Conditions Flashcards
Dupuytrens Contracture
Dupuytren’s contracture is a condition where the fascia of the hand becomes thickened and tight, leading to finger contractures.
A contracture is a shortening of the soft tissues that leads to restricted movement in a joint. In Dupuytren’s contracture, the finger is tightened into a flexed position and cannot fully extend.
Pathophysiology
The palmar fascia of the hand forms a triangle of strong connective tissue on the palm.
In Dupuytren’s contracture, the fascia of the hands becomes thicker and tighter and develops nodules. Cords of dense connective tissue can extend into the fingers, pulling the fingers into flexion and restricting their ability to extend (contracture).
It is unclear why the fascia becomes thicker and tighter. However, it is thought to be an inflammatory process in response to microtrauma.
Risk Factors
Age
Family history (autosomal dominant pattern)
Male
Manual labour, particularly with vibrating tools
Diabetes (more with type 1, but also type 2)
Epilepsy
Smoking and alcohol
Presentation
The first sign of Dupuytren’s contracture is the development of hard nodules on the palm. There may be skin thickening and pitting. Slowly, the fascia becomes thicker, and the finger is pulled into flexion. It becomes impossible to extend the affected finger fully.
A thick, nodular cord can be palpated from the palm into the affected finger.
The ring finger is most often affected. The index finger is least likely to be affected.
Dupuytren’s contracture can significantly affect the function of the hand. However, patients do not usually experience pain with the condition.
The table-top test is a straightforward test for Dupuytren’s contracture. The patient tries to position their hands flat on a table. If the hand cannot rest completely flat, the test is positive, indicating Dupuytren’s contracture.
Management
The options for Dupuytren’s contracture are essentially to do nothing (conservative management) or to treat it surgically. There are three options for surgical management.
Needle fasciotomy (also known as needle aponeurotomy) involves inserting a needle through the skin to divide and loosen the cord that is causing the contracture.
Limited fasciectomy involves removing the abnormal fascia and cord to release the contracture.
Dermofasciectomy involves removing the abnormal fascia and cord, as well as the associated skin. A skin graft is used to replace the removed skin.
Olecranon Bursitis
Olecranon bursitis refers to inflammation and swelling of the bursa over the elbow. The olecranon is the bony lump at the elbow, which is part of the ulna bone.
Bursae are sacs created by synovial membrane filled with a small amount of synovial fluid. They are found at bony prominences (e.g., at the greater trochanter, knee, shoulder and elbow). They act to reduce the friction between the bones and soft tissues during movement.
Bursitis is inflammation of a bursa. This causes thickening of the synovial membrane and increased fluid production, causing swelling. This inflammation can be caused by a number of things:
Friction from repetitive movements or leaning on the elbow
Trauma
Inflammatory conditions (e.g., rheumatoid arthritis or gout)
Infection – referred to as septic bursitis
Olecranon bursitis is sometimes called “student’s elbow”, as students may lean on their elbow for prolonged periods while studying, resulting in friction and mild trauma leading to bursitis. It can also occur with people with occupations that require leaning on the elbow, such as plumbers or drivers.
Presentation
The typical presentation is a young/middle-aged man with an elbow that is:
Swollen
Warm
Tender
Fluctuant (fluid-filled)
It is important to identify where bursitis is caused by infection. Features of infection are:
Hot to touch
More tender
Erythema spreading to the surrounding skin
Fever
Features of sepsis (e.g., tachycardia, hypotension and confusion)
An important differential diagnosis is septic arthritis. Consider septic arthritis if there is:
Swelling in the joint (rather than the bursa)
Painful and reduced range of motion in the elbow
Aspiration
The NICE clinical knowledge summaries (updated January 2021) recommend aspiration of fluid from the bursa when an infection is suspected. They advise that the appearance can give an indication of the underlying cause:
Pus indicates infection
Straw-coloured fluid indicates infection is less likely
Blood-stained fluid may indicate trauma, infection or inflammatory causes
Milky fluid indicates gout or pseudogout
Aspiration should ideally be performed before starting antibiotics. The fluid is sent to the lab for microscopy and culture. During microscopy, they will examine for crystals (gout and pseudogout) and gram-staining for bacteria.
Management
Management options for olecranon bursitis include:
Rest
Ice
Compression
Analgesia (e.g., paracetamol or NSAIDs)
Protecting the elbow from pressure or trauma
Aspiration of fluid may be used to relieve pressure
Steroid injections may be used in problematic cases where infection has been excluded
When infection is suspected or cannot be excluded, management involves:
Aspiration of the fluid for microscopy and culture
Antibiotics
The NICE CKS recommend flucloxacillin first-line, with clarithromycin as an alternative.
Patients that are systemically unwell (e.g., immunocompromised or have sepsis) need admission to hospital for further management, including:
Bloods (including lactate)
Blood cultures
IV antibiotics
IV fluids
Epicondylitis
Epicondylitis refers to inflammation at the point where the tendons of the forearm insert into the epicondyles at the elbow. It is a specific type of repetitive strain injury.
There is a medial epicondyle and a lateral epicondyle on the distal end of the humerus, either side of the elbow joint.
The tendons of the muscles that insert into the:
Medial epicondyle act to flex the wrist
Lateral epicondyle act to extend the wrist
Epicondylitis is the result of repetitive use and injury to the tendons at the point of insertion. Symptoms gradually worsen over weeks to months. It most commonly affects patients in middle age.
Lateral Epicondylitis
Lateral epicondylitis is often called tennis elbow.
Lateral epicondylitis causes pain and tenderness at the lateral epicondyle (outer elbow). The pain often radiates down the forearm. It can lead to weakness in grip strength.
Mill’s test involves stretching the extensor muscles of the forearm while palpating the lateral epicondyle. The elbow is extended, the forearm pronated, and the wrist is flexed. The examiner holds the patient’s elbow with pressure on the lateral epicondyle. If this causes pain, the test is positive, indicating lateral epicondylitis.
Cozen’s test starts with the elbow extended, forearm pronated, wrist deviated in the direction of the radius and hand in a fist. The examiner holds the patient’s elbow with pressure on the lateral epicondyle. The examiner applies resistance to the back of the hand while the patient extends the wrist. If this causes pain, the test is positive, indicating lateral epicondylitis.
Medial Epicondylitis
Medial epicondylitis is often called golfer’s elbow.
Medial epicondylitis causes pain and tenderness at the medial epicondyle (inner elbow). The pain often radiates down the forearm. It can lead to weakness in grip strength.
A golfer’s elbow test involves stretching the flexor muscles of the forearm while palpating the medial epicondyle. The elbow is extended, the forearm supinated, and the wrist and fingers are extended. The examiner holds the patient’s elbow with pressure on the medial epicondyle. If this causes pain, the test is positive, indicating medial epicondylitis.
Management
Epicondylitis is a clinical diagnosis based on the signs and symptoms.
In most patients, epicondylitis is self-limiting and resolves with time. However, symptoms can take several years to resolve.
Management options for epicondylitis include:
Rest
Adapting activities
Analgesia (e.g., NSAIDs)
Physiotherapy
Orthotics, such as elbow braces or straps
Steroid injections
Platelet-rich plasma (PRP) injections
Extracorporeal shockwave therapy
Rarely, surgery may be required to debride, release or repair damaged tendons.
Adhesive Capsulitis (Frozen Shoulder)
Frozen shoulder is also called adhesive capsulitis. It is a relatively common cause of shoulder pain and stiffness. The loss of range of motion and function in the shoulder joint can significantly impair activities.
It most commonly affects people in middle age. Diabetes is a key risk factor.
Adhesive capsulitis can be:
Primary – occurring spontaneously without any trigger
Secondary – occurring in response to trauma, surgery or immobilisation
Pathophysiology
The glenohumeral joint is the ball and socket joint in the shoulder. The glenohumeral joint is surrounded by connective tissue that forms the joint capsule.
In adhesive capsulitis, inflammation and fibrosis in the joint capsule lead to adhesions (scar tissue). The adhesions bind the capsule and cause it to tighten around the joint, restrict movement in the joint.
Presentation
There is a typical course of symptoms, with three phases:
Painful phase – shoulder pain is often the first symptom and may be worse at night
Stiff phase – shoulder stiffness develops and affects both active and passive movement (external rotation is the most affected) – the pain settles during this phase
Thawing phase – there is a gradual improvement in stiffness and a return to normal
The entire illness lasts 1 – 3 years before resolving (e.g., 6 months in each phase). However, a large number of patients (up to 50%) have persistent symptoms.
Differential Diagnosis
The main differentials in a patient presenting with shoulder pain not preceded by trauma or an acute injury are:
Supraspinatus tendinopathy
Acromioclavicular joint arthritis
Glenohumeral joint arthritis
Rare but important differentials to keep in mind are:
Septic arthritis
Inflammatory arthritis
Malignancy (e.g., osteosarcoma or bony metastasis)
Shoulder pain preceded by trauma or an acute injury may be due to:
Shoulder dislocation
Fractures (e.g., proximal humerus, clavicle or rarely the scapula)
Rotator cuff tear
Supraspinatus tendinopathy involves inflammation and irritation of the supraspinatus tendon, particularly due to impingement at the point where it passes between the humeral head and the acromion. The empty can test (AKA Jobe test) can be used to assess for supraspinatus tendinopathy. This involves the patient abducting the shoulder to 90 degrees and fully internally rotating the arm as though they are emptying a can of water. The examiner pushes down on the arm while the patient resists. The test is positive if there is pain or the arm gives way.
Acromioclavicular (AC) joint arthritis can be demonstrated on examination by:
Tenderness to palpation of the AC joint
Pain is worse at the extremes of the shoulder abduction, from around 170 degrees onwards when the arm is overhead
Positive scarf test – pain caused by wrapping the arm across the chest and opposite shoulder
Diagnosis
Adhesive capsulitis is a clinical diagnosis based on the history and examination and excluding other causes of shoulder pain and stiffness. Imaging investigations are not usually required.
X-rays are usually normal. However, they are helpful for diagnosing osteoarthritis as a differential.
Ultrasound, CT or MRI scans can show a thickened joint capsule.
Management
Non-surgical options for improving symptoms and speeding up recovery are:
Continue using the arm but don’t exacerbate the pain
Analgesia (e.g., NSAIDs)
Physiotherapy
Intra-articular steroid injections
Hydrodilation (injecting fluid into the joint to stretch the capsule)
Surgery may be used in particularly resistant or severe cases. The options are:
Manipulation under anaesthesia – forcefully stretching the capsule to improve the range of motion
Arthroscopy – keyhole surgery on the shoulder to cut the adhesions and release the shoulder
Breast Abscess
A breast abscess is a collection of pus within an area of the breast, usually caused by a bacterial infection. This may be a:
Lactational abscess (associated with breastfeeding)
Non-lactational abscess (unrelated to breastfeeding)
Pus is a thick fluid produced by inflammation. It contains dead white blood cells of the immune system and other waste from the fight against the infection. When pus becomes trapped in a specific area and cannot drain, an abscess will form and gradually increase in size.
Mastitis refers to inflammation of breast tissue. Often this is related to breastfeeding (lactational mastitis), although it can be caused by infection. Bacteria can enter at the nipple and back-track into the ducts, causing infection and inflammation. Mastitis caused by infection may precede the development of an abscess.
Smoking is a key risk factor for infective mastitis and breast abscesses. Damage to the nipple (e.g., nipple eczema, candidal infection or piercings) provides bacteria entry. Underlying breast disease (e.g., cancer) can affect the drainage of the breast, predisposing to infection.
Causes
The most common causative bacteria are:
Staphylococcus aureus (the most common)
Streptococcal species
Enterococcal species
Anaerobic bacteria (such as Bacteroides species and anaerobic streptococci)
TOM TIP: It is worth becoming familiar with the effective antibiotics against different classes of bacteria. Staph aureus, streptococcal and enterococcal bacteria are gram positive, meaning that penicillins are likely to be effective. Flucloxacillin, in particular, is used against staph aureus skin infections (this association is worth remembering). However, anaerobic bacteria can also cause breast abscesses, and simple penicillins (e.g., amoxicillin or flucloxacillin) do not cover anaerobic bacteria. Co-amoxiclav (amoxicillin plus clavulanic acid) covers anaerobes. Metronidazole gives excellent anaerobic cover (also worth remembering), so it can also be added to the mix.
Presentation
The presentation of mastitis or breast abscesses is usually acute, meaning the onset is within a few days.
Mastitis with infection in the breast tissue presents with breast changes of:
Nipple changes
Purulent nipple discharge (pus from the nipple)
Localised pain
Tenderness
Warmth
Erythema (redness)
Hardening of the skin or breast tissue
Swelling
The key feature that suggests a breast abscess is a swollen, fluctuant, tender lump within the breast. Fluctuance refers to being able to move fluid around within the lump using pressure during palpation. Where there is infection without an abscess, there can still be hardness of the tissue, forming a lump, but it will not be fluctuant as it is not filled with fluid.
There may be generalised symptoms of infection, such as:
Muscle aches
Fatigue
Fever
Signs of sepsis (e.g., tachycardia, raised respiratory rate and confusion)
Management
The diagnosis of mastitis or a breast abscess can usually be made clinically, with a history and examination.
The NICE clinical knowledge summaries (last updated January 2021) recommend different management for mastitis depending on whether it is lactational or non-lactational.
Lactational mastitis caused by blockage of the ducts is managed conservatively, with continued breastfeeding, expressing milk and breast massage. Heat packs, warm showers and simple analgesia can help symptoms. Antibiotics (flucloxacillin or erythromycin/clarithromycin where there is penicillin allergy) are required where infection is suspected or symptoms do not improve.
Management of non-lactational mastitis involves:
Analgesia
Antibiotics
Treatment for the underlying cause (e.g., eczema or candidal infection)
Antibiotics for non-lactational mastitis need to be broad-spectrum. The NICE clinical knowledge summaries (last updated January 2021) recommend either:
Co-amoxiclav
Erythromycin/clarithromycin (macrolides) plus metronidazole (to cover anaerobes)
Management of a breast abscess requires:
Referral to the on-call surgical team in the hospital for management
Antibiotics
Ultrasound (confirm the diagnosis and exclude other pathology)
Drainage (needle aspiration or surgical incision and drainage)
Microscopy, culture and sensitivities of the drained fluid
Women who are breastfeeding are advised to continue breastfeeding when they have mastitis or breast abscesses. They should regularly express breast milk if feeding is too painful, then resume feeding when possible. This is not harmful to the baby and is important in helping resolve the mastitis or abscess.
Galactorrhoea
Galactorrhoea refers to breast milk production not associated with pregnancy or breastfeeding. Breast milk is produced in response to the hormone prolactin.
Prolactin is produced in the anterior pituitary gland. It is also produced in other organs, such as the breast and prostate. Prolactin also regulates aspects of immune function and metabolism.
Dopamine blocks the secretion of prolactin. Therefore, dopamine antagonists (i.e., antipsychotic medications) can result in raised prolactin and galactorrhea. Dopamine agonists (e.g., bromocriptine or cabergoline) can be used to suppress prolactin secretion.
Pregnancy and Breastfeeding
Milk production may start in small amounts during the second or third trimester of pregnancy, and leaking can occur during that time. Oestrogen and progesterone inhibit the secretion of prolactin. In pregnancy, higher levels of oestrogen and progesterone inhibit breast milk production.
Oxytocin stimulates breast milk excretion. Full milk production starts shortly after birth in response to oxytocin release and a rapid drop in oestrogen and progesterone.
Breast milk production will taper off and stop once breastfeeding stops.
Hyperprolactinaemia
Galactorrhoea is usually associated with a raised prolactin level (hyperprolactinaemia).
There is a long list of causes of hyperprolactinaemia, but the key causes to remember are:
Idiopathic (no cause can be found)
Prolactinomas (hormone-secreting pituitary tumours)
Endocrine disorders, particularly hypothyroidism and polycystic ovarian syndrome
Medications, particularly dopamine antagonists (i.e., antipsychotic medications)
Prolactin suppresses gonadotropin-releasing hormone (GnRH) by the hypothalamus, leading to reduced LH and FSH release. Therefore, hyperprolactinaemia can also present with:
Menstrual irregularities, particularly amenorrhoea (absent periods)
Reduced libido (low sex drive)
Erectile dysfunction (in men)
Gynaecomastia (in men)
Prolactinomas
Prolactinomas are tumours of the pituitary gland that secrete excessive prolactin. This may be associated with multiple endocrine neoplasia (MEN) type 1, an autosomal dominant genetic condition.
Prolactinomas can be:
Microprolactinomas – smaller than 10 mm
Macroprolactinomas – larger than 10 mm
Macroadenomas can have adverse effects relating to their size:
Headaches
Bitemporal hemianopia (loss of the outer visual fields in both eyes)
The optic chiasm sits just above the pituitary gland. The optic chiasm is the point where the optic nerves coming from the eyes cross over to different sides of the head. Only the nerves fibres containing the signal from the outer visual fields cross over, whereas the fibres from the inner visual fields continue on the same side. A pituitary tumour of sufficient size will start to press on the optic chiasm, where the nerves cross, leading to a visual field defect, with loss of vision in the outer visual fields in both eyes (the inner visual fields are spared). This is called bitemporal hemianopia.
TOM TIP: It is worth properly understanding and remembering bitemporal hemianopia, as it is commonly tested in exams. If you find it a bit confusing, there is a Zero to Finals YouTube video explaining it in detail. Remember to examine the visual fields in any patient with symptoms that may be related to a pituitary tumour.
Non-Milk Discharge
Other conditions can cause nipple discharge that is not breast milk:
Mammary duct ectasia
Duct papilloma
Pus from a breast abscess
Investigations
A pregnancy test is essential in women with childbearing potential presenting with breast milk production.
Blood tests include:
Serum prolactin
Renal profile (U&Es)
Liver function tests (LFTs)
Thyroid function tests (TFTs)
An MRI scan is the investigation of choice for diagnosing pituitary tumours.
Management
Management is targeted at the underlying cause.
Dopamine agonists (e.g., bromocriptine or cabergoline) can be used to treat the symptoms of hyperprolactinaemia. They block prolactin secretion and improve symptoms.
Trans-sphenoidal surgical removal of the pituitary tumour is the definitive treatment of hyperprolactinaemia secondary to a prolactinoma. The pituitary gland and tumour are accessed and removed through the nose and sphenoid bone.
Breast Lumps
There are numerous causes of breast lumps, many of which are benign. Any breast lump needs a thorough assessment to exclude breast cancer.
Basic Breast Anatomy
The breasts sit in front of the chest wall, which contains the ribs and pectoral muscles. Most of the breast is adipose (fatty) tissue. The areola surrounds the nipple. Behind the nipple are the ducts, which lead into the lobules, where breast milk is produced. Milk is secreted through the ducts and out of openings on the nipple.
Breast Cancer
The most significant differential of a breast lump is breast cancer.
Triple assessment of a breast lump is standard practice to exclude or diagnose cancer. This involves:
Clinical assessment (history and examination)
Imaging (ultrasound or mammography)
Histology (fine needle aspiration or core biopsy)
Clinical features that may suggest breast cancer are:
Lumps that are hard, irregular, painless or fixed in place
Lumps may be tethered to the skin or the chest wall
Nipple retraction
Skin dimpling or oedema (peau d’orange)
The NICE guidelines (updated January 2021) recommend a two week wait referral for suspected breast cancer for:
An unexplained breast lump in patients aged 30 or above
Unilateral nipple changes in patients aged 50 or above (discharge, retraction or other changes)
The NICE guidelines recommend also considering a two week wait referral for:
An unexplained lump in the axilla in patients aged 30 or above
Skin changes suggestive of breast cancer
The NICE guidelines suggest considering non-urgent referral for unexplained breast lumps in patients under 30 years.
Fibroadenoma
Fibroadenomas are common benign tumours of stromal/epithelial breast duct tissue. They are typically small and mobile within the breast tissue. They are sometimes called a “breast mouse”, as they move around within the breast tissue.
They are more common in younger women, aged between 20 and 40 years. They respond to the female hormones (oestrogen and progesterone), which is why they are more common in younger women and often regress after menopause.
On examination, fibroadenomas are:
Painless
Smooth
Round
Well circumscribed (well-defined borders)
Firm
Mobile (moves freely under the skin and above the chest wall)
Usually up to 3cm diameter
Fibroadenomas are not cancerous and are not usually associated with an increased risk of developing breast cancer. Complex fibroadenomas and a positive family history of breast cancer may indicate a higher risk.
Fibrocystic Breast Changes
Fibrocystic breast changes were previously called fibrocystic breast disease. However, fibrocystic breast changes, and generalised lumpiness to the breast, is considered a variation of normal and not a disease. The connective tissues (stroma), ducts and lobules of the breast respond to the female sex hormones (oestrogen and progesterone), becoming fibrous (irregular and hard) and cystic (fluid-filled). These changes fluctuate with the menstrual cycle.
It is a benign (non-cancerous) condition, although it can vary in severity and significantly affect the patient’s quality of life if severe. It is common in women of menstruating age. Symptoms often occur prior to menstruating (within 10 days) and resolve once menstruation begins. Symptoms usually improve or resolve after menopause.
Symptoms can affect different areas of the breast, or both breasts, with:
Lumpiness
Breast pain or tenderness (mastalgia)
Fluctuation of breast size
Management of fibrocystic breast changes is to exclude cancer and manage symptoms. Options to manage cyclical breast pain (mastalgia) include:
Wearing a supportive bra
Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen
Avoiding caffeine is commonly recommended
Applying heat to the area
Hormonal treatments (e.g., danazol and tamoxifen) under specialist guidance
Breast Cysts
Breast cysts are benign, individual, fluid-filled lumps. They are the most common cause of breast lumps and occur most often between ages 30 and 50, more so in the perimenopausal period. They can be painful and may fluctuate in size over the menstrual cycle.
On examination, breast cysts are:
Smooth
Well-circumscribed
Mobile
Possibly fluctuant
Breasts cysts require further assessment to exclude cancer, with imaging and potentially aspiration or excision. Aspiration can resolve symptoms in patients with pain. Having a breast cyst may slightly increase the risk of breast cancer.
Fat Necrosis
Fat necrosis causes a benign lump formed by localised degeneration and scarring of fat tissue in the breast. It may be associated with an oil cyst, containing liquid fat. Fat necrosis is commonly triggered by localised trauma, radiotherapy or surgery, with an inflammatory reaction resulting in fibrosis and necrosis (death) of the fat tissue. It does not increase the risk of breast cancer.
On examination, fat necrosis can be:
Painless
Firm
Irregular
Fixed in local structures
There may be skin dimpling or nipple inversion
Ultrasound or mammogram can show a similar appearance to breast cancer. Histology (by fine needle aspiration or core biopsy) may be required to confirm the diagnosis and exclude breast cancer.
After excluding breast cancer, fat necrosis is usually treated conservatively. It may resolve spontaneously with time. Surgical excision may be used if required for symptoms.
Lipoma
Lipomas are benign tumours of fat (adipose) tissue. They can occur almost anywhere on the body where there is adipose tissue, including the breasts.
On examination, lipomas are typically:
Soft
Painless
Mobile
Do not cause skin changes
They are typically treated conservatively with reassurance. Alternatively, they can be surgically removed.
Galactocele
Galactoceles occur in women that are lactating (producing breast milk), often after stopping breastfeeding. They are breast milk filled cysts that occur when the lactiferous duct is blocked, preventing the gland from draining milk. They present with a firm, mobile, painless lump, usually beneath the areola. They are benign and usually resolve without any treatment. It is possible to drain them with a needle. Rarely, they can become infected and require antibiotics.
Phyllodes tumour
Phyllodes tumours are rare tumours of the connective tissue (stroma) of the breast, occurring most often between ages 40 and 50. They are large and fast-growing. They can be benign (~50%), borderline (~25%) or malignant (~25%). Malignant phyllodes tumours can metastasise.
Treatment involves surgical removal of the tumour and the surrounding tissue (“wide excision”). They can reoccur after removal.
Chemotherapy may be used in malignant or metastatic tumours.
Pre Op Care
Before going to theatre for an operation, there are a number of things that need to be addressed:
Pre-operative assessment (pre-op)
Consent
Bloods (including groups and save / crossmatch)
Fasting
Medication changes
Venous thromboembolism assessment
Pre-Operative Assessment
Patients need to be assessed to determine if they are fit to undergo the specific operation. This involves exploring their co-morbidities, risk from anaesthesia, their frailty status and their cardiorespiratory fitness.
They require a full history of:
Past medical problems
Previous surgery
Previous adverse responses to anaesthesia
Medications
Allergies
Smoking
Alcohol use
Pregnancy needs to be considered in women of childbearing age. Consider asking about a family history of sickle cell disease. A general examination is performed to look for cardiovascular and respiratory disease.
Patients who may be malnourished (e.g., BMI under 18.5 or significant unintentional weight loss) may need input from a dietician and additional nutritional support before surgery and during admission.
ASA Grade
The American Society of Anesthesiologists (ASA) grading system classifies the physical status of the patient for anaesthesia. Patients are given a grade to describe their current fitness prior to undergoing anaesthesia/surgery:
ASA I – normal healthy patient
ASA II – mild systemic disease
ASA III – severe systemic disease
ASA IV – severe systemic disease that constantly threatens life
ASA V – “moribund” and expected to die without the operation
ASA VI – declared brain-dead and undergoing an organ donation operation
E – this is used for emergency operations
Pre-Operative Investigations
NICE guidelines (2016) are available outlining recommendations for routine preoperative tests for elective surgery, based on individual patient factors and the size of the operation. There will also be local guidelines. If in doubt, get advice from an anaesthetist.
Investigations may be required prior to surgery depending on the co-morbidities:
ECG if there is known or possible cardiovascular disease
Echocardiogram if there are heart murmurs, cardiac symptoms or heart failure
Lung function tests may be required if there is known or possible respiratory disease
Arterial blood gas testing may be required if there is known or possible respiratory disease
HbA1C (within the last 3 months) for people with known diabetes
U&Es for patients at risk of developing an acute kidney injury or electrolyte abnormalities (e.g., taking diuretics)
FBC may be required if there is possible anaemia, cardiovascular or kidney disease
Clotting testing may be required if there is known or possible liver disease
Group and save refers to sending off a sample of the patient’s blood to establish their blood group. The sample is saved in case they require blood to be matched to them for a blood transfusion. A group and save is done routinely where there is a lower probability that they will require blood products. No blood is assigned to the patient at this stage. A group and save sample will only be valid for a certain period (e.g., 7 days) depending on the local trust policy, after which a repeat sample is required.
Crossmatching involves the process of actually taking a unit or more of blood off the shelf and assigning it to the patient in case they need it quickly. This is done where there is a higher probability that they will require blood products, so that the blood is ready to go if required.
MRSA screening is routinely performed on all patients being admitted to hospital. This is usually arranged automatically by the nursing staff, so you don’t need to think about this.
Fasting Before Surgery
Patients undergo ‘fasting’ before surgery to ensure they have an empty stomach for the duration of their operation. The aim is to reduce the risk of reflux of food around the time of surgery (particularly during intubation and extubation), which subsequently can result in the patient aspirating their stomach contents into their lungs.
Fasting for an operation typically involves:
6 hours of no food or feeds before operation
2 hours no clear fluids (fully “nil by mouth”)
TOM TIP: When you assess an acutely unwell surgical patient, always consider whether there is any possibility they require emergency surgery. Acutely unwell surgical patients that potentially require emergency surgery are made nil by mouth and given maintenance IV fluids. Allowing them to eat and drink could have significant consequences if they need emergency surgery, and the anaesthetist and senior surgeon won’t be happy. This decision will often be reversed on the post-take ward round if the consultant or senior surgeon decides they are unlikely to need to go to theatre.
Specific Medications
Follow local guidelines for medication alterations before and after an operation.
Anticoagulants need to be stopped before major surgery. The INR can be monitored in patients on warfarin to ensure it returns to normal before the operation. Warfarin can be rapidly reversed with vitamin K in acute scenarios. Treatment dose low molecular weight heparin or an unfractionated heparin infusion may be used to bridge the gap between stopping warfarin and surgery in higher-risk patients (e.g., mechanical heart valves or recent VTE), and stopped shortly before surgery depending on the risk of bleeding and thrombosis. DOACs (e.g., apixaban, rivaroxaban or dabigatran) are stopped 24-72 hours before surgery depending on the half-life, procedure and kidney function.
Oestrogen-containing contraception (e.g., the combined contraceptive pill) or hormone replacement therapy (e.g., in perimenopausal women) need to be stopped 4 weeks before surgery to reduce the risk of venous thromboembolism (NICE guidelines 2010).
Long-term corticosteroids, equivalent to more than 5mg of oral prednisolone, require additional management around the time of surgery. Surgery adds additional stress to the body, which normally increases steroid production. In patients on long-term steroids, there is adrenal suppression that prevents them from creating the extra steroids required to deal with this stress. Management involves:
Additional IV hydrocortisone at induction and for the immediate postoperative period (e.g., first 24 hours)
Doubling of their normal dose once they are eating and drinking for 24 – 72 hours depending on the operation
Diabetes
The stress of surgery increases blood sugar levels. However, fasting may lead to hypoglycaemia. In general, the risk of hypoglycaemia is greater than hyperglycaemia.
Certain oral anti-diabetic medications may need to be adjusted or omitted around surgery:
Sulfonylureas (e.g., gliclazide) can cause hypoglycaemia and are omitted until the patient is eating and drinking
Metformin is associated with lactic acidosis, particularly in patients with renal impairment
SGLT2 inhibitors (e.g., dapagliflozin) can cause diabetic ketoacidosis in dehydrated or acutely unwell patients
In patients on insulin going for surgery (follow the local policy):
Continue a lower dose (BNF recommends 80%) of their long-acting insulin
Stop short-acting insulin whilst fasting or not eating, until eating and drinking again
Have a variable rate insulin infusion alongside a glucose, sodium chloride and potassium infusion (“sliding-scale”) to carefully control their insulin, glucose and potassium balance
VTE Prophylaxis
Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE). Surgery, particularly where the patient is likely to be immobilised (e.g., orthopaedic surgery), significantly increases the risk of venous thromboembolism. There are local and national policies on reducing the risk that involve:
Low molecular weight heparin (LMWH) such as enoxaparin
DOACs (e.g., apixaban or rivaroxaban) may be used as an alternative to LMWH
Intermittent pneumatic compression (inflating cuffs around the legs)
Anti-embolic compression stockings
Post Op Care
Immediately after the operation, the patient will go to the recovery room to be monitored closely whilst they regain consciousness. Once they are conscious and stable, they can return to the ward. Patients may be transferred to HDU or ICU depending on their condition and the monitoring requirements post-operatively.
Enhanced Recovery
Enhanced recovery aims to get patients back to their pre-operative condition as quickly as possible, by encouraging independence, early mobility and appropriate diet. There are increased nutritional requirements after the physiological stress of surgery, so sufficient calories are very important. The aim is to discharge as soon as possible. This leads to better outcomes for the patient.
The principles of enhanced recovery are:
Good preparation for surgery (e.g., healthy diet and exercise)
Minimally invasive surgery (keyhole or local anaesthetic where possible)
Adequate analgesia
Good nutritional support around surgery
Early return to oral diet and fluid intake
Early mobilisation
Avoiding drains and NG tubes where possible, early catheter removal
Early discharge
Analgesia
Adequate analgesia in the post-operative period is important to encourage the patient to:
Mobilise
Ventilate their lungs fully (reducing the risk of chest infections and atelectasis)
Have an adequate oral intake
Analgesia is usually started in theatre by the anaesthetist, with regular paracetamol, NSAIDs and opiates if required (e.g., regular modified-release oxycodone with immediate-release oxycodone as required for breakthrough pain). The surgeon may put local anaesthetic into the wound to help with the initial pain after the procedure. Analgesia should be reduced and stopped as symptoms improve. There is more detail on analgesia in the anaesthetics section.
Non-steroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen, naproxen and diclofenac may be inappropriate or contraindicated in patients with:
Asthma
Renal impairment
Heart disease
Stomach ulcers
Patient Controlled Analgesia
Patient-controlled analgesia (PCA) involves an intravenous infusion of a strong opiate (e.g., morphine, oxycodone or fentanyl) attached to a patient-controlled pump. This involves the patient pressing a button as pain starts to develop, for example during a contraction in labour, to administer a bolus of this short-acting opiate medication. The button will stop responding for a set time after administering a bolus to prevent over-use. Only the patient should press the button (not a nurse or doctor).
Patient-controlled analgesia requires careful monitoring. There needs to be input from an anaesthetist, and facilities in place if adverse events occur. This includes access to naloxone for respiratory depression, antiemetics for nausea, and atropine for bradycardia. The anaesthetist may prescribe background opiates (e.g., patches) in addition to a PCA, but avoid other “as required” opiates whilst a PCA is in use. The machine is locked to prevent tampering.
Post-Operative Nausea and Vomiting
Nausea and vomiting are common in the 24 hours after an operation and is called post-operative nausea and vomiting (PONV). There are many causes, including the surgical procedure, anaesthetic, pain and opiates.
Risk factors for post-operative nausea and vomiting are:
Female
History of motion sickness or previous PONV
Non-smoker
Use of postoperative opiates
Younger age
Use of volatile anaesthetics
Prophylactic antiemetics are often given at the end of the procedure by the anaesthetist to prevent PONV from occurring. Common options for prophylaxis given at the end of the operation are:
Ondansetron (5HT3 receptor antagonist) – avoided in patients at risk of prolonged QT interval
Dexamethasone (corticosteroid) – used with caution in diabetic or immunocompromised patients
Cyclizine (histamine (H1) receptor antagonist) – caution with heart failure and elderly patient
Examples of “rescue” antiemetics used in the post-operative period if nausea or vomiting occur are:
Ondansetron (5HT3 receptor antagonist) – avoid in patients at risk of prolonged QT interval
Prochlorperazine (dopamine (D2) receptor antagonist) – avoid in patients with Parkinson’s disease
Cyclizine (histamine (H1) receptor antagonist) – caution with heart failure and elderly patients
Some local guidelines also refer to the P6 acupuncture point on the inner wrist. There is evidence that pressure to this area can reduce nausea.
Tubes
Post-operative patients may have a catheter, drains or nasogastric tube, and these will be monitored and removed when appropriate.
Drains are usually removed once they are draining minimal or no blood or fluid
Nasogastric tubes are removed when they are no longer required for intake or drainage of gas or fluid
Catheters are removed when the patient can mobilise to the toilet
Removal of a catheter is called a trial without catheter (TWOC). It is called this as there is a risk the patient will find it difficult to pass urine normally and go into urinary retention, and the catheter may need to be reinserted for a period before removal can be tried again. This is quite common, more so in male patients.
Nutritional Support
Good nutrition is important for healthy wound healing and overall recovery from surgery. A dietician may be involved.
Where possible, patients should get their nutrition via their gastrointestinal tract. Having nutrition via the gastrointestinal tract is called enteral feeding. This could be by:
Mouth
NG tube
Percutaneous endoscopic gastrostomy (PEG) – a tube from the surface of the abdomen to the stomach
Total parenteral nutrition (TPN) involves meeting the full ongoing nutritional requirements of the patient using an intravenous infusion of a solution of carbohydrates, fats, proteins, vitamins and minerals. This is used where it is not possible to use the gastrointestinal tract for nutrition. It is prescribed under the guidance of a dietician. TPN is very irritant to veins and can cause thrombophlebitis, so is normally given through a central line rather than a peripheral cannula.
Post-Operative Complications
Patients are monitored for a long list of complications that can occur in the post-operative period:
Anaemia
Atelectasis is where a portion of the lung collapses due to under-ventilation
Infections (e.g., chest, urinary tract or wound site)
Wound dehiscence is where there is separation of the surgical wound, particularly after abdominal surgery
Ileus is where peristalsis in the bowel is reduced (typically after abdominal surgery)
Haemorrhage with bleeding into a drain, inside the body creating a haematoma or from the wound
Deep vein thrombosis and pulmonary embolism
Shock due to hypovolaemia (blood loss), sepsis or heart failure
Arrhythmias (e.g., atrial fibrillation)
Acute coronary syndrome (myocardial infarction) and cerebrovascular accident (stroke)
Acute kidney injury
Urinary retention requiring catheterisation
Delirium refers to fluctuating confusion and is more common in elderly and frail patients
Anaemia
A post-op full blood count is used to measure the haemoglobin.
Treatment of anaemia is based on individual factors and preferences alongside local guidelines. As a rough guide (local policies will vary):
Hb under 100 g/l – start oral iron (e.g., ferrous sulphate 200mg three times daily for three months)
Hb under 70-80 g/l – blood transfusion in addition to oral iron
Patients with symptoms of anaemia or underlying cardiovascular or respiratory disease may need a transfusion with higher haemoglobin levels.
It is worth noting that Jehovah’s Witnesses may refuse blood transfusions. They often have a written advanced directive to state that even in an emergency scenario where they lose capacity, blood transfusions are prohibited. Provided they have capacity and are making an informed decision, they have the right to autonomy. Measures are taken before surgery to optimise any anaemia, and careful steps are taken during surgery to minimise blood loss.
Polycystic Kidney Disease
Polycystic kidney disease is a genetic condition where the kidneys develop multiple fluid-filled cysts. Kidney function is also significantly impaired. There are a number of associated findings outside the kidneys such as hepatic cysts and cerebral aneurysms. Palpable, enlarged kidneys may be felt on examination.
There is an autosomal dominant and an autosomal recessive type. The autosomal dominant type of PKD is more common than the autosomal recessive type.
Diagnosis is by kidney ultrasound scan and genetic testing.
Autosomal Dominant Type
Autosomal Dominant Genes
PKD-1: chromosome 16 (85% of cases)
PKD-2: chromosome 4 (15% of cases)
Extra-renal Manifestations
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation
Complications
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria can occur with cyst rupture (this usually resolves within a few days
Renal stones are more common in patients with PKD
End-stage renal failure occurs at a mean age of 50 years
Autosomal Recessive Type
Autosomal recessive polycystic kidney disease (ARPKD) is caused by a gene on chromosome 6. It is rarer and more severe. It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine.
Features
The oligohydramnios leads to underdevelopment of the lungs resulting in respiratory failure shortly after birth. Patients may require dialysis within the first few days of life. They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge. They usually have end-stage renal failure before reaching adulthood.
Management
Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease. It is recommended by NICE in certain situations although it should be initiated and monitored by a specialist.
Management of polycystic kidney disease is mainly supportive of the complications:
Antihypertensives for hypertension.
Analgesia for renal colic related to stones or cysts.
Antibiotics for infection. Drainage of infected cysts may be required.
Dialysis for end-stage renal failure.
Renal transplant for end-stage renal failure.
Other management steps:
Genetic counselling
Avoid contact sports due to the risk of cyst rupture
Avoid anti-inflammatory medications and anticoagulants
Regular ultrasound to monitor the cysts
Regular bloods to monitor renal function
Regular blood pressure to monitor for hypertension
MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history
Rhabdomylosis
Rhabdomyolysis is a condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.
The muscle cells (myocytes) undergo cell death (apoptosis). The cell death results in muscle cells releasing:
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine kinase
Potassium is the most immediately dangerous breakdown product, as hyperkalaemia can cause cardiac arrhythmias that can potentially result in a cardiac arrest.
These breakdown products are filtered by the kidney and cause injury to the kidney. Myoglobin in particular is toxic to the kidney in high concentrations. This results in acute kidney injury. The acute kidney injury causes the breakdown products to further accumulate in the blood.
Causes
Anything that causes significant damage to muscle cells can cause rhabdomyolysis:
Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)
Crush injuries
Seizures
Signs and Symptoms
Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine
Investigations
Creatine Kinase (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury.
Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood.
Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia.
ECG is important in assessing the heart’s response to hyperkalaemia.
Management
Suspect rhabdomyolysis in patients with trauma, crush injury, prolonged immobilisation or excessive exercise.
IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.
Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.
Consider IV mannitol. This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.
Treat complications, particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).
Renal Tubular Acidosis
Renal tubular acidosis is where there is a metabolic acidosis due to pathology in the tubules of the kidney. The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH. There are four types each with different pathophysiology.
Type 1 and type 4 are the two that may come up in your exams and are most relevant to clinical practice.
Type 1 Renal Tubular Acidosis
Type 1 renal tubular acidosis is due to pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions.
There are many causes:
Genetic. There are both autosomal dominant and recessive forms.
Systemic lupus erythematosus
Sjogren’s syndrome
Primary biliary cirrhosis
Hyperthyroidism
Sickle cell anaemia
Marfan’s syndrome
Presentation:
Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)
Results:
Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)
Treatment is with oral bicarbonate. This corrects the other electrolyte imbalances.
Type 2 Renal Tubular Acidosis
Type 2 renal tubular acidosis is due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood. Excessive bicarbonate is excreted in the urine. Fanconi’s syndrome is the main cause.
Results:
Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)
Treatment is with oral bicarbonate.
Type 3 Renal Tubular Acidosis
Type 3 renal tubular acidosis is a combination of type 1 and type 2 with pathology in the proximal and distal tubule. This is rare and unlikely to appear in your exams or clinical practice.
Type 4 Renal Tubular Acidosis
Type 4 renal tubular acidosis is caused by reduced aldosterone. This is probably the most common cause of renal tubular acidosis and the most likely to turn up in your exams and clinical practice.
This can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.
Results:
Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH
Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.
Acute Tubular Necrosis
Acute tubular necrosis is damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common cause of acute kidney injury. Damage to the kidney cells occurs due to ischaemia or toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.
Causes
Ischaemia can occur secondary to hypoperfusion in:
Shock
Sepsis
Dehydration
Direct damage from toxins can occur due to:
Radiology contrast dye
Gentamycin
NSAIDs
Urinalysis
“Muddy brown casts” found on urinalysis is a pathognomonic finding specific to acute tubular necrosis. There can also be renal tubular epithelial cells in the urine.
Management
Treatment is the same as with other causes of an acute kidney injury:
Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications
Interstitial Nephritis
Interstitial nephritis is term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney. This is different to glomerulonephritis, where there is inflammation around the glomerulus. There are two types of interstitial nephritis: acute interstitial nephritis and chronic tubulointerstitial nephritis.
Acute Interstitial Nephritis
Acute interstitial nephritis presents with acute kidney injury and hypertension. There is acute inflammation of the tubules and interstitium. This is usually caused by a hypersensitivity reaction to:
Drugs (e.g. NSAIDS or antibiotics)
Infection
Other features of a generalised hypersensitivity reaction can accompany the acute kidney injury:
Rash
Fever
Eosinophilia
Management involves treating the underlying cause. Steroids have a role in reducing inflammation and improving recovery.
Chronic Tubulointerstitial Nephritis
Chronic tubulointerstitial nephritis involves chronic inflammation of the tubules and interstitium. It presents with chronic kidney disease.
It has a large number of underlying autoimmune, infectious, iatrogenic and granulomatous disease causes.
Management involves treating the underlying cause. Steroids have a role when guided by a specialist.
Diabetic Nephropathy
Diabetic nephropathy is the most common cause of glomerular pathology and chronic kidney disease in the UK. The chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis.
Proteinuria is a key feature of diabetic nephropathy. This is due to damage to the glomerulus allowing protein to be filtered from blood to urine.
Patients with diabetes should have regular screening for diabetic nephropathy by testing the albumin:creatinine ratio and U&Es.
Management
Treatment is by optimising blood sugar levels and blood pressure.
ACE inhibitors are the treatment of choice in diabetics for blood pressure control. They should be started in patients with diabetic nephropathy even if they have a normal blood pressure.
