a history and perform an appropriate examination.

    Patient History:

    Bob, a 41-year-old gentleman, construction worker.

    A few weeks ago, your left shoulder started becoming stiffer than usual, affecting movements in all directions; stretching exercises help with stiffness slightly, but stiffness is the same throughout the day. This is causing problems for you as you now need help with overhead activities and putting on your clothes. You feel like your left shoulder can no longer move as it used to with a limited range of motions.

    Six months ago, you had a gradual worsening, constant left shoulder pain, which is often worse at night affecting your sleep- however, this is slowly getting better, so you are not too concerned, and you have a high pain tolerance. You describe the pain as a dull ache - rating it 2/10 currently. No radiation. No previous recent injury or known trigger. You tried many painkillers, such as paracetamol, with only minimal effects.

    Idea, Concern, Expectation:

    You have no idea what is going on. You work in construction, so this may be related. You had a few injuries towards your left shoulder in the past but nothing major. You are concerned as your work often involves very active use of your left shoulder, and you now have problems at work due to stiffness. You would like to see if you can have a sick note for this.

    Past Medical History:

    Type 2 diabetes, hypothyroidism

    Previous left shoulder rotator cuff injury, which was treated conservatively three years ago.

    No previous surgical history

    Drug History:

    Metformin, levothyroxine.

    Allergic to fish - Rash.

    Family History:

    Mother has osteoarthritis affecting both hips.

    Social History:

    Work as a builder

    Non-smoker

    Drink around 3-5 units a week over a weekend.

    Live with wife in a flat

    Examination Findings:

    Left shoulder stiffness on both active and passive movement in all directions with limited range of motions. However, external rotation is most affected. The whole shoulder joint is mildly tender to palpation.

    Positive coracoid pain test - tenderness with direct pressure on the coracoid

    Positive shoulder shrug test - inability to abduct arm to 90degree in the plan of body and to hold the position.

    No tenderness at acromioclavicular joint. No painful arc on shoulder abduction.

    Negative for other manoeuvres or shoulder tests.

    Differentials:

    Adhesive capsulitis (pain phase transitioning to stiff phase)

    Supraspinatus tendinopathy

    Acromioclavicular joint arthritis

    Glenohumeral joint arthritis

    Things to consider: septic arthritis, inflammatory arthritis, malignancy e.g. osteosarcoma, bony mets, fractures, shoulder dislocation, rotator cuff injury...etc.

    Investigations:

    Clinical diagnosis

    Consider routine bloods if indicated to rule out other pathologies

    Consider shoulder XR shoulder e.g. may show signs of arthritis

    Consider ultrasound, CT, MRI (may show thickened joint capsule in adhesive capsulitis)

    Management:

    Conservative:

    Continue using the left arm but don't exacerbate the pain

    Encourage active/passive exercises and stretching

    Analgesia e.g. paracetamol, NSAIDs

    Physiotherapy

    Psychosocial support

    Consider transcutaneous electrical nerve stimulation (TENS) machine for pain management

    Consider referral to pain clinic/orthopaedics if significant disability and poor pain control despite conservative/ medical management

    Medical:

    Intra-articular steroid injections

    Consider short-term oral steroids

    Surgical:

    Hydrodilation (injecting fluid into joint to stretch capsule)

    Manipulation under anaesthesia to improve range of motion

    Arthroscopy, e.g. keyhole to remove adhesions and release shoulder

    Arthroscopic capsulotomy

    Viva Questions:

    Explain the pathophysiology of adhesive capsulitis.

    Adhesive capsulitis, or frozen shoulder, involves inflammation in the shoulder joint. This triggers collagen buildup and adhesion formation in the joint capsule, leading to stiffness and restricted movement. Over time, inflammation subsides, but adhesions persist, causing ongoing limited range of motion. Physical therapy and treatments aim to break down adhesions and improve shoulder function. In severe cases, medical interventions may be necessary.

    What are the different phases of adhesive capsulitis?

    Freezing Phase: Pain and stiffness increase as inflammation sets in.

    Frozen Phase: Pain stabilizes, stiffness intensifies due to scar tissue and adhesions.

    Thawing Phase: Pain and stiffness decrease, range of motion improves gradually.

    How long can adhesive capsulitis generally last?

    Adhesive capsulitis can last from a few months to a couple of years, with treatment playing a role in its duration. Early intervention and therapy can help shorten the recovery time.

    What manoeuvre/ test can be used to test for supraspinatus tendinopathy?

    The Empty Can Test (Jobe's Test) is used for supraspinatus tendinopathy. The person raises arms forward at 90 degrees, thumbs down. Downward pressure is applied, and pain or weakness suggests a potential issue with the supraspinatus tendon.

    What are the complications of frozen shoulder?

    Complications of frozen shoulder include prolonged stiffness, pain, loss of function, muscle imbalances, reduced quality of life, secondary issues in other body parts, chronic pain, limited work and activities, and emotional distress. Timely treatment and therapy can help prevent or minimize these complications.

    What is the usual prognosis for frozen shoulder?

    The prognosis for frozen shoulder varies, but with proper treatment and therapy, most individuals can expect gradual improvement over several months to years. Early intervention and consistent care can lead to full or nearly full recovery of range of motion and function. In some cases, residual stiffness or recurrence can occur, and underlying health conditions can influence outcomes.

    B Stations

  • Orthopedic
    A admin

    Dupuytren's Contractur

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 65-year-old female called Mary, presenting with restricted hand movements. Please take a history and perform an appropriate examination.

    Patient History:

    Mary, a 65-year-old female, retired.

    Over the last few years, you have been developing increasing difficulty using your right hand. You are unable to straighten your right ring and little fingers fully at all. You tried to flick your finger back but it didn't help. Because of this, you have been dropping things easily on the floor as you couldn't let go of things properly - how embarrassing! You now have difficulties using your right hand, for example, washing your face or fitting your hand into a glove to do gardening. Because you are mostly right-handed - you are becoming more frustrated day by day! You haven't noticed any pain in your hands as of yet. No stiffness. No previous hand trauma/injury.

    Idea, Concern, Expectation:

    You think this might be arthritis, as your mother got it. You are concerned as you are struggling with activities at home. You often have to ask your husband to help. You want to become more independent and not rely on others. You would like to free up your hand to do more things on your own.

    Past Medical History:

    T1DM, epilepsy, hyperlipidaemia

    No previous surgeries.

    Drug History:

    Insulin injections, carbamazepine, atorvastatin

    NKDA

    Family History:

    Arthritis - mother

    Social History:

    Retired. Used to work in sewing for clothes for most of your life.

    You don't smoke, but you used to smoke around ten cigarettes for over 20 years.

    You drink a glass of gin and tonic a few times a week.

    You live with your husband in a small bungalow.

    Examination Findings:

    Skin thickening/ puckering/ pitting tethering/ dimpling in the palm of the right hand. Restricted extension of 4th and 5th digits of the right hand and appear in a flexed position at rest. 4th and 5th digits of right MCP joints are limited to 30°, and PIP joints are limited to 10° in the axis.

    Firm, longitudinal thickening cords can be palpated from the palm into the affected fingers.

    Firm nodules can be felt in the palm of the right hand - fixed to the skin and deep fascia at the distal palmar crease.

    Hueston's table-top test is positive - the patient is unable to lay their right hand completely flat on the table.

    Neurovascular intact upper limbs

    Differentials:

    Dupuytren's contracture

    Callus

    Ganglion

    Trigger finger

    Epithelioid sarcoma

    Ulnar nerve palsy

    Investigations:

    Clinical diagnosis

    Consider monitoring risk factors such as hba1c/glucose for diabetes

    Consider ultrasound of the hand

    Management:

    Conservative:

    Do nothing/reassurance if there is no contracture or loss of function

    Referring to plastic / orthopaedic surgery for specialist assessment

    Medical:

    Corticosteroid injections for those with painful nodules (without contracture/loss of function)

    Consider collagenase injection for ≤30° MCP joint contracture with no PIP joint contracture

    Surgical (usually done under regional block or GA as a day case):

    Needle fasciotomy/needle aponeurotomy - using a needle to divide and loosen the cord causing the contracture

    Percutaneous fasciotomy - using a scalpel to divide and loosen the cord causing the contracture

    Limited fasciectomy- removing abnormal fascia and cord to release the contracture

    Dermofasciectomy - removing abnormal fascia and cord and associated skin. A skin graft is used to replace the removed skin.

    Peri-operative antibiotic

    Surgery is generally followed by splinting and physiotherapy of the affected hand.

    In severe cases, consider finger amputation.

    Viva Questions:

    Explain the pathophysiology of Dupuytren's contracture.

    Dupuytren's contracture is a hand condition driven by genetic factors and abnormal tissue response. Fibroblasts, responsible for producing collagen, become overactive due to genetic triggers. This leads to excessive collagen production, forming nodules and cords in the palm. These cords exert a contractile force, causing finger bending. Myofibroblasts, with contractile abilities, contribute to this force. Inflammation and microvascular changes may also play roles. Overall, genetics, fibroblast activity, collagen accumulation, and contractile forces underlie the condition.

    What are the complications of Dupuytren's contracture surgery?

    Recurrence: Contracture can return after surgery.

    Scarring: Surgery can lead to visible scars.

    Infection: Risk of post-surgery infection.

    Nerve or Vascular Damage: Nearby structures can be harmed.

    Stiffness: Hand movement may be limited.

    Pain and Discomfort: Pain during recovery is common.

    Hematoma: Blood collection can occur.

    Skin Issues: Wound healing problems or skin changes.

    Complex Regional Pain Syndrome: Rare, severe pain condition.

    Joint Stiffness: Hand joints can become stiff.

    Allergic Reactions: Allergies to surgical materials.

    Cosmetic Changes: Hand appearance might alter.

    B Stations

  • Orthopedic
    A admin

    Epicondylitis

    Doctor Instruction:

    Your patient is a 45-year-old woman, Susan, presenting with elbow pain. Please take a history and perform an appropriate examination.

    Patient History:

    Susan - a 45-year-old female - farmer

    You have been experiencing elbow pain for the last few months. This pain is gradually getting worse. This pain is located at the lateral side of your right elbow. The pain is sharp and constant and can radiate down the forearm. Pain is not worsened by grasping objects, wrist flexion or pronation. It is made worse when bending your right wrist upwards (extension). You tried ibuprofen which improved the pain.

    You noticed the gripping strength of your right hand has reduced. You now find opening a jar of jam more difficult than usual. No known recent injuries. No abnormal sensation.

    Ideas, Concerns, Expectations:

    You think this might be related to your work as a farmer, as you often have to use heavy vibrating tools on the farm. You are concerned as you are beginning to have difficulty managing at home and at work due to the pain. You would like to find out what is going on and have strong painkillers.

    Past Medical History:

    Osteoarthritis affecting both hips and knees

    COPD

    Previous left Achilles tendon rupture

    Drug History:

    Ibuprofen as required for pain

    Fostair inhaler

    NKDA

    Family History:

    Inflammatory bowel disease

    Social History:

    You work on a farm involving raising animals and growing crops.

    You live with your husband in a detached house.

    You are usually independent at home. No carers.

    You smoke ten cigarettes a day for 20+ years.

    You drink a glass of wine every day during dinner.

    You play tennis when you are free, but you have been playing less than usual due to elbow pain.

    Examination Findings:

    Tenderness at the right lateral epicondyle of the humerus on palpation.

    Elbow pain is worsened on resisted dorsiflexion of the right wrist

    Weak right wrist extension and reduced grip strength of the right hand

    Mill's test positive

    Cozen's test positive

    Tinel's sign is negative

    Good range of movement of the right elbow.

    Normal sensation

    Differentials:

    Lateral epicondylitis (Tennis Elbow)

    Olecranon bursitis

    Elbow arthritis

    Cervical nerve root entrapment

    Radial tunnel syndrome

    Investigations:

    Clinical diagnosis

    Consider Elbow XRay/MRI/US if the diagnosis is uncertain

    Consider nerve conduction study and electromyography if ulnar nerve involvement is suspected in patients with golfer's elbow

    Consider Infra-red thermography and laser doppler flowmetry in difficult suspected cases of tennis elbow

    Management (Epicondylitis):

    Conservative:

    Self-limiting; resolving with time

    Rest

    Modifying activities that exacerbate symptoms e.g. avoid tasks that involve high force, hand-gripping/ pinching/ use of high-amplitude vibrating handheld tools

    Rehabilitation exercises - increase the strength

    Analgesia e.g. oral or topical NSAIDs/ paracetamol

    Apply heat/ ice to help relieve pain

    Physiotherapy

    Orthotics e.g. elbow braces, forearm strap

    Medical:

    Consider steroid injections for short-term relief

    Consider topical GTN for tendinopathies for up to six months

    Review in 6 weeks and reassess management and symptoms - may require a specialist referral if the diagnosis is in doubt, severe pain/functional impairment, symptoms non-responding for 6-12 months.

    Secondary Care:

    Platelet-rich plasma (PRP) injections

    Hyaluronan gel injections

    Biologic treatment may be considered

    Botulinum toxin in very severe cases

    Extracorporeal shock wave treatment

    Surgical:

    Debridement

    Release or repair of damaged tendons

    Prevention:

    Modify activities that led to overuse injury.

    Proper ergonomic positioning and functioning in both workplace and recreational environments.

    Viva Questions:

    Explain the pathophysiology of epicondylitis.

    Epicondylitis, commonly known as tennis or golfer's elbow, is a repetitive strain injury affecting the tendons at the elbow's bony prominences. It stems from microscopic tendon damage due to repeated wrist and forearm motions, like gripping and twisting. This leads to inflammation, impaired blood flow, and altered collagen structure in the tendons. Overuse strains the tendon attachments, causing pain, weakness, and limited function. Inflammation further exacerbates the issue. If untreated, chronic degeneration can occur.

    What are the differences between tennis vs golfer's elbows?

    Tennis elbow (lateral epicondylitis) affects the outer elbow and extensor tendons, caused by repetitive wrist extension motions. Golfer's elbow (medial epicondylitis) affects the inner elbow and flexor tendons due to repeated wrist flexion movements. Both cause pain and inflammation at tendon attachments.

    What are the risk factors for epicondylitis?

    Epicondylitis risk factors: Repetitive motions, occupational demands, sports involvement (tennis, golf), poor technique, age (30-50), gender (men for tennis elbow), fitness level, obesity, prior elbow issues, genetics. Prevent with proper form, ergonomic tools, warm-ups, and exercises.

    What is the usual prognosis for epicondylitis?

    The prognosis for epicondylitis varies. With early diagnosis and appropriate treatment, such as rest, physical therapy, and lifestyle adjustments, many individuals recover within a few weeks to a few months. However, if not managed properly, the condition can become chronic, leading to persistent pain and functional limitations. In some cases, more intensive treatments like corticosteroid injections or even surgery might be considered. To enhance prognosis, timely intervention, adherence to treatment recommendations, and preventive measures to avoid repetitive strain are crucial.

    B Stations

  • Orthopedic
    A admin

    Carpal Tunnel Syndrome

    Doctor Instruction:

    You are currently a Foundation Year Doctor working in the Emergency Department. Your next patient is a 44-year-old woman called Candy, who presents with hand numbness. Please take a history and perform an appropriate examination.

    Patient History:

    Your name is Candy (44-year-old woman) – office worker.

    Over the last few months, you noticed worsening numbness in your right hand – mainly affecting your right hand's thumb, index, and middle fingers. Sometimes around these sites, you will notice some pins and needles/ a burning sensation / aching pain, which tend to come up intermittently and worsen at night-time and can wake you up from sleep. You tried multiple methods of relieving symptoms, such as hanging your hand out of bed at odd angles or shaking your hand multiple times – which helped slightly. You occasionally have stiffness in the fingers of both hands, especially in the morning, lasting around 30-45 minutes, improving throughout the day.

    You also noticed you have been becoming clumsier as usual in the last few months. You feel weak in doing things with your right hand i.e. opening a jar or turning a wrench. Sometimes items just slip out from your right hand! Because of this, you dropped and broke a few cups in the kitchen, how embarrassing!

    Ideas, Concerns, Expectations:

    You think you might have arthritis but are not too sure. You are concerned because you are becoming less able to cope at home due to clumsiness. You would like to see if you can be seen by a rheumatologist about this.

    Past Medical History:

    Obesity, Hypothyroidism, Type 2 Diabetes, previous fracture at the right wrist when you were a child - this was managed conservatively.

    Drug History:

    Atorvastatin, levothyroxine, metformin

    NKDA

    Family History:

    Dad also has similar symptoms in the past – all you know is that he has acromegaly. Mother has arthritis, but you do not know which one.

    Social History:

    You work as an office worker (if asked specifically, your job involves heavily typing on a keyboard for various clients).

    Smoke five cigarettes daily for five years.

    Don't drink alcohol.

    Examination Findings:

    Overgrowth features of acromegaly might include large nose/tongue/hands/feet/ protruding jaw/ prominent forehead + brow

    Wasting/loss of sensation around the thenar muscles (right)

    Weaknesses in flexion of the index and middle fingers of the right hand. Weakness on right thumb abduction/opposition/ flexion. Weakness in grip strength(right hand).

    Difficulty with fine movement involving thumb (right)

    Reduced sensory innervation of the median nerve distribution of the right palm and full fingertips of the right hand's thumb, index and middle finger.

    Positive for Phalen’s test, Tinel’s test and carpal tunnel compression test of the right hand.

    Differentials:

    Carpal Tunnel Syndrome / Median Nerve Palsy

    Rheumatoid / Osteoarthritis

    Underlying undiagnosed acromegaly

    Tendonitis/ fibrositis

    Investigations:

    Bedside:

    Observations

    Perform a Carpal Tunnel Questionnaire

    Imaging:

    Consider XR of the hands for arthritis

    Ultrasonography Wrist + Hand (space-occupying lesion may be identified)

    MRI scan (space-occupying lesion may be identified)

    Special Test:

    Nerve conduction studies e.g. electroneurography/ electromyography (focal slowing of conduction velocity in median sensory nerves + prolongation of median distal motor latency)

    Management (Carpal Tunnel Syndrome):

    Conservative:

    Patient Education about the condition

    Rest

    Minimise activities that can exacerbate symptoms

    Wrist splints (to maintain a neutral position of the wrist at night)

    A trial of NSAIDs +/- PPI cover

    Acupuncture (symptom relief/ grip strength/ electrophysiological function)

    Physiotherapy (to improve strength/flexibility/mobility of median nerve)

    Secondary prevention: ergonomic changes to workplace e.g. ergonomic keyboards, wrist, rest, frequent breaks, wrist splint…etc.)

    Consider referring patients to orthopaedics or rheuamtology if e.g. uncertain about diagnosis or severe symptoms e.g. persistent motor/ sensory disturbance, or for long-term management

    Medical:

    Steroid injections (symptom relief)

    Surgical:

    Carpal tunnel decompression surgery (open or endoscopically) with rehabilitation treatment following surgery e.g. immobilisation of wrist orthosis, dressings, exercise, controlled cold therapy, multimodal hand rehabilitation, electrical modalities, scar desensitisation, arnica, laser therapy.

    Sonographically guided carpal tunnel release (new technique)

    Viva Questions:

    Explain the pathophysiology of carpal tunnel syndrome.

    Carpal Tunnel Syndrome (CTS) occurs when the median nerve in the wrist is compressed due to factors like inflammation and anatomical constraints in the carpal tunnel. Repetitive movements or medical conditions can cause swelling and increased pressure. This pressure on the nerve leads to symptoms such as pain, tingling, and weakness in the hand's thumb, index, and middle fingers. Over time, this compression can damage the nerve, causing further sensory and muscle issues. Treatment options range from conservative measures to surgery, depending on the severity of the condition.

    What nerve is affected in carpal tunnel syndrome?

    In carpal tunnel syndrome (CTS), the median nerve is the nerve that is primarily affected. The median nerve runs from the forearm into the hand through a narrow passageway called the carpal tunnel, which is located on the palm side of the wrist. Compression or irritation of the median nerve within the carpal tunnel leads to the characteristic symptoms of CTS, including pain, numbness, tingling, and weakness in the thumb, index finger, middle finger, and half of the ring finger.

    What are the risk factors/causes of carpal tunnel syndrome?

    Carpal tunnel syndrome (CTS) risk factors include repetitive hand motions, jobs with wrist strain, anatomy variations, diabetes, arthritis, hormonal changes (pregnancy, menopause), age (over 50), female gender, obesity, wrist injuries, genetics, fluid retention, and lifestyle factors like smoking and inactivity.

    What are the advantages of endoscopic surgery compared to open surgery?

    Endoscopic surgery has advantages over open surgery: smaller incisions, less tissue trauma, faster recovery, reduced blood loss, shorter hospital stay, lower infection risk, improved cosmetic outcome, enhanced visualization, less disruption to tissues, quicker return to activities, and potentially lower hernia risk. The approach depends on the procedure and patient, ensuring personalised and efficient treatment.

    B Stations

  • Orthopedic
    A admin

    Fractured Neck of Femur

    Doctor Instruction:

    You are a Foundation Year Doctor working in the Emergency Department. Your next patient is a 65-year-old woman, Mary, presenting following a fall. Please take a history and perform an appropriate examination.

    Patient History:

    Your name is Mary. You are 65 years old woman – retired.

    While walking down the stairs 2 hours ago, you slipped accidentally and fell down the stairs, and suddenly, you heard a crack at your left hip. Since then, you have had this sudden, ongoing severe pain and your husband called the ambulance. You can't remember how long you have been lying on the ground. You are not sure if you have hit your head during the fall. No dizziness/vertigo. No palpitation. No loss of consciousness. No chest pain/ palpitation. No shortness of breath. No neurological symptoms. No fits/ incontinence/ tongue biting. No weakness/ slurred speech/ vision change. No warning signs. Waterworks/bowel normal.

    You note you have pain in the groin and hip, which radiates to the knee. The pain is excruciating 10/10 – worsening by any movement, especially rotation. You have been given some morphine in the ambulance which helped. You are unable to stand or bear weight on the left side. You have some swelling in your left hip.

    Ideas, Concerns, Expectations:

    You think you have cracked a bone or something as your GP previously said you have brittle bones! You are concerned that you may need an operation! You want to avoid surgery as much as possible and get your pain under control.

    Past Medical History:

    Osteoporosis, Parkinson's disease. Diabetes type 2, paroxysmal atrial fibrillation, heart failure

    Drug History:

    Levodopa, alendronic acid weekly, metformin, furosemide, apixaban, omeprazole, vitamin D supplement

    Family History:

    Atrial fibrillation

    Social History:

    Drink 2-3 glasses of wine every other night

    Ex-smoker – used to smoke around 5-10cigarettes a day for 10 years

    Examination Findings:

    Left leg shortened, abducted, and externally rotated. Pain palpating the greater trochanter.

    Differentials:

    Neck of femur fracture

    Acetabular fracture

    Pubic rami fracture

    Femoral shaft or subtrochanteric femur fracture

    Femoral head fracture

    To rule out causes for falls e.g. Parkinson's, anaemia, electrolyte imbalance, arrhythmias, heart failure, MI, stroke, UTI, chest infection, dehydration, incorrect eyewear, poor footwear, obstacles at home…etc.

    Investigations:

    Bedside:

    Primary Survey (ABCDE)

    Observation including lying and standing BP

    ECG / 24-48h Holter monitor (arrhythmias e.g. AF)

    Consider Echo (aortic stenosis? fall)

    Assess fluid status

    Urine dip (rule out infection, +++blood in rhabdomyolysis)

    Dix-Hallpike test if suspecting BPPV for cause of fall

    Bloods:

    Bloods (FBC, CRP, anticoagulation screen, electrolytes, bone profile, LFTs – rule out potential causes for fall/ fracture e.g. anaemia, electrolyte imbalance, underlying infection, plan for surgery…etc.) + group and save/ cross-match for surgery + CK (potential long lie/rhabdomyolysis) + glucose (hypoglycaemia is a cause of falls)

    Imaging:

    XR hip (AP + Lateral) – look for fractures, disruption of Shenton's line/ trabeculae, inferior/superior cortices…etc

    MRI/ CT may be indicated if XR is negative, but fracture is suspected

    Consider CT head for head injuries if indicated e.g. on anticoagulants

    Consider XR Chest if suspecting pneumonia contributing to fall

    Management:

    Conservative :

    Appropriate analgesia e.g. opioids, nerve block

    VTE risk assessment + prophylaxis e.g. LMWH / stocking

    Prophylactic antibiotics (those at risk of MRSA/ open wound)

    Nutrition support if appropriate

    Review medications

    Review functional status

    Measure cognitive impairment/signs of delirium

    Prevention of pressure ulcers

    Patient/family education

    Falls assessment

    PT / OT input

    Medical:

    Treat any underlying infection if appropriate

    Management of co-morbidities

    Surgery:

    Refer to orthopaedics / orthogeriatric

    Pre-operative assessment for surgery

    Aim surgery within 48hours of admission for hip fractures

    Post-surgical care: analgesia, VTE prophylaxis, rehabilitation/ PT/ OT, fall risk assessment, treat the underlying cause for falls/fracture

    Intracapsular Hip Fracture:

    Undisplaced Intracapsular fracture – internal fixation with screws, otherwise arthroplasty in those who are less fit

    Displaced intracapsular fracture – arthroplasty (total / partial)

    Consider extramedullary implants such as sliding hip screw in preference to intramedullary nail in patients with trochanteric fractures above and including the lesser trochanter.

    Extracapsular Hip Fracture:

    Intramedullary nail used to treat subtrochanteric fracture

    Extracapsular fractures by internal fixation using intramedullary nails but hip arthroplasty is used if internal fixation fails in unstable fractures.

    Those not suitable for surgery but not receiving end-of-life care:

    Bed rest/non-weight bearing + regularly reassess suitability for surgery

    Not currently suitable for surgery + receiving end of life:

    Palliative care / symptomatic relief, ensure bed rest and non-weight bearing.

    Prevention of falls:

    Eye test/suitable eyewear, ensure good fitting footwear, remove environmental hazards e.g. rugs/ turn on lights, ensure good hydration, review medication, hearing assessment and correction,

    Viva Questions:

    Explain the pathophysiology of a fracture.

    A fracture occurs when a bone breaks due to trauma or excessive force. The body responds with an inflammatory phase, forming a blood clot (hematoma) at the site. A callus made of collagen and cartilage stabilizes the bone and eventually remodels into new bone tissue, healing the fracture.

    Tell me the different types of fractures.

    Fractures can manifest in various forms, each classified based on the pattern and characteristics of the break. The main types of fractures include:

    Simple or Closed Fracture: The bone breaks without puncturing the skin.

    Compound or Open Fracture: The broken bone protrudes through the skin, increasing the risk of infection.

    Transverse Fracture: The break occurs horizontally across the bone.

    Oblique Fracture: The break is at an angle across the bone.

    Comminuted Fracture: The bone shatters into multiple pieces.

    Greenstick Fracture: Common in children, where the bone bends and cracks but doesn't fully break.

    Compression Fracture: Common in the spine, involving a loss of height in the vertebral body.

    Stress Fracture: Tiny cracks in the bone due to repetitive stress or overuse, often seen in athletes.

    Describe the anatomy of a hip joint.

    Acetabulum: The socket-shaped cavity in the pelvis, formed by the fusion of three bones: ilium, ischium, and pubis. It accommodates the rounded head of the femur.

    Femoral Head: The ball-shaped top of the femur that fits into the acetabulum, creating the ball-and-socket joint.

    Articular Cartilage: Covers the surfaces of the acetabulum and the femoral head, providing a smooth, low-friction surface for movement.

    Ligaments: Several strong ligaments provide stability and support to the hip joint, including the iliofemoral, pubofemoral, ischiofemoral, and ligamentum teres.

    Labrum: A ring of cartilage that surrounds the acetabulum, deepening the socket and providing stability to the joint.

    Synovial Membrane: The inner lining of the joint capsule that produces synovial fluid, reducing friction and providing nourishment to the joint.

    What are the differences between an intracapsular and extra-capsular hip fracture? How does this affect management?

    Intracapsular Fracture:

    Location: Occurs at or within the hip joint capsule, specifically involving the femoral neck or the head of the femur.

    Effect on Blood Supply: Intracapsular fractures may disrupt the blood supply to the femoral head, potentially leading to avascular necrosis (loss of blood flow and subsequent death of bone tissue).

    Management Challenges: These fractures might necessitate surgical intervention, such as pinning, screw fixation, or replacement. However, the blood supply concerns can make healing more complex.

    Extracapsular Fracture:

    Location: Occurs outside the joint capsule, typically along the trochanteric or subtrochanteric region of the femur.

    Effect on Blood Supply: As these fractures are outside the capsule, the blood supply to the femoral head remains unaffected.

    Management: Extracapsular fractures are often more stable and tend to heal better than intracapsular fractures. Surgical treatment usually involves fixation using devices like screws, plates, or nails.

    When are total hip replacements preferred more than partial hip replacements? Vice-versa.

    Total Hip Replacement (THA):

    Preferred when the entire hip joint is damaged due to conditions like severe osteoarthritis, rheumatoid arthritis, avascular necrosis, or fractures that involve both the femoral head and acetabulum.

    Generally suitable for cases where both the femoral head and the acetabulum are significantly affected, requiring complete joint replacement.

    THA replaces both the femoral head and the hip socket (acetabulum) with artificial components.

    Partial Hip Replacement (Hemiarthroplasty):

    Preferable when only the femoral head is damaged or fractured, such as femoral neck fractures, and the acetabulum or hip socket is healthy.

    Appropriate for older, less active patients, especially with femoral neck fractures, where replacing only the femoral head may be sufficient.

    Hemiarthroplasty involves replacing the femoral head with a prosthesis, leaving the natural socket intact.

    How does a bone heal?

    Bone healing involves stages:

    Inflammation and blood clot formation.

    Soft callus formation with collagen.

    Hard callus formation with new bone.

    Bone remodeling to restore original form.

    What are the risk factors for fractures?

    Osteoporosis: Weakening of bones, especially in older individuals, which makes them more susceptible to fractures.

    Age: Advanced age increases the risk due to bone density reduction and the potential for reduced balance and coordination.

    Gender: Women are at a higher risk, particularly after menopause due to decreased estrogen levels that can lead to bone loss.

    Trauma or Falls: Accidents, falls, or high-impact injuries can lead to fractures, especially in vulnerable populations like the elderly.

    Medical Conditions: Certain medical conditions, such as osteogenesis imperfecta, cancer, or conditions affecting bone strength, can increase fracture risk.

    Medications: Prolonged use of certain medications like corticosteroids can weaken bones, elevating the risk of fractures.

    Lifestyle Factors: Lack of physical activity, poor nutrition, smoking, excessive alcohol consumption, and inadequate calcium and vitamin D intake can also contribute to increased fracture risk.

    What is the garden classification, e.g. for an intra-capsular neck of femur fracture?

    Garden I: This stage represents an incomplete fracture with minimal displacement or an incomplete fracture without any displacement.

    Garden II: It refers to a complete fracture with minimal displacement. The bone is completely fractured but remains relatively aligned.

    Garden III: In this stage, a complete fracture shows moderate displacement. The bone alignment is partially shifted.

    Garden IV: This stage indicates a complete fracture with severe displacement. The bone fragments are significantly displaced or completely separated.

    What are the complications of hip fractures?

    DVT (Deep Vein Thrombosis) and Pulmonary Embolism: Blood clots in the deep veins of the legs may form and travel to the lungs, causing a potentially life-threatening pulmonary embolism.

    Infection: Surgery and hospitalization increase the risk of infections, such as urinary tract infections or surgical site infections.

    Bedsores (Pressure Ulcers): Immobile patients are at risk of developing pressure ulcers due to prolonged bed rest.

    Pneumonia: Reduced mobility, particularly in elderly patients, can lead to an increased risk of developing pneumonia.

    Heterotopic Ossification: Abnormal bone formation in the soft tissues around the hip joint, leading to restricted movement.

    Muscle Weakness and Atrophy: Lack of mobility after a hip fracture can cause muscle weakness and wasting in the affected limb.

    Dislocation or Mal-union of Fracture: Improper healing or displacement of the fracture fragments can lead to mal-union or dislocation, affecting function.

    Chronic Pain or Disability: Inadequate healing, complications, or delayed rehabilitation may lead to chronic pain or permanent disability.

    What medications can increase the chances of falls/fractures?

    Benzodiazepines and Sleep Medications: These drugs used for anxiety, insomnia, or sedation can cause drowsiness, impaired coordination, and balance issues.

    Opioids: Medications like morphine, oxycodone, or hydrocodone used for pain relief can cause dizziness, sedation, and a higher risk of falls.

    Antidepressants: Some antidepressants, especially tricyclic antidepressants, can cause dizziness and orthostatic hypotension, increasing the risk of falls.

    Antipsychotics: Certain antipsychotic medications can affect balance and increase the risk of falls, particularly in the elderly.

    Antihypertensive Medications: Blood pressure medications might lead to orthostatic hypotension, causing dizziness upon standing and increasing the risk of falls.

    Antiepileptic Drugs: Medications used to manage seizures can cause dizziness or drowsiness, increasing the risk of falls.

    Corticosteroids: Long-term use of corticosteroids may decrease bone density, leading to an increased risk of fractures.

    What does fall assessment involve?

    Medical History: Reviewing medical conditions, medications, previous falls, and any specific concerns related to balance or mobility.

    Physical Examination: Assessing gait, balance, muscle strength, joint mobility, vision, and neurological functions.

    Home Safety Evaluation: Examining the home environment for potential hazards that might contribute to falls, such as loose rugs, poor lighting, or slippery surfaces.

    Medication Review: Evaluating the medications an individual is taking, as certain drugs can increase the risk of falls.

    Cognitive Assessment: Checking cognitive functions, especially in older adults, to assess mental alertness and decision-making abilities that might impact fall risk.

    Footwear Evaluation: Assessing the suitability of footwear, ensuring proper support and comfort.

    Functional Assessment: Evaluating an individual's ability to perform activities of daily living, such as standing from a seated position or walking up and down stairs.

    Balance and Mobility Testing: Conducting specific tests to evaluate balance, mobility, and risk of falls.

    Nutritional Assessment: Assessing nutritional status, particularly deficiencies that might affect muscle strength and bone health.

    B Stations

  • Orthopedic
    A admin

    Anterior Cruciate Ligament (ACL) Injury

    Doctor Instruction:

    You are an Emergency Department Doctor. Your next patient is a 28-year-old gentleman, Glen, presenting with knee pain. Please take a history and perform an appropriate examination.

    Patient History:

    Your name is Glen - a 28-year-old male- accountant.

    You remember while playing football on a grass pitch about 2 hours ago when you were tackled by an aggressive player wearing cleats from your front. It was raining heavily, and you slipped following the tackle and heard a pop sound. Following this, you suddenly developed pain in your right knee, which is worsening. 9/10 pain score. No radiation. Pain is worsened by movement, and you try to take some simple pain killers i.e. paracetamol and ibuprofen, without much effects. Your knee has also been getting more swollen rapidly at the same time when the pain started, and you were unable to carry on with the match and therefore decided to go to the hospital.

    You feel unsteady in the right knee. You do not have the confidence to walk without any support. You feel your right knee is weak and is giving way.

    No locking. No fever. No weight loss. No previous night pains. No previous knee pain before the injury. No back pains. No other previous injuries. No neurological symptoms

    Ideas, Concerns, Expectations:

    You think you might have snapped a tendon or something, but you are not sure. You are concerned about how this will affect your future ability to play sports and walk. You hope to find out what is happening – maybe have a scan or something.

    Past Medical History:

    Nil significant

    Drug History:

    Nil NKDA

    Family History:

    Osteoarthritis

    Social History:

    You work as an accountant. You live by yourself. You smoke 5 cigarettes daily for 2 years but aim to stop smoking. You occasionally drink a few pints of beer over the weekend.

    Examination Findings:

    Right knee – swelling, tenderness on touch + worsened by movement.

    Anterior drawer test (right) – positive (tibia moving excessively anterior with no clear endpoint while being pulled).

    Lachman test (right)- positive (increased movement/laxity between tibia and femur).

    Pivot shift test (right) – positive (internally rotate foot and tibia and apply abduction force at the knee + then flex the knee from 0° to 30° to detect any reduction between femur and tibia).

    Antalgic Gait/ unsteady gait. Tenderness at lateral femoral condyle, lateral tibial plateau. (right)

    McMurray Test negative (to check for a tear in the meniscus).

    Differentials:

    ACL Tear / Damage

    Fracture

    Patellar subluxation / dislocation

    Meniscal Tear

    Posterior capsular sprain

    To rule out other ligament / articular chondral/ osteochondral injuries

    Investigations:

    MRI Scan (first-line imaging for evaluating internal derangement of the knee)

    XR knee (can use Ottawa Knee Rules to decide if this is indicated: if patient unable to bear weight, flex knee to 90°, tenderness at the head of the fibula, isolated tenderness in patella, age 55 or over) – to look for impaction fracture of lateral femoral condyle + posterior aspect of lateral tibial plateau, anterior subluxation of tibia on femur, effusion, bony avulsion of ACL

    Arthroscopy (to visualise ligaments – gold standard).

    Consider knee joint aspiration for both diagnostic i.e. infection + therapeutic

    Management:

    Referral to orthopaedics

    Conservative:

    PRICER (Protect, Rest, Ice, Compression, Elevation, Rehabilitation)

    Analgesia i.e. NSAID: diclofenac, ibuprofen, naproxenKnee braces/ Crutches (protect knee while mobilising + non-weight bearing restriction)

    Physiotherapy

    Surgical:

    Ligament reconstruction (arthroscopic surgery) – In complete rupture where no local healing is detectable, a graft of tendon from another ligament is used to form a new ligament. The type and timing of surgery depend on patient activity levels + severity of ligament injury. Some patients can be managed conservatively alone.

    Viva Questions:

    Explain the pathophysiology of an ACL tear.

    An ACL tear typically occurs due to sudden trauma, such as a forceful twist or direct impact to the knee during sports or activities. This stress leads to the ligament partially tearing or completely rupturing.

    Describe the anatomy of the knee.

    Bones: Femur (thigh bone), Tibia (shinbone), and Patella (kneecap).

    Articular Cartilage: Provides a smooth surface for movement.

    Menisci: Cartilage discs acting as shock absorbers.

    Ligaments: ACL and PCL inside the joint, MCL and LCL on the sides, providing stability.

    Muscles and Tendons: Quadriceps, hamstrings, and associated tendons for movement and support.

    Name the ligaments of the knee and their roles.

    ACL (Anterior Cruciate Ligament): Prevents excessive forward movement and rotational instability in the knee.

    PCL (Posterior Cruciate Ligament): Limits excessive backward movement and stabilizes the knee against various forces.

    MCL (Medial Collateral Ligament): Resists inward forces and stabilizes the inner part of the knee.

    LCL (Lateral Collateral Ligament): Provides stability against outward forces and supports the outer part of the knee.

    What are the complications of ACL Injury?

    Knee instability, making movements challenging.

    Increased risk of secondary knee injuries.

    Potential early development of osteoarthritis.

    Reduced knee mobility and function.

    Muscle weakness and possible psychological impact.

    B Stations

  • Orthopedic
    A admin

    Acute Compartment Syndrome

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 26-year-old gentleman presenting with leg pain. Please take a history and perform an appropriate examination.

    Patient History

    Your name is Joe – a 26-year-old rugby player.

    While playing rugby 1-2 hours ago, you tripped and fell over while running at high speed after being tackled. Afterwards, You noticed severe pain in your right lower leg following the accident – rating it 10/10. The pain also tends to radiate up and down the leg. It is worsened by any movement. Your coach thinks you fractured one of your bones in the leg and therefore called for an ambulance. Since then, you put a tight splint in place to help stabilise a potential fracture and stop it from getting any worse. You were given morphine in the ambulance which helped a bit.

    Since the injury, you can feel numbness and tingling sensation over the lower right leg, it is also becoming increasingly pale and swollen. You are unsure if there's any weakness as it is too painful to move your leg. Your calf feels extremely tight.

    No fever. No recent infection. No rigours. No involvement in joints.

    Ideas, Concerns, Expectations:

    You think you have a fracture for sure because of the pain you are having. You are concerned because it is getting worse, and you start to not be able to feel the leg, and it is getting more swollen. You hope to get this fixed as soon as possible in any way and want a stronger pain killer. You cannot bear this anymore!

    Past Medical History:

    Von Willebrand disease

    Drug History:

    Nil Adverse reaction to penicillin (sickness)

    Family History:

    Nil significant

    Social History:

    You work as a chef in a busy restaurant in town.

    You do not smoke or drink.

    You live with your partner in a flat currently.

    Examination Findings:

    Tenderness on palpation on the lower leg (right) with swelling and paleness. Pulses are present at the posterior tibialis + dorsalis pedis and popliteal/femoral region. Weakness and limited movement in active/passive movement below the right ankle due to pain and swelling. Increased capillary refill time at right lower leg. Reduced sensation below the right ankle.

    Differentials:

    Compartment Syndrome secondary to trauma + worsened by splint

    Fracture

    Other soft tissue injuries

    Haematoma

    Investigations:

    Clinical diagnosis

    Urine dip (urine dip/urine myoglobin if rhabdomyolysis/ tissue necrosis is suspected)

    Bloods (routine bloods, blood culture if infection suspected, CK + U&Es)

    Needle manometry/ slit catheter/infusion techniques (to measure compartment pressure)

    XR (rule out fracture as a cause)

    US with doppler (exclude thrombus/occlusion)

    Consider MRI scan if unsure

    Management:

    Urgent orthopaedic referral for fasciotomy to relieve pressure within the compartment and restore blood flow + prevent tissue necrosis/permanent damage (to be done as soon as possible – within 6 hours) compartment is then explored to identify and debride necrotic tissues.

    Analgesia i.e. morphine sulphate

    Oral hydration +/- sodium bicarbonate (to achieve urine output of >0.5ml /kg + target urine pH 6.5)

    Remove any external dressing/bandages

    Elevate leg to heart level

    Maintain good blood pressure (avoiding hypotension)

    Continuous compartment pressure monitoring

    All potentially constricting dressing, splints, cases…etc. must be removed

    Amputation in delayed diagnosis / significant muscle necrosis

    Consider haemodialysis if patients are anuria unresponsive to hydration

    Viva Questions:

    Explain the pathophysiology of compartment syndrome.

    Compartment syndrome occurs when increased pressure within a muscle compartment restricts blood flow due to swelling from injury or exertion. This reduced blood flow leads to tissue damage and can become a medical emergency if not promptly treated.

    What are the four compartments of the lower leg?

    The lower leg subdivides into four compartments which are the anterior, lateral, superficial posterior and deep posterior compartments.

    What is chronic compartment syndrome?

    Chronic compartment syndrome involves increased pressure in a muscle compartment during exercise, leading to pain or cramping. Symptoms occur during activity and improve with rest. It often affects athletes and is managed with rest, activity modification, and sometimes surgery to release the pressure.

    What are the causes of acute compartment syndrome?

    Trauma or Injury: Fractures, crush injuries, severe bruising, or significant trauma that damages muscles, blood vessels, or nerves within a compartment can lead to swelling and increased pressure.

    Prolonged Compression: Prolonged pressure on a limb due to tight bandages, splints, or immobilization can restrict blood flow and lead to compartment syndrome.

    Reperfusion Injury: Restoration of blood flow following a period of reduced or absent circulation (as seen after a prolonged surgery or treatment for blocked arteries) can cause swelling and increased pressure in the compartment.

    Bleeding Disorders: Bleeding within a compartment due to coagulation disorders or anticoagulant therapy can cause increased pressure, especially if not adequately managed.

    Excessive Exercise: Rarely, extreme exertion or unaccustomed, vigorous exercise may lead to acute compartment syndrome, particularly in athletes.

    What are the complications of compartment syndrome?

    Tissue Damage: Insufficient blood flow due to increased pressure can cause tissue damage and cell death (necrosis) within the affected compartment.

    Nerve Damage: Prolonged pressure on nerves can result in sensory and motor deficits or even permanent nerve damage.

    Muscle Dysfunction: Severe cases can lead to impaired muscle function or muscle death, affecting strength and movement.

    Ischemia-Reperfusion Injury: When pressure is suddenly released, the influx of blood to the compromised tissue can lead to further damage or inflammation.

    Infection: In severe cases or if left untreated, tissue death can lead to an increased risk of infection or gangrene.

    Complications from Treatment: Surgical procedures to relieve compartment syndrome can lead to potential risks, such as infection or nerve damage.

    Long-Term Disability: Severe or untreated cases may result in long-term disability, affecting limb function and potentially requiring extensive rehabilitation.

    What are the late signs of compartment syndrome?

    Paresthesia: Numbness, tingling, or a "pins and needles" sensation in the affected area. This can indicate nerve damage due to compromised blood flow.

    Weakness or Paralysis: In advanced cases, there may be weakness or inability to move the affected area due to muscle and nerve damage.

    B Stations

  • Orthopedic
    A admin

    Rotator Cuff Tear

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is Joe- a 45-year-old gentleman presenting with shoulder pain. Please take a history and perform an appropriate examination.

    Patient History:

    Your name is Joe 45 year old – construction worker.

    Your right shoulder has been getting gradually worse every day. The right shoulder pain first started around a few months ago. The pain is sharp and does not radiate. You rate the pain as 7/10. It is worsened by movement and improved with rest.

    You play tennis regularly (if asked specifically, you are right-handed) but since the pain started, you no longer play as much with your mates, which is bothering you. You also have night pain around your right shoulder, which sometimes can make it difficult to fall asleep.

    You feel your right shoulder has weakened since the pain started, and you now struggle to lift your right arm up from your waist.

    No numbness/ tingling/ abnormal sensations in the limbs. You haven't noticed any shoulder mass, swelling, or deformity. No fever. No red skin. Other than the pain and shoulder weakness. You feel well in general. No night sweats/weight loss. No shortness of breath. No recent trauma or fall. No neck pain. No previous history of fracture/ dislocation. No stiffness.

    Ideas, Concerns, Expectations:

    You have no idea what is going on - you are usually fit as a fiddle. You are concerned that the pain is causing many physical problems at work ( you work as a construction worker). You are now unable to lift any heavy objects with your right arm due to the pain. You hope to get better as soon as possible.

    Past Medical History:

    Nil

    Drug History:

    Nil

    NDKA

    Family History:

    Rheumatoid arthritis

    Type 2 diabetes

    Social History:

    You work as a construction worker, which often involves lifting heavy objects.

    You smoke around 5-10 cigarettes a day for ten years.

    You occasionally drink around 1-2 pints of beer when going out with friends for a meal.

    Examination Findings:

    Pain and weakness in initiating shoulder abduction – indicating supraspinatus tear. Tenderness over rotator cuff structure on palpation. Muscle wasting at regions of the right rotator cuff muscles might be present.

    Drop arm test positive (passively abduct shoulder, then ask patient to lower abducted arm slowly to the waist. If arm drops after reaching 90degree- indicates massive rotator cuff tear)

    Pain elicited and range of movement limited by pain in shoulder movements.

    Cross-arm test – negative (acromioclavicular problems). No shoulder pain arc elicited (70° – 120°) (subacromial impingement). No localised pain/tenderness over the acromioclavicular joint and no restriction of passive, horizontal movement of the arm across the body when the elbow is extended (acromioclavicular disorder).

    Differentials:

    Rotator cuff disorders: rotator cuff Injury/ tear, tendonitis…etc.

    To rule out rotator cuff rupture

    Other considerations:

    Fracture

    Adhesive capsulitis

    Osteoarthritis

    To rule out joint infection/dislocation

    Investigations:

    Bedside:

    Observations

    Bloods:

    Consider routine blood tests for baseline

    Imaging:

    Consider XR Shoulder to exclude bony pathology e.g. fracture/osteoarthritis/dislocation/opacities in calcific tendonitis/ anatomical abnormalities such as superior migration of humeral head relative to glenoid, pseudo subluxation of the humeral head relative to glenoid.

    U/S to assess rotator cuff structure / detect tears, effusion

    MRI shoulder to look for any underlying soft tissue shoulder pathology, i.e. shoulder instability, full/ partial tears, effusion…etc.

    MR/CT arthrography – to look for tears/effusion if appropriate

    If referred neck pain is suspected, consider cervical spine XR

    Management (Rorator Cuff Injury):

    Conservative:

    Patient Education

    Consider psychosocial support if appropriate i.e. stress, job pressure, job satisfaction

    Rest and adapted activities e.g. at work/home/hobbies – avoid overhead activities

    Analgesia e.g. NSAID (ibuprofen, diclofenac, naproxen) / opioids +/- PPI cover

    Ice Packs – reduce pain

    Physiotherapy to optimise shoulder function

    Consider occupational therapy input

    Consider sling if an acromioclavicular joint injury is suspected

    Surgical:

    Consider referral to orthopaedics for rotator cuff disorder or in suspected joint infection, unreduced dislocation or acute trauma

    Consider subacromial steroid injections – symptomatic relief (Avoid if significant rotator cuff tear is suspected) – patient will continue to have weakness despite pain relief.

    Consider suprascapular nerve block

    Arthroscopic rotator cuff repair depending on the degree of tendon damage

    Consider joint aspiration or lavage in patients with calcified tendonitis

    Viva Questions:

    Explain the pathophysiology of a rotator cuff tear.

    A rotator cuff tear involves:

    Mechanical Stress: Repetitive use or acute injury causes stress on the rotator cuff tendons, leading to microtears.

    Degeneration: Cumulative wear and tear can weaken the tendons, making them more prone to tearing.

    Acute Trauma: Sudden force or injury can also cause an immediate tear in the tendons.

    Reduced Healing Capacity: Tendons may have limited blood supply, hindering their natural healing process, leading to a partial or complete tear.

    Explain the anatomy of the shoulder joint and surrounding structure.

    The shoulder joint and surrounding structures include:

    Bones: Humerus, scapula, and clavicle.

    Glenohumeral Joint: Where the humerus fits into the scapula's socket.

    Rotator Cuff: Group of muscles and tendons stabilizing the joint.

    Labrum: Cartilage rim supporting the joint.

    Bursae: Fluid-filled sacs reducing friction.

    Ligaments, Muscles, Tendons: Supporting and connecting structures for stability and movement.

    Name the rotator cuff muscles and their function.

    Supraspinatus: Located on the top of the shoulder blade, this muscle initiates the abduction (raising the arm sideways) of the arm and assists in stabilizing the shoulder joint.

    Infraspinatus: Positioned on the back of the shoulder blade, it aids in external rotation of the arm (outward rotation) and contributes to shoulder joint stability.

    Teres Minor: Situated beneath the infraspinatus, this muscle also contributes to the external rotation of the arm and helps in stabilizing the shoulder.

    Subscapularis: Positioned on the front of the shoulder blade, it is responsible for internal rotation of the arm and stabilization of the shoulder joint.

    What are the risk factors for shoulder pain?

    Age: As individuals get older, the risk of shoulder pain due to wear and tear on the joints increases.

    Overuse and Repetitive Movements: Activities involving repetitive overhead motion or lifting can strain the shoulder muscles and tendons, leading to pain.

    Poor Posture: Incorrect posture while sitting or standing can contribute to shoulder strain and discomfort.

    Muscle Imbalances: Weakness or imbalance in the muscles around the shoulder can lead to instability and pain.

    Trauma or Injury: Falls, accidents, or direct impact can result in shoulder injuries and subsequent pain.

    Medical Conditions: Conditions like arthritis, tendonitis, bursitis, or rotator cuff tears can lead to shoulder pain.

    Lifestyle Factors: Factors such as smoking, obesity, and inadequate physical conditioning can contribute to shoulder issues.

    Which soft tissues heal slowly and why?

    Tendons: Tendons are the connective tissues that attach muscles to bones. They have relatively poor blood supply, which can slow down the healing process. Limited blood flow restricts the delivery of nutrients and oxygen necessary for efficient healing.

    Ligaments: Ligaments are another type of connective tissue that connects bones to other bones, providing joint stability. Similarly, they have a relatively low blood supply, hindering the healing process.

    Cartilage: Cartilage is a firm, rubbery tissue found in joints, providing cushioning and facilitating smooth movement. Due to its avascular nature (lack of blood vessels), cartilage has a limited ability to repair itself, leading to slow healing in case of injury.

    B Stations

  • Orthopedic
    A admin

    Achilles' Tendinopathy

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is Ed, a 26-year-old gentleman presenting with ankle pain. Please take a history and perform a relevant examination.

    Patient History:

    Your name is Ed, a 26-year-old professional tennis player.

    Over the past few weeks, you noticed that your left ankle pain has gradually worsened. It's getting more painful at the heel and worsens whenever you try to play more tennis. You tried to use some ibuprofen gel which only improved the pain slightly. You rate the pain as 5/10 on average, but when it is worse, it can go up to a 7/10. The pain doesn't radiate anywhere. Your left ankle is also becoming gradually more swollen than usual. Because of this, you have been having trouble walking and running especially during tennis practices.

    The movement of your left ankle is limited due to pain in all directions. You feel your left foot has gotten weaker, especially while pushing off the ground. You are not sure if you have ruptured any tendons - you hope not, as your profession is being a sportsman. No injuries you can recall, but you play tennis a lot.

    No fever, but recently, you were diagnosed with prostatitis and were given antibiotics.

    Ideas, Concerns, Expectations:

    You don't know, but you think you might have accidentally injured your left ankle without yourself noticing. You are concerned that it is becoming more difficult to continue playing tennis because of the pain and swelling in your left ankle. You want to know what is causing the problem and have a scan or some sort.

    Past Medical History:

    Ankylosing spondylitis, type 1 diabetes

    Drug History:

    Ciprofloxacin (for recent prostatitis five days ago).

    Allergic to penicillin (Rash)

    Family History:

    Rheumatoid Arthritis

    Social History:

    You live with your parents. You think you are very healthy.

    You do not smoke or drink.

    You currently play tennis professionally.

    Generally independent at home.

    Examination Findings:

    When Achilles is relaxed in a dangled position, the ankle is hyper-dorsiflexed

    Altered gait (weakness in pushing off with the affected left foot; worse during tiptoeing)

    Tenderness is noted in the left ankle region with posteriorly localised swelling

    A palpable defect in the Achilles tendon (but no rupture)

    Limited movement in ankle movement due to pain.

    Weakness in left ankle plantar flexion

    Simmond 's calf squeeze test / Thompson test – negative in tendinopathy (but positive in rupture)

    No tenderness or warmth palpating the calcaneus region. No crepitus. No obvious deformity, no nodularity or thickening on palpation of the Achilles tendon.

    Differentials:

    Achilles Tendinopathy

    Tendon Rupture

    MSK sprains and strains

    Retro calcaneal bursitis

    Investigations:

    Clinical diagnosis

    Observations

    XR foot/ankle: fractures/ calcific tendinopathy / talar shift

    US ankle – to rule out Achilles tendon tendinopathy /rupture

    MRI ankle – if the diagnosis is unclear (to rule out tendinopathy/rupture)

    Consider diagnostic arthroscopy if appropriate

    Management (Achilles Tendinopathy):

    Conservative:

    Rest + immobilisation e.g. applying specialist boot first involving from full plantar flexion of the ankle to neutral position - can take 6-12 weeks for Achilles tendon to heal in tendinopathy

    Night splints to hold the foot in a neutral position to dorsiflexion to main passive dorsiflexion

    Ice / Analgesia e.g.. NSAIDs

    Elevation to reduce swelling

    Heel lifts (orthotic devices to prevent gait imbalance)

    VTE prophylaxis

    Protective footwear

    Physiotherapy input + rehabilitation e.g. gentle stretching, eccentric heel-drop exercises…etc.

    Consider casting for resistant Achilles tendinopathy

    If ruptured:

    Period of non-weight bearing and a brace (orthosis) or plaster cast, surgical review for intervention, followed by early weight-bearing and mobilisation using removable orthosis for 4- 6 weeks.

    Medical:

    Consider glyceryl trinitrate transdermal (to decrease pain by improving tendon healing)

    Surgery (especially those with a high level of physical activity/ competitive athletes/ recurrent rupture):

    Orthopaedic referral

    Reattaching / repair of Achilles Tendon

    Excision of fibrous adhesion/ degenerative nodules

    Tendon stripping

    Percutaneous tenotomy

    Other considerations:

    Consider autologous blood injection (whole blood/ platelet-rich plasma containing growth factors)

    Consider low-level laser therapy to treat pain/disability in short-term

    Consider Extracorporeal shock wave therapy (ESWT) to reduce pain from tendinopathy

    Future Prevention:

    Stretching, warm-up exercises, and rehabilitation following minor injuries. Steroid injections are avoided due to increasing risk of tendon rupture.

    Viva Questions:

    What is the function of the Achilles tendon?

    The Achilles tendon is a strong fibrous band of tissue that connects the calf muscles (the gastrocnemius and soleus muscles) to the heel bone (the calcaneus). The primary function of the Achilles tendon is to facilitate movement by enabling the contraction of the calf muscles, allowing the foot to point downwards (plantarflexion) and providing the power necessary for activities such as pushing off the ground while walking or running.

    What are the risk factors for Achilles tendinopathy/rupture?

    The key risk factors for Achilles tendinopathy or rupture include:

    Overuse or sudden increase in physical activity.

    Age, with increased risk as individuals get older.

    Participation in sports, especially those involving jumping or sudden movements.

    Muscular imbalances, weakness, or tightness in the calf muscles.

    Improper footwear, training techniques, or biomechanical issues.

    Certain medical conditions or medications that weaken tendons.

    Previous history of tendon problems or injuries.

    Explain the pathophysiology of Achilles tendinopathy/ rupture.

    The pathophysiology of Achilles tendinopathy and rupture involves:

    Tendinopathy: Gradual breakdown due to repetitive stress, causing microtears and collagen fiber degeneration.

    Degeneration: Weakened tendon structure due to chronic overuse, leading to decreased capacity to handle stress.

    Inflammation: Early stages might involve inflammation, but chronic cases focus on failed healing responses.

    Rupture: Severe force or trauma, often in an already weakened tendon, can cause a partial or complete tear.

    Vascular Changes: Chronic tendinopathy can alter blood supply, impacting tendon health and healing.

    Describe the anatomy surrounding the Achilles tendon.

    The Achilles tendon, linking the calf muscles to the heel bone, is surrounded by:

    Gastrocnemius and Soleus Muscles: These form the tendon, enabling movement.

    Calcaneal Bursae: Fluid-filled sacs reducing friction.

    Paratenon: Thin sheath reducing friction around the tendon.

    Surrounding Ligaments, Muscles, Skin: Supporting structures and tissue of the ankle and heel region.

    What are the complications associated with Achilles tendinopathy/rupture?

    Complications associated with Achilles tendinopathy or rupture may include:

    Chronic Pain: Tendinopathy can cause persistent pain, discomfort, and stiffness, affecting mobility and daily activities.

    Reduced Functionality: Both tendinopathy and rupture can impair movement, such as walking, running, or jumping.

    Re-injury Risk: After healing, the Achilles tendon might remain vulnerable to re-injury or continued degeneration.

    Muscle Weakness: Reduced strength and function of the calf muscles due to limited use during recovery.

    Surgical Risks: In cases of severe rupture or chronic tendinopathy requiring surgery, potential risks associated with surgical intervention exist, including infection, nerve damage, or prolonged rehabilitation.

    Scar Tissue Formation: Following a rupture or surgery, scar tissue may form, affecting tendon flexibility and strength.

    Altered Gait: During recovery, individuals may experience changes in their gait, leading to imbalances or stress on other joints or muscles.

    Risk of DVT (Deep Vein Thrombosis): Immobilization or reduced mobility after a rupture or surgery might increase the risk of blood clot formation in the legs.

    B Stations

  • Orthopedic
    A admin

    Osteoarthritis

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is Jane, a 35-year-old woman presenting with joint pain. Please take a history and conduct a relevant examination.

    Patient History:

    Jane, 35 y/ F, dog trainer.

    For 8 months, you have been getting worsening knee pain in both knees. The pain is present on most days and worsens towards the end of the day. You spend most of the day on your feet as part of your job, and recently you have been progressively becoming less able to keep up with the demands of your work. To seek relief from the pain, you have to take frequent breaks throughout your work day, and this slows you down so much that you have been forced to cut down on the number of clients you see daily. You try to keep off your feet on the weekend and find that this helps limit the pain.

    Besides brief stiffness in your knees lasting less than 30 minutes in the morning, you don't have any other symptoms. You deny symptoms of locking or giving way, shortness of breath, chest pain, palpitations, rashes, visual problems, or changes in bowel habits. You have not had any recent short-lived episodes of illness.

    Ideas, Concerns, Expectations:

    You are worried that you have rheumatoid arthritis, as this is what your mother has. She is currently fully dependent on others for activities of daily living - this terrifies you as you do not want to be in her position when you reach her age. You would like to begin treatment as soon as possible to preserve your independence.

    Past Medical History:

    Obstructive sleep apnoea

    Polycystic ovarian syndrome

    Asthma – well-controlled. You haven’t used an inhaler in years!

    If asked about previous trauma, reveal that you tore your right knee meniscus during a hockey game as a teenager.

    Drug History:

    Lansoprazole

    No known drug allergies.

    Family History:

    Mother has rheumatoid arthritis.

    Father has oesophageal cancer.

    Social History:

    Non-smoker

    No recreational drug use

    You live at home with 3 dogs. You are independent in activities of daily living like shopping, cooking and cleaning.

    You work full-time as a dog trainer. As working has become increasingly difficult, lately you have been considering engaging in part-time work instead.

    Examination Findings:

    On general inspection:

    Large body habitus

    Gait is slow but symmetrical.

    On examination of the knees:

    There is no evidence of redness, swelling or heat bilaterally.

    No effusions can be detected on the patellar tap or sweep tests.

    Bilateral crepitus is ascertained on passive movement.

    There is pain in passive and active movement throughout the range of motion of both knees.

    Differentials:

    Osteoarthritis of the knees

    Rheumatoid arthritis

    Referred pain from the hip joint e.g. osteoarthritis of the hip, greater trochanteric pain syndrome

    The above history and examination are strongly suggestive of osteoarthritis. This is the most likely diagnosis despite the family history of rheumatoid arthritis. The presence of a past meniscal tear and current obesity can confer a higher risk of developing early-onset osteoarthritis – do not be deceived by the patient's age or family history!

    Investigations:

    Bedside:

    Measurement of BMI (obesity is associated with the development of osteoarthritis)

    Bloods:

    Inflammatory markers (usually normal in osteoarthritis)

    Serum autoantibodies (serum autoantibodies like rheumatoid factor and anti-CCP antibodies are negative in osteoarthritis )

    Imaging:

    X-rays of affected joints

    The 4 radiological features of osteoarthritis are:

    Loss of joint space

    Osteophytes

    Subchondral sclerosis

    Subchondral cysts

    Other investigations:

    Synovial fluid aspiration - carried out to investigate painful effusions

    Management:

    Conservative:

    Lifestyle measures

    Weight loss– obesity is a risk factor for osteoarthritis.

    Muscle strengthening exercises

    Walking aids: Shock-absorbing footwear, walking sticks

    Transcutaneous Electrical Nerve Stimulation

    Occupational health assessment: help with adapting work to the patient’s functional limitations.

    Physiotherapy: help with muscle strengthening exercises, stretching and provision of aids like joint supports.

    Podiatry: advice on footwear.

    Analgesia:

    Paracetamol and/or topical NSAIDs

    Consider substituting paracetamol or topical NSAIDs with oral NSAIDs +/- PPI co-prescription

    Add an opioid e.g. codeine

    Topical capsaicin

    Intra-articular corticosteroid injections

    Surgical:

    Surgical management of osteoarthritis can be considered if the patient's quality of life and pain control remain poor on conservative and medical management alone. The options include:

    Replacement arthroplasty

    Joint fusion

    Arthroscopic lavage and debridement

    Viva Questions:

    What are the ‘red flags’ of joint pain?

    Sudden, Severe Pain: Abrupt onset of intense joint pain that is not easily explained by an injury or overuse.

    Swelling and Redness: Unexplained swelling, warmth, or redness around the joint, which might be a sign of inflammation or infection.

    Fever and Chills: Joint pain accompanied by fever or chills could be indicative of an infection.

    Loss of Function: Significant loss of mobility or function in the joint, such as difficulty moving the joint, bending, or weight-bearing.

    Unexplained Weight Loss: Joint pain accompanied by unexplained weight loss could indicate systemic issues such as autoimmune diseases or malignancies.

    Multiple Joints Affected: If multiple joints are affected simultaneously or in quick succession, it might suggest conditions like rheumatoid arthritis, lupus, or other systemic autoimmune disorders.

    History of Cancer or Immunosuppression: Individuals with a history of cancer or those with weakened immune systems are at higher risk for certain joint-related complications.

    Pain at Rest or Night Pain: Joint pain that worsens at night or disturbs sleep might indicate inflammatory conditions.

    Numbness or Tingling: If joint pain is accompanied by numbness or tingling, it could indicate nerve involvement, such as in conditions like peripheral neuropathy.

    Skin Changes: Any changes in the skin overlying the joint, like rashes or lesions, might indicate a systemic issue affecting the joint.

    What are some examples of the different types of arthritis?

    Osteoarthritis (OA): This is the most common type of arthritis. It occurs due to the breakdown of cartilage in the joints, causing pain, stiffness, and reduced mobility.

    Rheumatoid Arthritis (RA): An autoimmune disorder that primarily affects the joints, causing inflammation, pain, and joint deformity.

    Psoriatic Arthritis: Associated with the skin condition psoriasis, it leads to joint pain, swelling, and stiffness, often affecting those with psoriasis.

    Juvenile Idiopathic Arthritis (JIA): Arthritis that affects children, causing joint inflammation and stiffness.

    Infectious/Septic Arthritis: Occurs due to a bacterial, viral, or fungal infection in the joints, leading to inflammation.

    Reactive Arthritis: Develops as a reaction to an infection in another part of the body, causing joint pain, swelling, and stiffness.

    What are the risk factors for osteoarthritis?

    Age: Risk increases with age.

    Obesity: Excess weight stresses joints.

    Joint Injuries: Previous injuries raise risk.

    Genetics: Family history can contribute.

    Occupation and Overuse: Repetitive stress in certain jobs or activities.

    Gender: More common in women, especially after menopause.

    Muscle Weakness: Weak muscles strain joints.

    Other Medical Conditions: Conditions like gout or rheumatoid arthritis can increase risk.

    Bone Deformities or Joint Alignment Issues: Misaligned joints or unusual bone shapes.

    Joint Stress: High-impact sports and activities can contribute.

    B Stations

  • Gen Surg
    A admin

    Gastro-Oesophageal Reflux Disease

    Doctor Instruction:

    You are a Foundation Year 1 Doctor working in the Emergency Department. Your next patient is a 42-year-old woman (Anne) presenting with abdominal pain. Please take a history and perform an appropriate examination.

    Patient History:

    Anne, a 42-year-old retired hairdresser.

    This morning at around 3am, you woke up from having tummy pain. Described as a sharp/burning sensation that started at the bottom chest centrally and radiated up to the neck. It is intermittent and lasts for a few seconds. Pain score: 5/10. You are known to have angina, and so you took a GTN spray, but it didn't help. You feel a bit nauseous but no vomiting; you had some retching (and a bad taste in the back of the throat). Pain tends to be worsened or triggered when you try to go back to bed and lay flat.

    If asked specifically, you remember having quite a big family meal when your friend came to visit the night before.

    No weight loss. No tiredness. No erosion in teeth. No bad-smelling mouth. No lump in the throat. No bloating. No nocturnal cough. No hoarse voice. Bowels working normally with no bloody stool. No breathing difficulty. No dysphagia. No LOC. No dizziness. No palpitation. No obvious chest pain.

    Ideas, Concerns, Expectations:

    You are not sure what is going on. You are worried that you had a heart attack and may die because of this since it is quite close to the chest. You want to be seen by a cardiologist and have some medications to help prevent having this pain again. You want to live!

    Past Medical History:

    Hypertension

    Stable angina - well-controlled

    Obesity

    Chronic Lower Back Pain

    Drug History:

    Amlodipine, GTN spray PRN, Atovastatin, ibuprofen

    NKDA

    Family History:

    Type 2 DM (Dad, age 44)

    Colon Cancer (Dad, age 65)

    Social History:

    Smoker – 10 cigarettes/day for 20 + years

    Drink a small glass of gin and tonic every night

    Hairdresser

    Drink 2 cups of coffee a day.

    Examination Findings:

    The patient is alert + comfortable at rest, with no signs of breathing difficulties.

    No clinical signs of anaemia.

    Some mild discomfort palpating the epigastric region.

    Abdominal examination is otherwise normal.

    PR exam is normal - no melena or blood in the stool.

    Differentials:

    GORD

    Gastritis

    Peptic ulcer

    Hiatus Hernia

    Oesophagitis / Oesophageal spasm

    To rule out cardiovascular causes: Stable Angina / ACS / AAA

    Investigations:

    Bedside:

    Observations

    ECG – rule out cardiac cause

    Bloods:

    FBC, CRP, U&Es, LFTs, Bone Profile, Troponin (if suspecting cardiac cause)

    Imaging:

    CXR/AXR (?Hiatus hernia)

    Special Tests:

    Consider serology/ urea breath test/ stool antigen, rapid urease test (H-pylori testing - ensure not taken PPI 2 weeks prior to testing)

    Barium swallow - assess dynamics, assess motility disorder, assess for hiatus hernia

    Oesophageal pH monitoring / Manometry - Assess for motility & regurgitative Disorders

    Consider OGD (Savary-Miller grading/ Los Angeles Classification) - allows direct visualisation and biopsy for histology.

    Data Interpretation:

    Patient Details: Alexander Great

    Age: 42

    Date of Request: 18/04/2023

    ​

    Value

    Reference Range

    ​

    Hb

    125 g/L

    115 - 165 g/L

    ​

    White Cell Count

    7.5 x10^9/L

    3.6 - 11.0 x10^9/L

    ​

    Platelets

    257 x10^9/L

    140 - 400 x10^9/L

    ​

    Haematocrit

    0.47 x10^12/L

    0.40 - 0.54 x10^12/L

    ​

    MCV

    94 fL

    80 - 100 fL

    ​

    Neutrophils

    3.7 x10^9/L

    1 - 7.5 x10^9/L

    ​

    Monocytes

    0.7 x10^9/L

    0.2 - 0.8 x10^9/L

    ​

    Lymphocytes

    3 x10^9/L

    1 - 4 x10^9/L

    ​

    Basophils

    0.03 x10^9/L

    0.02 - 0.1

    ​

    Eosinophils

    0.1

    0.1 - 0.4

    ​

    ​

    ​

    ​

    ​

    H. Pylori Stool Antigen Test

    Negative

    ​

    Interpretation of Blood Results:

    ree

    Interpretation of OGD Image:

    Management (GORD):

    Conservative:

    Lifestyle changes: stop smoking, weight loss, reduce alcohol intake, sleep more upright, small + regular meals, avoid eating big meals/ alcohol/ hot drinks before bed, avoid triggering diet e.g. spicy food, citrus, chocolate, caffeine, carbonated drinks, alcohol, manage stress level

    Review medications that can cause reflux, e.g. NSAID, steroids, bisphosphonates, nitrates, calcium channel blockers, alpha/beta agonists, theophylline, anticholinergics

    Antacids e.g. Gaviscon

    PPI e.g. omeprazole

    H2 antagonist e.g. Ranitidine

    Patient Education

    Safety netting for uncontrolled and red flag symptoms e.g. ACS

    Medical:

    Eradication therapy if tested positive for H. Pylori (PPI plus 2 antibiotics e.g. amoxicillin and clarithromycin) for 7 days.

    Surgical:

    Surgery for reflux e.g. fundoplication, magnetic sphincter augmentation.

    Viva questions:

    What are the complications of untreated acid reflux?

    Esophagitis: Inflammation and pain in the esophagus.

    Barrett's Esophagus: Increased risk of esophageal cancer.

    Strictures: Narrowing of the esophagus.

    Esophageal Ulcers: Painful sores in the esophagus.

    Respiratory Issues: Coughing, wheezing, and asthma exacerbation.

    Dental Problems: Tooth enamel erosion and oral health issues.

    Chronic Cough: Persistent cough unrelated to respiratory problems.

    Laryngitis/Voice Changes: Hoarseness and vocal cord inflammation.

    Asthma Aggravation: Worsening of asthma symptoms.

    Difficulty Swallowing: Dysphagia due to esophageal changes.

    Esophageal Cancer: Increased cancer risk over time.

    What are the complications of long-term management with omeprazole?

    Electrolyte disturbance e.g. magnesium

    Low bone mineral density - interference in gastric pH which can alter calcium absorption

    What is Barrett's Oesophagus?

    Barrett's esophagus develops due to chronic acid reflux (GERD). Acid irritates the esophagus, prompting the lining to transform into a type more resistant to acid, called columnar cells. This change is known as metaplasia, resulting in Barrett's epithelium. This condition increases the risk of esophageal cancer, making regular monitoring crucial.

    What are the red flag symptoms or signs for urgent OGD?

    Haematemesis or melena

    Dysphagia

    Unintentional weight loss

    Treatment-resistant

    Early satiety

    Recurrent vomitting

    B Stations

  • Gen Surg
    A admin

    Haemorrhoids

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 45-year-old male called Alex, presenting with constipation. Please take a history and perform an appropriate examination.

    Patient History:

    45-year-old male, Alex, a bodybuilder.

    In the past few weeks, you have been getting worsening constipation. You are not sure why. You usually eat healthily and avoid junk food. Yesterday, you noticed bright red blood on the toilet tissue paper while trying to wipe yourself, and you saw your stool was coated with fresh blood! You were very shocked because of this. You are not sure if this is yet another flare of your IBD - but you have no tummy pain, and you feel well. Your IBD is usually well controlled with azathioprine. Straining in the toilet can sometimes make your anus slightly sore – you feel like there’s something in your anus, but you are not sure if there's anything. You don’t want to look at your anus or feel around it with your finger – yuck! This grosses you out.

    You do have a sensation that your back passage is always full, especially when you strain yourself, and this is starting to affect your ability to work out at the gym. You can sometimes soil yourself by chance – which is embarrassing!

    Not sexually active currently. No weight loss. No night sweats. No abdomen pain. No nausea or vomiting. No fever. No SOB. No tiredness. Good energy level.

    Ideas, Concerns, Expectations:

    You have no idea what this might be; it might be another flare of your IBD. You are, however, worried that you might have cancer because your dad developed bowel cancer and died. You do not want to die so soon! You are still looking for the "one" to marry and happily live with!

    Past Medical History:

    Ulcerative colitis

    Drug History:

    Azathioprine.

    Allergic to penicillin (anaphylactic reaction)

    Family History:

    Bowel cancer (father)

    Social History:

    You work in the gym and often travel to different countries to enter bodybuilding competitions – you have won so many trophies since you were a teenager - you are quite proud of your achievements. You live alone in a flat. You do not smoke or drink. You are generally independent and manage well at home.

    Examination Findings:

    The abdomen is soft and non-tender. Bowel sound present.

    Digital Rectal Examination: non-tender wart-shaped swelling can be felt at the 3 o’clock position proximal to the anal verge – if ask the patient to strain, the swelling becomes visible at the anal verge- appearing bluish, bulging vessels covered with mucosa. No other internal/ external / prolapsed masses can be seen or felt. The prostate gland is normal. Normal anal tone. No PR bleeding or melena.

    Differentials:

    Haemorrhoid (non-thrombosed)

    To rule out Colorectal Cancer

    Inflammatory Bowel Disease

    Anal Fissures

    Diverticulosis

    Investigations:

    Observations (assess haemodynamic stability and rule out fever)

    Proctoscopy to visualise swelling at the rectum

    Consider FIT testing if rectal bleeding is not confirmed

    Consider Faecal calprotectin – (higher level, more severe IBD)

    Consider FBC + iron studies for anaemia (if prolonged PR bleeding + signs of anaemia/infection), CRP (raised in active IBD), baseline bloods: U&Es, LFT, Bone profile, coagulation screen.

    Consider Colonoscopy / flexible sigmoidoscopy to exclude other serious pathology and confirm the diagnosis with biopsy i.e. IBD and cancer.

    Consider anorectal physiological studies or anorectal US if associated with soiling/incontinence.

    Management:

    2ww referral if suspecting Lower GI Cancer

    Simple analgesia e.g. paracetamol, ice packs if required

    Topical treatment to reduce swelling/ pain of haemorrhoids: Anusol (astringent), Anusol HC (hydrocortisone), Hermoloids Cream (lidocaine), Proctosedyl Ointment (cinchocaine + hydrocortisone) - care should be taken how long the course should be

    To treat constipation: increasing fibre in diet e.g. raw fruits, vegetables, fibre supplements, hydration, laxative when required – bulk-forming laxative such as ispaghula husk. Alternatives include lactulose or sodium docusate, avoiding straining while opening bowels, avoid too much caffeine or alcohol.

    Non-surgical treatments of haemorrhoids: rubber band ligation (cut off blood supply by fitting a tight rubber band at the base of haemorrhoid), injection sclerotherapy (injection of phenol oil causing sclerosis and atrophy), infra-red coagulation (to damage blood supply of haemorrhoids), bipolar diathermy (electrical current to remove haemorrhoids)

    Surgical treatment of haemorrhoids: haemorrhoidal artery ligation (cutting off blood supply), haemorrhoidectomy, stapled haemorrhoidopexy

    Consider admission to those presenting with thrombosed haemorrhoids for excision under local anaesthetic/ incision and drainage of the clot

    Viva Questions:

    What are haemorrhoids?

    Hemorrhoids, also known as piles, are swollen and inflamed veins in the lower rectum and anus. They can be internal (inside the rectum) or external (under the skin around the anus). Common causes include increased pressure on the veins due to straining during bowel movements, chronic constipation or diarrhea, pregnancy, obesity, and prolonged sitting or standing. Symptoms may include pain, itching, bleeding during bowel movements, and discomfort. Treatment often involves dietary changes, improved hygiene, topical creams, and in severe cases, procedures to remove or shrink the hemorrhoids.

    What are thrombosed haemorrhoids?

    Thrombosed hemorrhoids are swollen and painful veins in the anal area that have a blood clot. They cause severe pain, swelling, and a hard lump near the anus.

    Where would you commonly find haemorrhoids in the rectum?

    Hemorrhoids can occur throughout the rectum, but they are most commonly found at positions like "3 o'clock" and "9 o'clock" inside the anus (internal) or outside the anus (external).

    What is the classification/grading of haemorrhoids?

    Hemorrhoids are often classified or graded based on their severity and the extent to which they protrude from the anal canal. The most commonly used classification system is the one developed by Goligher, which categorizes hemorrhoids into four grades:

    Grade I (First-degree hemorrhoids):
    Hemorrhoids that bleed but do not prolapse (protrude) or cause any significant protrusion.

    Grade II (Second-degree hemorrhoids):
    Hemorrhoids that prolapse during a bowel movement and retract spontaneously (go back inside) afterward.

    Grade III (Third-degree hemorrhoids):
    Hemorrhoids that prolapse during a bowel movement and require manual repositioning (pushed back inside) afterward.

    Grade IV (Fourth-degree hemorrhoids):
    Hemorrhoids that are always prolapsed and cannot be manually repositioned.

    What are the risk factors for haemorrhoids?

    Straining during bowel movements: Putting excessive pressure on the rectal area.

    Chronic constipation or diarrhea: Disrupting normal bowel movements can contribute.

    Sedentary lifestyle: Lack of physical activity can lead to poor circulation and increased pressure on veins in the rectal area.

    Obesity: Excess weight can contribute to increased pressure on the rectal veins.

    Pregnancy and childbirth: The pressure on the abdomen during pregnancy and the strain of childbirth can increase the risk.

    Aging: The risk increases with age due to weakened rectal tissue and veins.

    Genetics: Family history of hemorrhoids may play a role.

    Low-fiber diet: Insufficient fiber intake can lead to constipation, which is a risk factor.

    Heavy lifting: Straining while lifting heavy objects can contribute to the development of hemorrhoids.

    Chronic cough or sneezing: Persistent, forceful coughing or sneezing can increase abdominal pressure.

    When does a haemorrhoid become painful?

    Hemorrhoids become painful when there is inflammation or swelling in the blood vessels in the rectal or anal area. This can occur due to various factors, including:

    Thrombosis: When a blood clot forms within a hemorrhoidal vein, causing significant pain and swelling.

    Strangulation: If internal hemorrhoids prolapse (extend outside the anal opening) and the blood supply is cut off, it can lead to pain.

    Inflammation: Irritation and inflammation of hemorrhoids, often due to straining during bowel movements or other contributing factors.

    External hemorrhoids: These can be more painful than internal ones, as they are located under the skin around the anus and are more sensitive.

    What are the complications of haemorrhoidectomy

    Pain and Discomfort: Postoperative pain is common, and patients may experience discomfort during the recovery period.

    Bleeding: Some bleeding is normal after surgery, but excessive bleeding may occur in rare cases.

    Infection: Infections at the surgical site are possible, though they are uncommon.

    Urinary Retention: Difficulty in passing urine may occur temporarily after the procedure.

    Anal Stenosis: Narrowing of the anal opening, though rare, can occur as a result of scarring.

    Fecal Incontinence: Loss of control over bowel movements is a rare but potential complication.

    Delayed Healing: In some cases, the surgical site may take longer to heal than expected.

    Recurrence of Hemorrhoids: While hemorrhoidectomy is effective, there is a small chance that hemorrhoids may return.

    Allergic Reactions: Rarely, individuals may experience allergic reactions to medications or materials used during surgery.

    What are the complications of haemorrhoids?

    Thrombosis: Formation of blood clots in hemorrhoidal veins, leading to pain and swelling.

    Bleeding: Hemorrhoids can cause bleeding, especially during bowel movements.

    Prolapse: Internal hemorrhoids may protrude outside the anal opening, causing discomfort.

    Strangulation: Prolapsed hemorrhoids may have blood supply issues, resulting in pain.

    Infection: Scratching or irritation can lead to infections in the anal area.

    Anaemia: Chronic bleeding from hemorrhoids may contribute to low blood iron levels and anemia.

    Anal Fissures: Tears in the anal lining can occur in conjunction with hemorrhoids, causing pain.

    B Stations

  • Gen Surg
    A admin

    Acute Pancreatitis

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is Guy – a 45-year-old gentleman presenting with abdominal pain. Please take a history and perform a relevant examination.

    Patient History:

    Your name is Guy – a 45-year-old gentleman who works in a pub.

    You noticed in the past two days that you developed a sudden abdominal pain at the top of your tummy and the belly button region. It comes on intermittently, and it is worsening. You described the pain as dull. The pain also radiates towards the back (when this happens, you feel like you are being stabbed with a knife in the back) and is associated with vomiting (no blood/bile – just food content). The pain is 6/10. The pain is worsened by eating food in general. You have tried to use paracetamol to ease the pain, but it hasn't helped that much.

    You have had a bad appetite since yesterday and haven't been eating or drinking. You feel sick when you eat – but haven't vomited yet. You are quite constipated lately (no blood/offensive smell in stool /diarrhoea otherwise in previous stools) – haven't been opening your bowel for around 3 days. The stool has not been paler lately or difficult to flush. No urinary problems.

    You also have been a little more breathless, but you do not know why. No cough. No fever. No recent trauma. No recent surgery/ procedure. No recent infection. No itchy skin.

    Ideas, Concerns, Expectations:

    You think this is related to the gallstones. You had similar symptoms in the past. You are concerned if you need any surgery for this as last time, the doctor said they are considering gallbladder removal. You don't want any surgeries; your grandmother died during an operation. You would like to have something to ease the pain.

    Past Medical History:

    Known to have gallstones and fatty liver, polymyalgia rheumatica (recently diagnosed), hyperlipidaemia, heart failure

    Drug History:

    Started on steroids 2 days ago, omeprazole, furosemide, statin NKDA

    Family History:

    Rheumatoid arthritis, gallstones

    Social History:

    You drink around 2-3 cans of lager per day

    Don’t smoke

    Live by yourself

    Work in a pub

    Examination Findings:

    Corneal arcus

    Tachycardia

    Warm peripherals

    Appears to be Jaundice/icterus

    Epigastric/ umbilical region tenderness with rigidity but no guarding (no signs of peritonitis)

    Bowel sound reduced

    No signs of ascites

    Cullen's sign / Grey Turner's sign

    Murphy's sign is negative

    Mild pitting oedema bilaterally

    Calves soft and non-tender

    On chest auscultation – it may show signs of pleural effusion: localised reduced air entry and dullness to percussion/ coarse crackles at bases

    Signs of dehydration may include dry mouth, reduced skin turgor, and prolonged capillary refill time

    Differentials:

    Acute pancreatitis secondary to alcohol/ gallstone/ steroid/ hyperlipidaemia

    Cholangitis/ Cholecystitis

    Rule out other causes of acute abdomen e.g. peptic ulcer

    Decompensated heart failure

    To rule out ARDS

    To rule out AAA

    Investigations:

    Bedside:

    Observations (low grade pyrexia / tachycardia/ hypoxia/ low sat)

    ECG (tachycardia)

    ABG e.g. PaO2, lactate, glucose (Glasgow score)

    Bloods:

    Pancreatitis Glasgow score includes in bloods: WCC (neutrophil) in FBC, LDH/ AST in LFTs, albumin + Calcium in bone profile, glucose, Urea in U&Es

    Additionally: CRP (inflammation) + amylase/lipase (raised in pancreatitis – >x3 normal level for amylase, bilirubin in LFTs (may be raised) + other routine bloods to assess for baseline

    Blood culture if signs of infection

    Emerging test: Urinary trypsinogen-2 (elevated in pancreatitis), Serum IL-6/8 (if raised – may indicate severe risk of pancreatitis)

    Imaging:

    Abdominal XR (faecal loading / rule out obstruction / perforation)

    CXR (acute respiratory distress syndrome / pleural effusions / basal atelectasis)

    Ultrasound Abdomen/ endoscopic US (to assess for gallstone/dilated bile duct/ fluid collection/ pancreatic inflammation, peripancreatic stranding, calcification/ biliary sludge)

    CT Abdomen +/- contrast – can be diagnostic / assess for complications of pancreatitis e.g. abscess/ fluid collections/pseudocyst/ necrosis + rule out lesions e.g. malignancy) + rule out other causes of acute abdomen

    Consider MRCP in gallstone present/ dilatation of biliary tract for further assessment

    Special Test:

    Fine needle aspiration and culture/biopsy (infected pancreatic necrosis/ unknown lesion)

    Management (Acute Pancreatitis):

    Conservation:

    Patient Education e.g. condition

    Sociopsychology support

    IV Fluids

    Nil by mouth initially, and once symptoms are resolved/ improving blood tests – food can be introduced (consider a low-fat diet for patients with gallstones)

    NG tube if severe vomiting

    Antiemetics

    Analgesia

    Careful monitoring

    Nutritional support / dietician input e.g. NG feed / TPN + electrolyte/vitamin replacement as appropriate(potential risk of refeeding syndrome)

    Laxative if appropriate

    Electrolyte replacement if appropriate

    Oxygen when required (ARDS)

    Medical:

    Consider antibiotics if evidence of infection e.g. abscess / infected necrotic areas

    Consideration for admission for high dependency unit (HDU) / Intensive care unit (ICU) for moderate/severe cases).

    Surgical:

    Consider ERCP+/- stenting/ cholecystectomy in gallstone pancreatitis

    Treatment of complications e.g. endoscopic/ percutaneous drainage of collections + culture/sensitivity e.g. peritoneal fluid/ pseudocysts/ abscesses

    To treat obstruction of biliary system / pancreatic duct e.g. pancreaticojejunostomy instead of ERCP

    Removal of inflamed tissues + debridement of necrotic tissues/ pancreatoduodenectomy for pancreatic cancer/ other pancreatic resection procedures.

    Newer management: pancreatectomy followed by islet cell transplantation

    Long-term management:

    Reduce / quit / prevent : alcohol/smoking / other risk factors e.g. via support group / lifestyle advice e.g. dietary

    Consideration of replacement pancreatic enzymes (Creon) – for malabsorption

    Consideration of subcutaneous insulin regimes if required for diabetes

    Viva Questions:

    Explain the pathophysiology of acute pancreatitis.

    Acute pancreatitis begins with enzymes prematurely activating within the pancreas, causing tissue damage. This triggers inflammation, attracting immune cells and causing local effects like necrosis and pseudocysts. The inflammatory response can also affect other organs, potentially leading to multiple organ failure. Prompt diagnosis and treatment are essential to manage the condition and prevent severe complications.

    What are the complications of pancreatitis?

    Complications of pancreatitis can be serious and life-threatening. They include:

    Necrotizing Pancreatitis: Severe inflammation leads to tissue death (necrosis) in the pancreas.

    Pancreatic Abscess: Accumulation of infected fluid or pus within or near the pancreas.

    Pseudocysts: Fluid-filled sacs containing pancreatic enzymes, blood, and tissue debris.

    Organ Failure: Severe cases can cause failure of multiple organs, such as kidneys, lungs, or heart.

    Sepsis: Widespread infection that can lead to a life-threatening systemic response.

    Acute Respiratory Distress Syndrome (ARDS): Severe lung dysfunction due to inflammation.

    Acute Kidney Injury: Sudden kidney dysfunction due to reduced blood flow or inflammation.

    Disseminated Intravascular Coagulation (DIC): Abnormal blood clotting throughout the body.

    Diabetes Mellitus: Damage to the pancreas can lead to long-term insulin production issues.

    Chronic Pancreatitis: Continuous inflammation can lead to irreversible changes and chronic pain.

    How do we assess the severity of pancreatitis?

    Clinical: Evaluate symptoms and physical signs.

    Lab Tests: Check amylase, lipase, CBC, LFTs, and renal function.

    Imaging: Use CT, MRI, or ultrasound to visualize the pancreas.

    Scoring Systems: Use APACHE-II, Ranson's Criteria, or Glasgow-Imrie Criteria.

    Complications: Identify organ failure, necrosis, abscesses, or pseudocysts.

    Monitor Progression: Watch for changes and treatment response to adjust care.

    What are the potential causes of pancreatitis?

    I: Idiopathic

    G: Gallstone, Genetic - Cystic Fibrosis

    E: Ethanol (alcohol)

    T: Trauma

    S: Scorpion sting or Spider bite

    M: Mumps

    A: Autoimmune conditions (like lupus)

    S: Steroids

    H: Hyperlipidemia or Hypercalcemia

    E: ERCP (Endoscopic Retrograde Cholangiopancreatography)

    😧 Drugs e.g. tetracycline, furosemide, azathioprine, thiazide.

    Why is lipase more sensitive + specific than amylase for pancreatitis?

    Lipase is preferred for diagnosing pancreatitis because it's more specific to pancreatic issues, has a longer detection window, and is more sensitive than amylase. It provides clearer results and is endorsed by clinical guidelines.

    B Stations

  • Gen Surg
    A admin

    Diverticulitis

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 51-year-old gentleman called Isaac, presenting with bloody stool. Please take a history and perform an appropriate examination.

    Patient History:

    Your name is Isaac – a 51-year-old – estate agent.

    In the past three days, you have been having maroon-red diarrhoea with clots (not bright red or dark black, smelly stools). This is not settling or getting worse. You don't think you have eaten anything abnormally lately, but you generally eat a low-fibre diet. You did have some constipation a few days before having diarrhoea. You haven't noticed any lumps or bumps around your tummy. You have lost your appetite. Feeling sick and have been vomiting slightly (just food contact / no blood or bile). You also noticed aching pain on your tummy's lower left side. It comes on intermittently. Worsen by eating and improved slightly by emptying stool and passing gas. You feel your tummy is a little more bloated than usual. You also noticed you had been feeling warm with a bit of shivering last night. You do feel tired lately, but you are not sure whether this is from your stressful work or lack of sleep. You are not sure if you have lost any weight recently. Waterworks normal.

    Ideas, Concerns, Expectations:

    You have no idea what this might be. You hope it is not cancer – you have much more to live for! You are concerned because the stool is red; you might be bleeding somewhere in your bowels. You really want to know what is happening- your wife is concerned about this.

    Past Medical History:

    Ankylosing spondylitis, atrial fibrillation, diverticular disease, obesity, hypercholesterolaemia

    Drug History:

    Ibuprofen, apixaban, lansoprazole

    Allergic to shellfish (rash)

    Family History:

    Ulcerative Colitis

    Social History:

    Ex-smoker – used to smoke 10 cigarettes a day for 10 years.

    Drink a bottle of wine every other week.

    Work as an estate agent.

    Live with wife.

    Examination Findings:

    Lower left quadrant pain tenderness

    No guarding or signs of peritonitis

    No rebound tenderness

    No hernia/ lump

    No signs of testicular torsion

    Bowel sound present

    Murphy's sign negative

    Rovsing's sign negative

    PR exam – may show tenderness or mass suggesting pelvic abscess.

    Differentials:

    Diverticulitis +/- complications

    IBD

    Ischaemic colitis

    Gastroenteritis

    To rule out GI cancer

    Other causes of abdominal pain to rule e.g. peptic ulcers (use of NSAIDs + apixaban)

    Investigations:

    Bedside:

    Observations (pyrexia/ tachycardia)

    ECG (tachycardia/rule out arrhythmias) +/- echo (cause of embolism/ valvular pathology)

    Urine dip (rule out UTI as a cause of abdominal pain)

    Bloods:

    CRP/WCC (raised in diverticulitis)

    Hb (blood loss- anaemia)

    Lactate (raised in ischaemic colitis)

    U&Es (baseline + urea raised in dehydration/GI bleeding)

    CRP

    Group and Save

    Coagulation Screen (bleeding + ischaemia?)

    Blood Culture if suspected infection/sepsis

    LFT/Amylase (rule out abdominal pain causes)

    Imaging:

    XR Abdomen ( to look for dilated bowel loops, thumbprinting in ischaemic colitis…etc.)

    Erect CXR (to rule out air under the diaphragm)

    Urgent CT scan with contrast (aim with 24 hours) for suspected complicated diverticulitis + high CRP (alternative non-contrast CT, MRI, US)

    Consider CT angiography for suspected bowel ischaemia (gold standard)

    Special Test:

    Colonoscopy (to confirm diagnosis/ rule out other possible diagnoses)

    Flexible sigmoidoscopy (to rule rectosigmoid lesion)

    If no bleeding source can be identified with sigmoidoscopy, consider a non-invasive approach e.g. (nuclear scintigraphy) or an invasive approach e.g. angiography/ colonoscopy to localise/treat the bleeding source.

    Consider cystoscopy/ cystography, contrast radiographs or methylthionium chloride (methylene blue) studies for colovesciular fistula tracts.

    Management:

    Consider admission when:

    Pain is not managed with simple paracetamol

    Poor hydration with oral fluids

    Oral antibiotics cannot be tolerated

    Bleeding requiring transfusion

    Frailty + significant comorbidities

    Symptoms persist for over 48 hours despite conservative management at home

    Features of complications

    Conservative (especially in uncomplicated, asymptomatic diverticular disease – consider management at home +/- antibiotics if symptomatic + safety netting):

    Rest

    Bulk-forming / stimulant laxatives should be avoided

    Nil by mouth or clear fluids only until symptoms improve

    IV fluids/ hydration

    Analgesia e.g. paracetamol – avoid NSAID / opioids if possible

    Consider antispasmodic may for cramping

    Consider NG/antiemetics if vomiting

    Medical:

    Consider Oral co-amoxiclav 625mg TDS (at least 5 days) – in uncomplicated diverticulitis but systemically unwell / immunosuppressed/ significant comorbidities (alternative: cefalexin + metronidazole)

    Consider IV antibiotics in severe acute diverticulitis e.g. severe pain / complications (IV co-amoxiclav or IV cefuroxime + metronidazole) + stepping down regime following review in 48 hours / CT scan results)

    Consider blood transfusion due to significant blood loss + stop blood thinning medication + consider vitamin K / tranexamic acids

    Surgery:

    General Surgery Input/ referral

    Surgery may be required for complications e.g. perforation, purulent/faecal peritonitis, uncontrolled sepsis, peri-diverticular abscess, fistula, ileus, obstructions, haemorrhage…etc.

    In free perforation with generalised peritonitis - it may involve urgent surgical laparoscopic lavage and resection surgery. Primary anastomosis +/- diverting stoma or Hartmann's procedure are standards for routine or emergency surgery.

    Management of further complications:

    Abscess might involve antibiotics, bowel rest, percutaneous drainage, and standard surgery.

    Fistula – resection with fistula closure + repair

    Obstruction- might involve resection, endoscopic balloon dilation, stenting

    Haemorrhage – fluid/blood resuscitation, vasopressin, angiographic embolisation, surgery e.g. resection

    Prevention:

    High fibre diet e.g. fruits and vegetables, whole grain, good fluid intake + bulk-forming laxative, exercise, smoking cessation, weight loss

    Viva Questions:

    Explain the pathophysiology of diverticulitis?

    Diverticulitis starts with the formation of pouches (diverticula) in the colon due to increased pressure and weakened colon walls. When fecal matter gets trapped in these pouches, it can lead to bacterial growth and inflammation. The immune system responds, causing further inflammation and potential complications like abscesses, perforation, and bowel obstruction. High pressure, low-fiber diet, and aging are key factors in this process.

    What are the risk factors for diverticular diseases?

    Aging (especially over 40)

    Low-fiber diet

    Lack of physical activity

    Obesity

    Smoking

    Genetics (family history)

    Previous history of diverticular disease

    Connective tissue disorders

    What are the complications of diverticulitis?

    Abscess formation

    Perforation (rupture)

    Peritonitis (inflammation of the abdominal lining)

    Fistula formation (abnormal connections)

    Bowel obstruction

    Stricture formation (narrowing of the colon)

    Hemorrhage (severe bleeding)

    Septicemia (bloodstream infection)

    Psoas abscess (infection in the lower back muscle)

    At what sites does diverticulum most occur in the GI tract?

    Diverticula primarily occur in the sigmoid colon, followed by other parts of the colon, and rarely in other areas of the digestive tract.

    B Stations

  • Gen Surg
    A admin

    Bowel Obstruction

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is a 56-year-old gentleman (Adam) coming in due to vomiting. Please take a history and perform a relevant examination.

    Patient History:

    Your name is Adam – You are currently 56-year-old – retired, and used to work as an accountant.

    Since yesterday you have been vomiting, and it is only worsening – you also noticed you were starting to vomit green stuff today, which looked horrible and shocked you! Vomit doesn't contain any blood/faecal matter. You have been struggling to keep food down. You have a poor appetite. You feel weak and tired. You haven't had a good sleep since yesterday.

    You also started to develop sudden, intermittent excruciating tummy pain throughout your tummy, which is widespread. No radiation. Pain score 9/10. You tried to take paracetamol and Oramorph, but it didn't help. Any movement only makes the pain worse, so you try to stay still as much as possible. You also feel your tummy has gotten a little bigger than usual. You do not feel well at all. You feel feverish with some chills.

    You have not been passing bowel content/wind in the past week. No diarrhoea or bloody stool recently. No weight loss. No night sweats. No recent infection / surgery/ admission. No recent weight loss.

    Ideas, Concerns, Expectations:

    You are not sure what is going on. You don't think you have eaten anything abnormal lately. Maybe you have some constipation. You are concerned that the pain is now getting worse today. You hope to find out what is going on and receive some medications to help control your pain!

    Past Medical History:

    Hypothyroidism, type 2 diabetes, appendectomy, cholecystectomy, previous inguinal hernia operation, paroxysmal atrial fibrillation

    Drug History:

    Levothyroxine NKDA, metformin, apixaban

    NKDA

    Family History:

    Bowel cancel >60 years old, diverticular disease

    Social History:

    You smoke 10 cigarettes/ day for the last 20 years.

    You drink about 1-2 pints of beer every week.

    You use oramorph recreationally, but you haven't been taking this last week until the pain started.

    You live in a house with your partner currently.

    Examination Findings:

    Patient looks uncomfortable. Generalised abdominal tenderness – worst at the umbilical region. Voluntary guarding suggesting peritonitis. Bowel sound is absent. Abdominal distension with hyper-resonant on percussion. No palpable mass/lump. Previous surgical scars are present.

    Signs of dehydration might include prolonged capillary refill time, tachycardia, reduced skin turgor, and dry mouth.

    Differentials:

    Bowel obstruction secondary to e.g. adhesions (due to extensive history of abdominal surgeries), strangulated hernia, malignancy, volvulus…etc.

    Need to rule out bowel perforation

    Bowel ischemia

    Diverticular disease

    Gastroenteritis

    Acute pancreatitis

    Constipation e.g. secondary to opioid use/ dehydration / hypothyroidism

    Investigations:

    Bedside:

    ABCDE assessment

    Observation (tachycardia, hypotension / pyrexia may indicate perforation/ infarction)

    ECG (tachycardia/ rule out arrhythmias)

    ABG (metabolic alkalosis/electrolyte imbalance due to vomiting + raised lactate if bowel ischaemia)

    Fluid charts for input/out monitoring/ consider catheterisation (may show signs of dehydration e.g. oliguria)

    BM /ketones (DKA/HHS)

    Urinalysis (rule out UTI cause of abdominal pain / may show high ketones for DKA)

    Admit all patients with bowel obstruction/ perforation

    Urinalysis

    Serum hCG in women of childbearing age.

    Bloods:

    FBC(high WCC/neutrophilia, low haematorcrit or hb indicates blood loss), CRP, LFTs, U&Es (electrolyts imbalance from vomiting/ reduced kidney function from dehydration/ pseudoobstruction), Bone Profile, Amylase, Lactate, Cross-match / cross match (for surgery / plan for blood transfusion), serum/urine osmolality (HHS), blood culture (for suspected infection)

    Imaging:

    Supine and erect XR Abdomen (rule out gas in peritoneum/ bowel dilatation / may show fluid level)

    Barium swallow (can also be therapeutic)

    Erect CXR (rule out referred pain from pneumonia/ gas under diaphragm)

    Consider water-soluble contrast enema XR for diagnosis

    CT scan (rule out obstruction + perforation or other causes of abdominal pathology/plan for surgery)

    Consider MRI / US for diagnosing bowel obstruction or other causes.

    Special Test:

    Consider endoscopy e.g. flexible sigmoidoscopy/colonoscopy (can be diagnostic/therapeutic e.g. stenting) Care should be taken due to the risk of perforation / exacerbating complications. Should be in the absence of sepsis/ ischaemia/ perforation/ peritonitis/ closed loop obstruction/ abscesses/ distal rectal lesions/ persistent coagulopathy, dilated caecum more than 9cm.

    Management:

    Conservative:

    Urgent referral to General Surgery for suspected bowel obstruction

    Nil by mouth + bowel rest

    IV fluids resuscitation

    Consider NG tube for persistent vomiting / prevent aspiration

    Electrolyte replacement if appropriate

    Consider dietician input

    Ice to suck to moisten mouth and lips / reduce the sense of thirst

    Analgesia e.g. morphine sulphate

    VTE assessment and prophylaxis

    Consider conservative approach e.g. watchful waiting in incomplete obstruction, previous surgery suggesting ?adhesion, advanced malignancy, pseudo-obstruction, sigmoid volvulus?

    Avoid stimulant laxatives if the patient has colic/ stop all laxatives in complete obstruction

    Consider antiemetics – Care should be taken for prokinetic metoclopramide

    Medical:

    Consider (prophylactic) antibiotics in those with suspected perforation / bowel ischaemia / for surgery.

    Consider neostigmine to aid recovery of intestinal pseudo-obstruction alongside with correction of fluid and electrolyte imbalance

    Surgery

    Consider endoscopy for bowel decompression, dilatation of strictures via stenting for patients in palliative care or awaiting elective surgery

    Consider sigmoidoscopy + passage of flatus tube in sigmoid volvulus without perforation or decompression via colonoscopy in caecum volvulus / pseudo-obstruction.

    Early laparotomy/ laparoscopic surgery e.g. exploratory surgery/ adhesiolysis/ hernia repair/ resection if persisting obstruction, ischaemic, perforation / peritonitis/ irreducible hernia / palpable mass + failure to improve. Ischaemic bowel may require resection. A stoma may be created following an operation

    Post-op care

    Prior to discharge, advise on diet, emotional changes, weight management, adapting physical activity, expectation for recovery, smoking/alcohol use, when and where to seek help if appropriate.

    Palliative such as in those with advanced malignancy and unfit for surgery:

    Analgesia

    Antiemetics

    Antispasmodics

    Antisecretory

    Corticosteroids e.g. dexamethasone (may reverse partial obstruction)

    Colonic stenting

    Viva Questions:

    What are the different types of bowel obstruction and their likely causes?

    Small Bowel Obstruction:

    Adhesive obstruction (scar tissue after surgery)

    Hernia (protrusion through weakened abdominal wall)

    Volvulus (twisting of the small intestine)

    Intussusception (telescoping of intestine)

    Strictures (narrowing due to inflammation or scarring)

    Large Bowel Obstruction:

    Colorectal cancer

    Diverticulitis (inflammation or infection of diverticula)

    Strictures (narrowing due to scarring)

    Volvulus (twisting of the colon)

    What is paralytic ileus?

    Paralytic ileus is a condition where normal muscle contractions in the gastrointestinal tract are temporarily disrupted, leading to a slowdown or cessation of movement of contents. It can result from surgery, inflammation, infection, medications, or other medical conditions. Symptoms include abdominal bloating, nausea, vomiting, and constipation. Treatment involves addressing the underlying cause, supportive care, and, in severe cases, surgery.

    What are the complications of bowel obstruction?

    Ischemia (Lack of Blood Supply): Obstruction can compromise blood flow to the affected segment of the bowel, leading to ischemia. Prolonged ischemia can result in tissue damage and necrosis (death of tissue).

    Bowel Perforation: Increased pressure within the obstructed bowel can cause the bowel wall to rupture, leading to bowel perforation. This can result in peritonitis, a severe inflammation of the abdominal cavity.

    Sepsis: Bowel perforation can lead to the release of bacteria and digestive contents into the abdominal cavity, causing infection. Severe infection can progress to sepsis, a life-threatening condition.

    Fluid and Electrolyte Imbalances: Vomiting, dehydration, and the loss of fluids into the obstructed bowel can lead to imbalances in electrolytes (such as sodium and potassium) and dehydration.

    Malnutrition: Prolonged obstruction can lead to malabsorption of nutrients, causing malnutrition.

    Distension and Rupture of the Bowel: Obstruction can cause significant distension of the bowel, leading to increased pressure. In severe cases, the distended bowel may rupture.

    Renal Failure: In some cases, bowel obstruction can lead to reduced blood flow to the kidneys, potentially causing kidney dysfunction or failure.

    Respiratory Complications: Severe abdominal distension can affect diaphragmatic movement, leading to respiratory difficulties.

    Shock: In cases of severe complications, such as bowel perforation and sepsis, the patient may go into shock, which is a life-threatening condition characterized by inadequate blood flow to vital organs.

    Give some examples of how a "closed loop" obstruction may occur?

    Closed-loop bowel obstruction can occur in various ways:

    Adhesion Formation:

    Scar tissue from surgery causes the bowel to close at two points.

    Volvulus:

    Twisting of the bowel at two points leads to a closed loop.

    Intussusception:

    Telescoping of the bowel results in closure at both ends.

    Hernia:

    Trapped bowel within a hernia forms a closed loop.

    Internal Herniation:

    Bowel herniates internally, creating a closed loop.

    What are the upper limits of normal diameter of the bowel e.g. small bowel, colon, and caecum?

    Normal bowel diameter can vary among individuals and may be influenced by factors such as age, body size, and imaging technique. However, there are general reference ranges for the normal diameter of the small bowel, colon, and cecum which can be measured in imaging like XRays:

    Small Bowel:

    Normal diameter: Less than 3 cm

    Large Bowel:

    Normal diameter: Up to 6 cm

    Cecum:

    Normal diameter: Up to 9 cm

    What XR findings would you expect to see in large bowel obstruction vs small bowel obstruction?

    Large Bowel Obstruction (LBO):

    Dilated Colon: Visible dilation of the large bowel with haustral markings.

    Transition Point: Distinct transition point, often in the sigmoid colon or rectum.

    Small Bowel Obstruction (SBO):

    Dilated Small Bowel Loops: Multiple, uniformly dilated small bowel loops.

    Valvulae Conniventes: Visible circular folds crossing the entire width of the small bowel.

    "Umbilical" or "Triangle" Sign: Converging loops creating a triangle or "umbilical" shape.

    How do you get third-spacing in bowel obstruction, and what is the complication of this?

    In bowel obstruction, third-spacing occurs due to increased pressure within the obstructed bowel, causing fluid to move from blood vessels into surrounding tissues. Complications include dehydration, hypovolemic shock, electrolyte imbalances, and organ dysfunction.

    What are the symptoms/signs of dehydration/hypovolaemia?

    Thirst: Increased thirst is a natural response to fluid loss.

    Dark Yellow Urine: Concentrated urine with a dark yellow color indicates reduced fluid intake.

    Dry Mouth and Dry Skin: Insufficient fluid levels may lead to dryness of the mouth and skin.

    Fatigue: Dehydration can cause fatigue and a feeling of weakness.

    Dizziness or Lightheadedness: Reduced blood volume can affect blood pressure and lead to dizziness.

    Rapid Heartbeat: The heart may beat faster to compensate for decreased blood volume.

    Sunken Eyes: Dehydration may cause the eyes to appear sunken.

    Infrequent Urination: Reduced fluid intake can result in decreased urine output.

    Headache: Dehydration may contribute to headaches.

    Confusion or Irritability: Severe dehydration can affect cognitive function and mood.

    What are the different types of shock?

    Shock is a life-threatening medical emergency characterized by inadequate blood flow to the body's tissues and organs. There are several types of shock, each with distinct causes and features:

    Hypovolemic Shock:

    Cause: Severe loss of blood or other fluids (e.g., from trauma, bleeding, dehydration).

    Features: Rapid heart rate, low blood pressure, cold and clammy skin, confusion.

    Cardiogenic Shock:

    Cause: Heart-related problems, such as a heart attack, severe heart failure.

    Features: Weak pulse, rapid breathing, cold and clammy skin, confusion.

    Distributive (Vasodilatory) Shock:

    Subtypes:

    Septic Shock: Caused by severe infection leading to systemic inflammation.

    Neurogenic Shock: Resulting from a disruption of the autonomic nervous system (e.g., spinal cord injury).

    Anaphylactic Shock: Triggered by a severe allergic reaction.

    Features: Vasodilation, low blood pressure, rapid heart rate, warm and flushed skin (except in neurogenic shock), respiratory distress.

    Obstructive Shock:

    Cause: Obstruction of blood flow due to a physical barrier (e.g., pulmonary embolism, cardiac tamponade).

    Features: Signs vary based on the specific cause but may include difficulty breathing, chest pain, rapid heart rate.

    B Stations

  • Gen Surg
    A admin

    Acute Cholecystitis

    Doctor Instruction:

    You are currently a senior surgical doctor on call. Your next patient is Katie, a 45-year-old lady complaining of abdominal pain. Please take a history and perform a relevant examination.

    Patient History:

    You have some dreadful pain below your right ribs; it started gradually before you went to bed last night. But it's suddenly much worse today. It is a constant deep but sharp 7/10 pain in your right upper quadrant. You've been feeling the pain shooting up to your back on the right. Nothing seems to make it worse, and nothing's improving it either!

    This isn't the first time you've had tummy pain. For the past few months, you've been getting episodes of sharp pain in that area, which usually lasts a few hours and then goes away, usually starting after lunch. You've been taking ibuprofen for the pain. But the pain this time is different, and you don't feel like yourself at all!

    You vomited once about four hours ago and have generally been sick. You've had no change to your bowels. You last opened your bowels this morning. The stool was not pale and wasn't difficult to flush. You have no jaundice. You have chronic reflux, and no recent changes have happened. No difficulty swallowing. You haven't had any cough or chest pain.

    Gynae-wise, you haven't had any issues, your last period was two months ago, but they have been a bit irregular recently – you wonder why! No problems with waterworks thankfully!

    You have been feeling hot and flushy this morning. You haven't noticed any recent changes in your weight. You cannot recall eating anything troublesome before this.

    Ideas, Concerns, Expectations:

    You were warned by your GP that you were at risk of getting ulcers because of your reflux, so you're worried this is what's going on. The pain is quite severe, and you just want to get something stronger than ibuprofen.

    Past Medical History:

    GORD

    NAFLD

    Drug History:

    Omeprazole

    Allergic to penicillin (swollen mouth)

    Family History:

    None.

    Social History:

    You are an office worker, but you've been working from home this past year and have gained quite a bit of weight.

    You also broke up with your partner last year, so you now live alone in a flat.

    Your diet isn't the greatest, often buy fast foods and the occasional Indian takeaway.

    You stopped smoking 3 years ago but restarted smoking about 10 cigarettes a day last year.

    You occasionally drink alcohol, but nothing over 5-6 units per week.

    Examination Findings:

    Sweaty and hot to touch

    Tachycardic (104bpm)

    No jaundice

    Abdomen tender to light palpation

    Murphy's positive (only mention if tested or whilst palpating for hepatomegaly)

    Abdominal aorta palpable and pulsatile, not expansile

    Differentials:

    Cholecystitis (RUQ pain on a background of biliary colic associated with fever in the absence of jaundice. Worry about associated sepsis)

    Other biliary pathology e.g. biliary colic, choledocholithiasis, cholangitis

    Peptic ulcer disease (history of reflux and taking ibuprofen)

    Ectopic pregnancy

    Hepatitis

    Pancreatitis

    Investigations:

    Bedside:

    Vital signs (shock, sepsis)

    Pregnancy test

    Bloods:

    FBC (bleeding ulcer, infection)

    U&E (dehydration, AKI)

    LFT (obstructive picture, bilirubin levels)

    CRP/ESR (infection)

    Amylase (pancreatitis)

    Imaging:

    Abdominal USS (look for gallstones, gallbladder wall thickening and surrounding fluid)

    MRCP

    Erect CXR (perforated PUD)

    AXR (Rigler's sign may indicate perforated PUD)

    Endoscopy

    Management:

    Conservative:

    NBM + surgical preparation

    Stop ibuprofen and advise against it in cases of reflux - consider a PPI trial of increasing dose of omeprazole.

    Medical:

    Analgesia

    Antibiotics (according to local guidelines for pen allergy)

    Surgical:

    Urgent laparoscopic cholecystectomy

    Viva Questions:

    What is the Charcot's triad?

    Charcot's triad is a set of three classic symptoms that are traditionally associated with acute cholangitis, a condition characterized by inflammation and infection of the bile ducts. The triad includes:

    Fever: Patients with acute cholangitis often experience an elevated body temperature, which is a common sign of infection.

    Jaundice: Jaundice refers to the yellowing of the skin and eyes. In acute cholangitis, the inflammation and obstruction of the bile ducts can lead to impaired bile flow, resulting in the accumulation of bilirubin in the bloodstream and causing jaundice.

    Right Upper Quadrant Abdominal Pain: Pain or discomfort in the right upper quadrant of the abdomen is another component of Charcot's triad. This pain is often associated with inflammation and distension of the bile ducts.

    What are the risk factors for developing cholecystitis?

    Risk factors for cholecystitis include gallstones, age (over 40), female gender, obesity, rapid weight loss, pregnancy, diabetes, genetic predisposition, certain medical conditions (such as Crohn's disease), and specific ethnic backgrounds (Native American or Mexican American).

    How does cholecystitis cause shoulder tip pain?

    Cholecystitis can cause shoulder tip pain due to referred pain involving the phrenic nerve. Inflammation of the gallbladder irritates the diaphragm, and the shared nerve pathways, particularly the phrenic nerve (C3-C5), can lead to the brain interpreting pain signals from the diaphragm as originating from the shoulder area.

    What is Murphy's sign, and what does it indicate?

    Murphy's sign is a clinical test for gallbladder inflammation (cholecystitis). It involves placing fingers below the right costal margin and asking the patient to take a deep breath. If pain and cessation of inhalation occur due to gallbladder tenderness, the test is positive, suggesting possible cholecystitis, often caused by gallstones. Additional diagnostic tests are usually needed for confirmation.

    Name some complications of cholecystitis.

    Gangrenous Cholecystitis: Severe inflammation can lead to tissue death in the gallbladder wall.

    Perforation: Inflammation may cause the gallbladder to rupture, leading to bile leakage into the abdominal cavity.

    Abscess Formation: Pus collection within or around the gallbladder.

    Bile Duct Obstruction: Inflammation or gallstones can obstruct the common bile duct, affecting the flow of bile.

    Pancreatitis: Inflammation of the pancreas can occur due to the spread of inflammation from the gallbladder.

    Empyema: Accumulation of infected pus within the gallbladder.

    Gallstone Ileus: Large gallstones can migrate into the intestine, causing a bowel obstruction.

    Sepsis: Severe infection that can spread throughout the body.

    B Stations

  • Gen Surg
    A admin

    Hernia

    Doctor Instruction:

    You are currently a senior surgical doctor on call. You are asked to see Wan, a 35-year-old accountant, complaining of a lump in his groin. Please take a history and perform a relevant examination.

    Patient History:

    It's all a bit embarrassing, really, but you've got a groin lump. You noticed the lump last week, and it's been there ever since. It's like you've got a tennis ball under your skin. It's making things like wearing pants very awkward and sometimes a bit uncomfortable. You haven't noticed any change in size with coughing, straining or standing for prolonged periods. It was uncomfortable to touch.

    You've come in today because you've been getting waves of 5/10 abdominal pain today at the site. Paracetamol didn't seem to make much of a difference. You've been feeling sick on and off, and actually vomited once this morning - just normal food content. You last opened your bowels the night before yesterday and passed urine as normal without straining. There was no blood in your stool. You have had no difficulty swallowing, indigestion, fever or weight loss.

    Ideas, Concerns, Expectations:

    You are not sure what this is. You can concerned the lump is cancer. You wish to get it checked out.

    Past Medical History:

    Appendicectomy 10 years ago. Asthma.

    Drug History:

    Ventolin inhaler PRN. Steroid inhaler.

    NKDA.

    Family History:

    None.

    Social History:

    You are currently working as an accountant. It's good work, and you're able to work from home, so you have plenty of time to go to the gym for your weightlifting.

    You don't smoke or drink.

    You live with your wife and two young girls at home, where you are normally independent.

    Examination Findings:

    Left groin mass superior and medial to the pubic tubercle 2x2cm soft

    Tender on palpation at the hernia site.

    Non-reducible. Non-pulsatile

    Positive cough impulse

    No guarding or signs of peritonitis.

    Differentials:

    Direct inguinal hernia

    To rule out bowel obstruction/ perforation

    Incisional hernia if the site of hernia is at the site of incision for appendicectomy

    Vascular e.g. saphena varix, femoral artery aneurysm. (would be pulsatile).

    Subcutaneous e.g. lipoma, sebaceous cyst.

    Lymphoma

    Investigations:

    Clinical diagnosis. If uncertain, can use ultrasound as first line.

    Other abdominal imaging - AXR (bowel dilatation/ free air), CT Abdo (look for obstruction/bowel perforation)

    Management:

    In asymptomatic and reducible cases, conservative management is an option with general surgery follow-up.

    He will require surgery e.g. open/laparoscopic mesh repair if there's a high risk of complications when hernia is incarcerated/ causing bowel obstruction/ strangulated/ irreducible. For this, he will need admission and preparation for surgery e.g. NBM, IV fluids, catheterise, fluid balance, VTE prophylaxis, analgesia...etc.

    Viva Questions:

    What are the risk factors for the development of an inguinal hernia?

    The main risk factors for inguinal hernia development include:

    Age: Risk increases with age.

    Gender: Men are more susceptible.

    Family History: Genetic predisposition.

    Premature Birth/Low Birth Weight: Higher risk in such cases.

    Chronic Cough or Straining: Increases intra-abdominal pressure.

    Obesity: Excess weight strains abdominal muscles.

    Heavy Lifting: Especially if done improperly.

    Pregnancy: Especially with multiple pregnancies.

    Ascites: Fluid accumulation in the abdomen.

    Previous Abdominal Surgery: Weakens abdominal muscles.

    How do you differentiate between a femoral and inguinal hernia? Between a direct and indirect inguinal hernia?

    Location:

    Inguinal Hernia: This type of hernia occurs in the inguinal canal, which is a passage in the lower abdominal wall. Inguinal hernias are further divided into two types: direct and indirect:

    Direct Inguinal Hernia: This hernia occurs when abdominal contents push through a weakened area in the lower abdominal wall, often in the Hesselbach's triangle.

    Indirect Inguinal Hernia: This hernia occurs when abdominal contents protrude through the deep inguinal ring and into the inguinal canal. It may follow the pathway of the descent of the testes during fetal development.

    Femoral Hernia: This type of hernia occurs lower down in the groin area, just below the inguinal ligament. It protrudes through the femoral canal, which is a passageway through which blood vessels and lymphatics pass.

    Anatomy:

    Inguinal Hernia: Inguinal hernias are more common in both men and women. They are located in the inguinal region, which is near the groin and may cause a bulge in the scrotum in men or the labia in women.

    Femoral Hernia: Femoral hernias are more common in women, especially those who have been pregnant. They occur just below the inguinal ligament and may cause a bulge in the upper thigh.

    Talk me through your examination for inguinal hernia.

    Patient Positioning: Stand, expose groin with chaperone.

    General Inspection: Check for asymmetry, swelling, or skin changes.

    Scrotal Examination: Inspect for masses, tenderness.

    Palpate along inguinal canal.

    Cough test for dynamic assessment.

    Differentiate Hernia Types: Direct vs. Indirect.

    Auscultation: Listen for bowel sounds over the hernia.

    Documentation: Record size, location, tenderness, and dynamic changes.

    Repeat examination with the patient lying down.

    What are the causes of bowel obstruction?
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    B Stations
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