Kyphosis and Scheuermann’s disease

Kyphosis is the apical-dorsal curvature of the spine in the sagittal plane (i.e. curves away from the body).  There is normal thoracic kyphosis of around 20-40°.  Abnormal kyphosis is a curvature (measured as Cobb’s angle (between T2-T12)) of >45°.

Background/Aetiology

• Pathological kyphosis most commonly occurs in the thoracic spine although rarely can occur elsewhere in the spine.
• It is not uncommon amongst the elderly population (occurs in around 20-30% of patients >65) and is more common in women
• Risk factors include
  • Osteoporosis; vertebral (wedge) fractures and degenerative disc disease
  • Problems with proprioception; poor posture; spinal muscle weakness/attenuation
  • Other causes include trauma; ankylosing spondylysis and other arthritides; and rarely neoplasms and infections
• Kyphosis can impair physical functioning; quality of life and mortality directly and indirectly
  • Increased risk of vertebral fracture
  • May affect balance and likelihood of falls
  • Decline in gait speed/mobility
  • In some cases, can impair pulmonary, GI and gynaecological function

Presentation

• Most patients are asymptomatic and kyphosis is purely aesthetic
• Some may present with back pain
• On examination, there is usually a thoracic kyphosis and there may also be compensatory lumber hyperlordosis
  • Tight hamstrings/difficulty with straight leg raise may also be present
• Rare but important features include those of myelopathy i.e. neurological problems (including pain/altered sensation, weakness, altered tone/reflexes, problems with gait etc)
• Indications for surgical management (note not absolute)
  • Neurological deficits
  • Kyphosis >70° (no pain) or >65° with pain
  • Loss of anterior vertebral height >50%

Management

• For purely postural related kyphosis, exercises and education about posture may benefit patient symptoms (may not entirely relieve kyphosis)
• Surgical management is reserved only for severe cases
  • Smith-Peterson osteotomy, pedicle subtraction and vertebral column resection can all be options for corrections
  • Anterior release spinal fusion may also be used in Scheuermann’s disease/severe cases

Scheuermann’s disease

• In children and adolescents, abnormal kyphosis can occur as what is thought to be the result of a genetic defect causing collapse of the vertebrae
  • A family history is common
  • Patients
• Classically defined as anterior wedging of >5° across three consecutive vertebrae, and is different from postural kyphosis by the rigidity of the kyphosis (not corrected by hyperextension)

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Mild Cognitive Impairment

Definition

Isolated cognitive impairment(s) identified as abnormal (compared to expected) and representing a decline from previous level of function.  The cognitive impairment should not be so severe as to affect social or occupational functioning (at which point the diagnosis of dementia would be more appropriate).

Background

• It is uncertain whether MCI is a normal sequelae of the aging process or whether there is a pathological process underlying it
  • Risk/contributing factors include
    • Cerebrovascular events
    • Hypothyroidism and parathyroid disease
    • Malnutrition and vitamin deficiencies (e.g. B12 and folate)
    • Polypharmacy (especially sedating medications)
    • Mood disorders
    • Drug/alcohol abuse
• It is a significant risk factor for dementia (around 15% of patients with MCI progress to dementia per year (usually Alzheimer’s); and up to 50% later develop dementia)
• There are several different ‘types’ of MCI
  • Amnesic (poor memory function)- most likely to go on to develop Alzheimer’s type dementia
  • Non-amnesic MCI
    • Usually impairment of executive function e.g. ability to make sound decisions, judge time or sequences involved in complex tasks, visual perception etc

Presentation

• Most present with vague symptoms of cognitive decline (e.g. poor memory- forgetting conversations, recent events etc)
  • Quite often, relatives or close friends are more concerned
• Note that it can be difficult to tease apart what is MCI, what is normal and what could be secondary to other problems e.g. sensory impairments

Assessment

• There are several assessments commonly used to identify cognitive impairment
  • The Mini-mental state examination (MMSE) is the most commonly used in practice to quickly assess cognition
    • Addenbrooke’s testing is more extensive and is usually used for formal assessments
  • Other tests include the 6-CIT, AMT, GPCOG and the 7 minute screen.
• Other routine tests (e.g. FBC, U&Es, Calcium, Glucose, LFTs, B12/folate, TFTs) should be performed to rule out an potentially reversible cause

Management

• Coping mechanisms e.g. lists; tackling one job at a time; memory aids (clocks/watches/calendars; storage places for items such as keys/glasses; setting reminders etc)
• Patients with MCI should be followed up every so often to check that there has not been a deterioration
  • Referral to a specialist should be made if cognitive decline is thought to be impacting on daily living (i.e. dementia is being considered)

 

Pre-operative assessment

NB Many trusts will have a preassessment form which will guide you through the assessment and cover all the questions needed to be asked

• WIPE 
  • wash hands, introduce self, check patient details and explain
    • NB When checking patient details, you should also check what operation they are to have (and what kind of anaesthesia) and when this is going to be
• History
  • Ask about present health:
    • Presenting complaint and history
    • General systems history (CVS; Resp; GI; GU; Endo/Diabetes; Neuro)
    • Any recent or current illness
    • Current exercise tolerance
    • Any smoking? Any alcohol? Who is with them at home?
    • Any sleep apnoea?
  • Ask about PMHx and Rx
    • In particular any diabetes, epilepsy, any CVD, asthma/COPD, hypertension (and how well each is controlled)
    • What medication is the patient taking?
      • Some medications may require advice re: stopping before surgery (and when to restart)
      • Make sure to ask about aspirin, clopidogrel, rivaroxiban (and other NOACs), warfarin… in particular
    • ANY ALLERGIES?
    • Previous surgical history
  • Anaesthetic Hx
    • Previous general anaesthetics; reactions/complications
      • If the patient has not had any GAs, ask about family history of reactions/complications
    • Dental prosthesis
  • Social
    • Smoking and Drinking
    • Exercise tolerance
    • Support (independent/family/care etc)
  • Family Hx
  • Full systemic review (cardiorespiratory; gastrointestinal; neurological; musculoskeletal; urological/gynaecological etc)
• Examination
  • Anaesthetic assessment
    • Examine neck movement and any limitation in ROM
    • Examine how wide the patient can open their jaw and grade this (Mallampati grading)
      1. See all of soft palate and uvula
      2. See half of uvula
      3. See a small gap at end of soft palate
      4. Only see hard palate
  • Multi-system assessment (Head to toe)
    • Examine Cardiorespiratory system fully; abdomen; calves +/- any systems involved in the surgery

NICE recommends various investigations based on the severity of the surgery (minor; intermediate; major and major +; as well as cardiovascular surgery and neurosurgery) as well as patient baseline function and comorbidities (ASA graded depending on severity of co-morbidity).

In general, an investigation is only required to confirm a diagnosis or exclude a differential; assess the appropriateness of the surgical intervention; assess fitness for surgery.  In short- will the investigation alter the surgical management of the patient.  Investigations may include (if they have not been requested a week prior to surgery)

• CXR
• ECG
• Bloods (FBC; U&Es; clotting +/- others e.g. LFTs; glucose; amylase)
• Urinalysis
• Blood gases
• Lung function tests

Other things to consider pre-operatively

• VTE Prophylaxis
• Drugs
  • In particular, diabetes drugs e.g. oral antihyperglycaemics (see also Diabetes and Surgery)
  • When to stop antiplatelets and anticoagulants
  • Antihypertensives (diuretics and ACEIs usually withheld on the day of surgery)
• Fasting information
• Consent

Assessing a patient with memory problems

History

• NB It is vital to get a corroborative history from a relative close friend, particularly where it is them that are more concerned about memory problems than the patient themselves.
  • It may be useful to interview them separately
  • If the patient comes alone worried about memory problems, it is often a sign that lessens the likelihood of dementia
• In general, consider the age of the patient
• Assess what the patient means by memory problems
  • Are they having trouble finding words?  Are they losing/forgetting things?  Are they getting lost?
    • i.e. is it a problem with working memory? (immediate memory)
    • is it a problem with episodic memory? (short term/anterograde or old/retrograde)
    • is it a problem with semantic memory? (word meaning and general knowledge)
    • is it a problem with implicit memory? (learned/automatic responses- can be complex tasks e.g. driving, or more simple ones e.g. dressing)
  • What sort of problems is this causing? (impact on life)
• Take a history of PC
  • Onset
    • Particularly- any triggers such as adverse life events
      • Depression is not an uncommon cause of memory problems- important to ask about mood and other associated symptoms e.g. sleep
  • Tempo/progression
    • Have things been deteriorating?  Are the problems constant or are there particular times of day when things are worse (sunset- ‘sundowning’)
    • Is there a step-wise progression?
  • Impact on work/family and any issues about safety e.g. driving/cooking, or self-care/hygiene e.g. shopping
  • Ask about associated symptoms/features
    • Mood, enjoyment in activities, personality changes, psychotic symptoms etc
    • Appetite and sleep changes
    • Walking or balance problems
    • Anorexia, weight loss, incontinence, change in bowel habits
    • Any changes in consciousness
• Past medical history
  • Detailed medical and drug history (including compliance) are very important, particularly in identifying an iatrogenic cause (drug induced problems)
    • Vascular disease e.g. TIA/stroke, hypertension, ischaemic heart disease
  • Past psychiatric history
• Family history
  • e.g. Alzheimer’s disease
• Social history
  • Are they living alone (in own home or another residence)?
  • Do they have any routine?
  • Alcohol consumption (past and present)?

Examination

• Cognitive testing (most commonly tested using Mini-mental state examination ©– good screening tool)
  • Orientation (time, place, person)
  • Attention
  • Memory
  • language
  • executive function
  • praxis e.g. hand movement/coordination
  • visuaspatial function
• If there is concern over whether the memory problems are associated with delirium, the patient can be screened for features (e.g. 4AT score)
• For a thorough assessment, the Addenbrookes cognitive assessment (ACE) is a more in depth assessment used for the formal diagnosis of dementia
  • see here for ACE example along with other forms of cognitive tests
• Perform a routine physical exam to note any signs which may suggest a treatable underlying cause

Investigations

• Imaging
  • CT scan of the brain is usually done in all patients to rule out an organic cause of confusion/dementia
  • SPECT/PET/MRI imaging is becoming more useful at diagnosing different types of dementias e.g. fronto-temoral
• Blood tests
  • B12, TFTs

Differential Diagnosis

• Dementia (of which there are differentials within this)
• Delirium
• IMPORTANT TO RULE OUT OTHER POTENTIALLY TREATABLE CAUSES OF COGNITIVE IMPAIRMENT
• 

Depression

Background

• Characterised by persistent low mood and/or loss of pleasure in most activities and a range of associated features.
• Extremely common: about 1 in 20 adults experience an episode of depression every year (majority mild and reactive)

Risk Factors

• Complex interaction of:
  • Biological factors e.g. family history; head injury; physical illness
  • Psychosocial factors e.g. abuse, unemployment, lack of social relationships, poverty
  • Personality
• High risk factors include
  • History of depression, suicide or abuse
  • Significant physical illness
  • Other mental health condition (including learning disability)
  • Family history
  • Frequent GP/A&E visits

Assessment of a patient who is at risk or presents with low mood

• To screen ask about whether the patient has one of the core symptoms of depression
  • Have you been feeling down, depressed or hopeless recently (low mood)?
  • Do you have little pleasure or interest in doing things?
  • (Have you felt like you have no energy recently? While this is a core feature according to ICD, it is less specific for depression than the others.  NICE no longer consider it a core feature but as a minor feature)
• Other symptoms of depression include
  • Worthlessness/excessive or inappropriate guilt
  • Suicidal ideation; recurrent thoughts of death
  • Diminished concentration/indecisiveness
  • Psychomotor agitation or retardation
  • Poor sleep pattern (insomnia/hypersomnia)
  • Loss or gain of appetite +/- weight change
  • (Reduced self-confidence)
  • (Bleak and pessimistic views of the future)
• Ask about other psychiatric features, commonly anxiety
  • IMPORTANT to ask about mania/hypomania (e.g. feeling abnormally happy/high, irrational behaviour, expenditure etc) to exclude bipolar
  • Also eating disorders
  • Alcohol/substance misuse
  • Features of psychosis
• ALWAYS ask about thoughts of suicide and self harm and go into detail where possible
• Ask about possible triggers (e.g. relationship problems; employment issues; family problems etc), onset, timing, progression etc (i.e. take a full HPC)
• It is important to take an extensive history in patients with possible depression, including HPC; Past psychiatric history; PMHx and drugs; FHx; Social Hx (drugs and alcohol are extremely important; as are housing, employment history, acitivities/hobies, relationships); Personal Hx (including developmental hx; childhood/growing up/school; family relationships; personal relationships; etc)
  • In reality, this may not be possible due to time constraints, so screening questionnaires e.g. PHQ-9 and HAD scale, may be useful
• On MSE
  • Appearance and behaviour can vary from normal to unkempt, poor communication and eye contact, weepy, frustrated
  • Speech can be slowed and in extreme cases words may be few (word poverty)
  • Mood is often subjectively and objectively low and affect can be flat
  • There is rarely any disorder of thought or perception although the patient may obsess over ideas of suicide or self harm; guilt or worthlessness
  • Insight can be preserved or the patient may be so depressed as to be pessimistic about treatments
  • Cognition is rarely impaired significantly by depression but may be impaired by co-existent dementia

Diagnosis

• NB Different associations have different criteria
  • NICE
    • At least 5 out of 9 NICE features (at least one out of two core symptoms)
    • Mild depression is where all symptoms are relatively mild, with little impairment of daily living
    • Moderate depression is defined as ‘symptoms and functional impairment between mild and severe depression’ (some marked symptoms)
    • Severe depression would be 7-9 symptoms, some of which are severe and impair daily living
  • ICD-10
    • At least 2 core symptoms and at least two minor symptoms (mild)
      • 3-4 minor symptoms (moderate)
      • All three core symptoms plus 4 or more minor symptoms with impairment of daily activity (severe)

Management

• For mild/subthreshold depression- provide information and wait, giving follow-up in 2 weeks to see if they are better
  • Consider psychological therapy if symptoms persist
• For moderate/severe depression
  • offer pharmacological therapy and high intensity psychotherapy
• Psychological
  • Low intensity for subthreshold/mild depression
    • e.g. individual guided self-help or computerised therapy based on CBT principles (e.g. MoodJuice website and phoneline); group based activity programmes e.g. Dundonald centre/group based peer support
  • High intensity for moderate-severe depression
    • Group or individual CBT; interpersonal therapy; behavioural activation; couples therapy
• Pharmacological
  • NB Consider toxicity and suicide risk; explain symptoms of anxiety may worsen initially and that most take some time to work
  • Usually, start with generic SSRI for most individuals (citalopram is often used first line, but fluoxetine, paroxetine and sertraline are alternatives)
    • Sertraline is often used in patients with significant physical illness due to its side effect profile
  • Antidepressant treatment should be trialled for minimum of 6 weeks (unless there are side effects after week 1)
    • If successful should be continued for 6 months before being reviewed and at least 2 years if the patient is at risk of relapse
    • If unsuccessful, trial another SSRI*
      • subsequently, other groups of antidepressants may be trialed
      • in general, stop the SSRI over 4 weeks before trialing a second (with fluoxetine, wait 4-7 days before starting alternative)
        • Venlafaxine may be cross-tapered

Dysthymia/Persistent low mood

• Defined as subthreshold features of depression lasting >2 years

Treatment refractory depression

• There are multiple definitions of treatment refractory depression
  • Some quote a minimum trial of at least 2 antidepressants of different classes (i.e. if followed guidelines- at least 3)
  • Some say at least four
• Chronic depression is defined as criteria for depression lasting >2 years
• In any case, it is important to rule out pseudo-resistance i.e. patient not taking medications
• Treatment options include pharmacological combination treatment (namely SSRI or venlafaxine with mirtazapine); augmentation therapy (usually with lithium, although the evidence for this is minimal); ECT which has been shown to be effective but does include side effects such as impaired cognition; Vagal nerve stimulation/DBS (rarely used due to highly specialist nature).

Psychotic depression

• Usually, there is pervasive low mood and marked psychomotor disturbance with accompanying delusions and/or hallucinations.  Constipation may be a feature (patients can think that their bowels have been sewn up or have turned to dust.
• Typically paranoid and mood-congruent, or hypochondriacal:
  • “People are out to get and kill me.”  “I’m being poisoned  to punish me for my sins.”  “I’ve got cancer because I deserve it.”
• Cotard’s syndrome
  • More commonly found in the elderly, Cotard’s is characterised by classic nihilistic delusions:
    • I’m dead- the world around me isn’t real.
• Treatment
  • For many of these patients, ECT will be an option for first line treatment (particularly effective).
  • Antipsychotic plus an antidepressent should be only used in combination with caution as both can enhance the side effect profile of the other. Careful monitoring is required.  Alternatively, drugs with dual-effects e.g. Amoxapine (TCA with D2 antagonism) or Olanzapine may be used, especially for episodic attacks.

Atypical Depression

• Clinical features seem depressive but are atypical (funnily enough).
  • Mood is low but reactive (i.e. able to ‘enjoy’ activities- maybe not as much as usual)
• PLUS 2 or more of
  • Hypersomnia (>10hrs/day at least 3 days/wk for 3 months)
  • Weight gain/ increase in appetite
  • Leaden paralysis (heavy arms and legs)- at least 1 hour/day, 3 days/week for 3 months
  • Over-sensitivity to perceived rejection- can result in significant social impairment/work problems.
• It is often associated with anxiety and often responds well to treatment with phenelzine (MAOI- which are usually 3rd line in depression).

Somatiform Depression

• This subtype of depression is often more described as ‘biological’ depression.  It can often be more severe that other forms but is also more amenable to pharmacological treatment.  ECT is also often effective in these patients
• It can be diagnosed in the presence of 4 or more of the following clinical features:
  • Marked loss of enjoyment/pleasure/interest in activities that are normally enjoyable (anhydonia)
  • Lack of emotional reaction to events or activites that normally produce an emotional response (blunt affect)
  • Early morning waking (>2hours before normal)
  • Depression worse in morning
  • Objective evidence of marked psychomotor retardation or agitation (reports from others)
  • marked loss of appetite and weight loss (>5% of body mass in 1 month)
  • marked loss of libido

Hyponatraemia and Syndrome of Inappropriate Antidiuretic hormone production (SIADH)

Background

• Hyponatraemia is the most common electrolyte disturbance encountered.  Up to 30% of hospitalised patients will be hyponatraemic.  SIADH is the most common cause.
• Usually asymptomatic but can manifest as anorexia, nausea, vomiting, confusion, lethargy, seizures and coma.
  • Severity of symptoms are usually representative of the rate of change rather than the severity of change (chronic hyponatraemia is rarely symptomatic)

Classifications of hyponatraemia

• Hypovolaemic (sodium deficit with a relatively smaller water deficit)
  • e.g. renal sodium loss; diuretic therapy (esp thiazide diuretics); adrenocortical failure (e.g. Addison’s disease); GI sodium losses (diarrhoea/vomiting); burns
    • i.e. cause is often apparent (except perhaps in Addison’s/hypoadrenalism)
  • may have features of hypovolaemia e.g. thirst, dizziness, weakness, dry mucous membranes, reduced urine output etc
• Euvolaemic (water retention alone)
  • Polydipsia; excessive electrolyte-free (e.g. 5% dextrose solution) infusions; SIADH (see below); hypothyroidism
• Hypervolaemic (sodium retention with relatively greater water retention)
  • Congestive heart failure; cirrhosis; nephrotic syndrome; chronic renal failure

SIADH

Physiology

• During resting states (normal homeostasis)- ADH is produced in the hypothalamus and stored in the posterior pituitary
• Osmoreceptors in the hypothalamus detect changes in the ECF osmolality (most commonly as a result of serum sodium concentrations)
• In the hyperosmolar state, they stimulate ADH secretion.  In the hypoosmolar state, they result in decreased production of ADH.
• The action of ADH is primarily renal: increasing the number of aquaporin receptors in the collecting tubule, allowing for a greater reabsorption of water and dilution of the blood i.e. lower sodium concentration is actually due to higher ECF water content than actual number of moles of sodium
• SIADH is characterised by
  • hyponatraemia
  • inappropriately elevated urine osmolality (>100mmol/kg) (can be higher than plasma osmolality)
  • excessive urine sodium concentrations (>30mmol/l)
  • decreased serum osmolality (<270mmol/kg)
  • in a euvolaemic patient, with no evidence of renal, cardiac or hepatic disease potentially associated with hyponatraemia

Causes

• Tumours
• CNS disorders e.g. stroke, trauma, infection, psychosis, porphyria
• Pulmonary disorders: pneumonia, tuberculosis, obstructive lung disease
• Drugs: anticonvulsants; psychotropics; antidepressants; cytotoxics; oral hypoglycaemics; opiates
• Idiopathic

Investigations

• Plasma and urine electrolytes/osmolaltiy
  • NB U&Es should be measured more than once in case of false positives
    • Low Na
    • Potassium- can be raised in Addison’s
• Imaging can be useful e.g. CXR in heart failure

 

Management

• Correct any underlying cause e.g. stop diuretic
  • Beware of correcting too rapidly- particularly in chronically hyponatraemic patients (no more than 8-10 mmol/l/day)
    • can cause myelinolysis (demyelination)
• If hypovolaemic- fluid replacement (0.9% saline)
  • NB beware of subsequent diuresis and rapid conversion to hypernatraemia (if this occurs, give desmopressin (ADH analogue) and 5% glucose (water))
• If normovolaemic/hypervolaemic
  • Fluid restrict (500-1000ml/day)
    • Consider adding furosemide if symptomatically hypervolaemic
    • Consider adding NaCl tablets/3% saline if the urine osmolality exceeds that of plasma
• NB If also hypokalaemia, potassium will raise both K and Na in the serum.

Urinary Incontinence

Background/Classifications

Involuntary leakage of urine

• Functional incontinence: e.g. due to poor mobility (unable to reach the toilet)
• Stress incontinence: involuntary leakage on effort/exertion e.g. sneezing/coughing.  Most commonly in women due to weakness of the pelvic floor muscles
• Urge incontinence: involuntary leakage immediately preceded by urgency, usually due to bladder dysfunction
• Overflow incontinence: usually due to chronic bladder outflow obstruction (e.g. prostatic disease in men) and can be accompanied by urinary retention
• Much more common in women than in men and the elderly (46% of women >80 and 34% of men >80)

Risk factors

• Women
  • Parity (more pregnancies and vaginal deliveries- more risk) – particularly of stress incontinence
  • BMI
  • Menopause

History

• Determine type of incontinence (stress, urge, mixed)
  • NB if mixed focus mainly on the predominant symptoms
• Ask about other urinary symptoms
  • Frequency, nocturia, dribbling/incomplete emptying, dysuria
  • Also ask about any sexual dysfunction, bowel habit
• Ask about previous medical history and current/past medications
  • In women, this should a full PMHx for Obs/Gynae (particularly parity, deliveries, surgery etc)
  • Ask about any neurological conditions (personal or family history)
• Ask about social circumstances, including functionality/mobility
  • e.g. access to the bathroom, family support
  • Also ask about caffeine, alcohol and diet/fluids
• Patients may also be asked to fill out a symptom scoring checklist to estimate the severity/impact of symptoms

Examination

• Women
  • Perform a full gynaecological examination including testing the tone of the pelvic floor
    • Assess also any prolapse
• Men
  • DRE: prostate examination
• Also examine the abdomen, pelvis and nervous system

Investigations

• Urinalysis/MSSU
  • Important to exclude treatable cause like UTI
• Residual volume scan (USS) or catheterisation
• Urinary (voiding) diaries
• NB Urodynamic testing is not often used first line but can be used in
  • patients with symptoms of over-active bladder/detrusor overactivity
  • symptoms suggestive of voiding dysfunction e.g. poor flow
  • patients who have had previous surgery for stress incontinence

Management

• 1st line
  • Lifestyle
    • Reduce caffeine intake
    • Consider altering fluid intake
    • Weight loss
  • Physiotherapy
    • pelvic floor muscle training for stress incontinence
    • bladder re-training for urge incontinence
• 2nd line
  • Drug treatment
    • Oxybutynin or tolterodine can be offered for urge incontinence
      • Review in 4 weeks (benefit) and 6 months (review)
    • The use of drugs in treating stress incontinence is limited although duloxetine may be used in conjunction with pelvic floor exercises (SIGN not NICE)
• 3rd line
  • Surgery/Invasive
    • Consider retropubic mid-urethral tape procedure with synthetic tape
    • Other procedures include open colposuspension and autologous rectus fascial sling procedures
  • Intramural bulking agents (rare)
• Others
  • Catheterisation can be considered (first line for relief in obstructive incontinence)

Urinary Tract Infection (lower)

Usually describes acute urethritis and cystitis caused by a microorganism.

Background/Epidemiology

• Common- accounts for around 1-3% of consultations in GP; affects around 3% of women at age 20 and increasing by ~1% every decade.
  • In men, UTI is uncommon except in neonates/infants and in men >60 with LUTS.

Risk

• More common in women because, the urethra is shorter and there is closer proximity between the urethra and the vagina and anus.
• Patients with catheters (or other instrumentation or foreign bodies- technically including renal stones) are also much higher risk
• Bladder outflow obstruction e.g. BPH, Prostate Cancer, urethral stricture
• Uterine prolapse
• Neurological conditions e.g. MS, diabetic neuropathy
• Diabetes mellitus
• NB Have a high clinical suspicion in elderly people (particularly females) who have acute onset fever or delirium of unknown cause, as this is the most common cause.

Pathophysiology

• The most common organisms to cause UTIs are
  • E coli (from the GI tract- account for ~75%)
  • Proteus spp
  • Staphylococcus saprophyticus
  • Other organisms include
    • Pseudomonas spp, streptococci and staph epidermidis
    • In hospital, Klebsiella and streptococci are more common (E coli still most common)
• Entry of the organisms may be retrograde (via the urethra), via the bloodstream (particularly in immunosuppressed) or direct (via instrumentation)

Clinical Presentation

• abrupt onset frequency and urgency of micturition
• scalding/burning pain (dysuria) in the urethra during micturition
• suprapubic pain during and after voiding
• feeling of incomplete emptying (due to spasm of the inflamed bladder wall)
• cloudy urine which may have an offensive smell
• there may also be haematuria
• Systemic symptoms e.g. fever, rigors, nausea/vomiting, confusion etc are usually only mild in simple UTI.  If these signs are present, suspect pyelonephritis and/or bacteraemia.
• Make sure to ask about previous UTIs and PMHx

Investigations

• NB UTI in females is a clinical diagnosis and investigations aren’t completely necessary.  UTI in males should be investigated with culture (male UTI is often immediately classed as complicated)
• Urinalysis
  • Leucocytes and nitrites are suggestive of UTI
• Urine microscopy/culture & sensitivity
• In some cases, particularly if the patient is having recurrent episodes or if there is a history suspicious of renal stones, USS imaging may be of benefit.

Management

• In uncatheterised patients
  • 1st line- Trimethoprim 200mg BD for 3 days (female- unless pregnancy is suspected/known) or 7 days (male) OR Nitrofurantoin MR 100mg BD or 50mg QDS for 3 or 7 days.
  • 2nd line- culture sample and treat as sensitivities

Special cases

• Patients with chronic kidney disease
  • In patients with CKD 3B/4/5, consider pivmecillinam (400mg stat then 200mg TDS for 3 days)
• UTI in pregnancy
  • 1st line nitrofurantoin MR 100mg BD or 50mg QDS for 7 days in the 1st and 2nd trimester
    • In the 3rd trimester, trimethoprim 200mg BD for 7 days
  • 2nd line cefalexin 500mg every 8 hours for a minimum of 7 days or as per sensitivities
• Recurrent UTIs in women (≥2/month or ≥3/year)
  • Treat for 6 months then review
  • 100mg trimethoprim at night/post-coital OR nitrofurantoin 50-100mg at night/post-coital
    • (Cranberry juice/extract also has evidence)
• Catheterised patients
  • In the presence of a catheter, antibiotics will NOT eradicate bacteria
  • Change catheter prior to treatment
  • Send sample
  • Treat only if symptomatic/systemically unwell
  • If in the community
    • Co-amoxiclav 625mg TDS for 14 days or cotrimoxazole 960mg BD for 14 days
      • 2nd line, base on sensitivities
  • If in hospital
    • IV Amoxicillin and Gentamicin (cotrimoxazole + gentamicin)
      • Aztreonam can be used as an alternative to gentamicin in patients with kidney failure (AKI/CKD)
      • Step down to co-trimoxazole or adjust as sensitivities suggest for 14 days total

Hypercalcaemia

Background

• Hypercalcaemia is mostly asymptomatic and is commonly an incidental finding after investigation for another reason.  It is relatively uncommon- so all cases should be investigated further
• A note about calcium measurements:
  • About 50% of serum calcium is bound to plasma proteins (majority of which is albumin) and organic ions e.g. citrate/phosphate.  The rest is free and under hormonal control.
  • Labs routinely measure total serum calcium (free and bound).  However, they also routinely report a Corrected Calcium level which is the calcium level adjusted to the level of binding products e.g. albumin
    • E.g. if albumin is low, the corrected calcium levels increase (as more is free/unbound)
    • Both are relevant, but the corrected calcium levels show a more accurate representation of the physiological calcium levels (NB In practice, the two are often extremely close in the majority of patients.  Differ mainly in patients with underlying liver/kidney disease)

Presentation

• Levels >2.21 (normal) but <2.8mmol/l
  • Patients may have polyuria/polydipsia; dyspepsia (calcium stimulates gastrin release); depression/low mood; mild cognitive impairment (may be acute or chronic)
• Levels < 3.5mmol/l
  • + Muscle weakness; constipation; anorexia; nausea; fatigue (all general effects of calcium in muscle physiology)
• Levels >3.5mmol/l
  • + Abdominal pain; vomiting; dehydration; lethargy; cardiac arrhythmias (shortened QT interval); pancreatitis; coma
• Patients can also present with stone disease if the levels are chronically and insidiously raised.

Investigation

• Repeat serum calcium (confirm hypercalcaemia)
  • Also look at albumin and urea levels (if raised, possible dehydration)
  • Other factors to inspect include Alk Phos; TFTs (thyrotoxicity)
• Serum PTH
  • Raised/normal- diagnostic for primary hyperparathyroidism
    • Further tests may be considered by a specialist e.g. Urinary 24 hour calcium
      • Raised or normal suggest hyperparathyroidism
      • Low suggests familial hypocalciuric hypercalcaemia (found particularly in young people with a family history)
  • Low- consider another cause
    • Most commonly malignant hypercalcaemia
      • Radionucleotide bone scan is useful to look for malignant bone disease
• Calcidiol testing can be done if no clear diagnosis is found from other tests (looking for Vit D toxicity
• Other tests for complications which may be warranted include renal USS (for stone disease- may be an indication for removal of parathyroid glands); bone mineral density
• Parathyroid imaging (USS, spect technetium scan)

Causes

• Primary hyperparathyroidism is the most common cause (0.1-0.3% of the population)
• Malignancy (myeloma or bony metastases)- suggested by rapidly progressive hypercalcaemia; second most common
• Drugs e.g. lithium, thiazide diuretics
• Rarer causes include
  • Tertiary hyperparathyroidism in end-stage renal disease
  • Granulomatous disease e.g. sarcoid, tuberculosis
  • Lymphoproliferative disorders
  • Vit D toxicity
  • Thyrotoxicosis
  • Addison’s disease
  • Familial Hypocalciuric Hypercalcaemia (1 in 78000) (see below)

Management (of hypercalcaemia)

• If the patient is asymptomatic and hypercalcaemia is mild, identification of the underlying cause (+/- treatment) is all that is required
• With acute/severe hypercalcaemia (>3mmol/l)
  • Rehydrate with saline (this can reduce the calcium by 0.5mmol/l
  • If severe, IV bisphosphonates e.g. disodium pamidronate or zoledronic acid may be helpful
    • Note that if this is due to hyperparathyroidism, bisphosphonates will only reduce calcium from bone resorption, not from renal reabsorption.

Familial Hypocalciuric Hypercalcaemia

• Autosomal dominant disorder caused by inactivating mutation of the calcium sensing receptor gene, which reduces the ability of the parathyroid gland to sense calcium concentrations and an inability of renal receptors causing increased reabsorption of calcium.
  • Important to diagnose as these patients do NOT require parathyroid surgery
  • As well as calcium, PTH and urinary calcium tests, genetic tests may be available.
  • Patients only ever have mild hypercalcaemia (extremely rare to be symptomatic due to FHH) and no treatment is required.

Visual Loss/Disturbance

NB Most visual disturbance diagnoses are based on examination but a good history is key too.

History

• What kind of disturbance?
  • Central vs peripheral? (macular degeneration vs retinitis pigmentosa)
  • Fields? (neurological/optic pathways)
  • Blurriness? (Acuity problem/cataract)
  • Double vision? (cranial nerve palsy/strabismus)
  • Curtain-like? (occlusion/amaurosis fugax)
  • Haloes? (glaucoma)
  • Floaters/flashes? (detachment/vitreous haemorrhage)
• Timing?
  • Superacute vs Acute vs Gradual vs Chronic
  • Progressive/single episode/episodic
• Associated symptoms?
  • Pain?
  • Headache?
  • Vomiting/nausea? (closed-angle glaucoma)
  • Confusion?
• Family History; Medical History; Drug History (antihistamines, anticholinergics, thiazides, indomethacin, ethambutol, antimalarials etc); social history

Examination

NB This is the full visual examination.  Most patients will only require certain sections of this where there is a relevant history and/or clinical suspicion.

Inspection

• The eye, eyelids and lacrimal ducts should be looked at to check for any redness, proptosis, lid abnormalities etc etc
• Lid lag should be looked for when appropriate by asking the patient to follow your finger down in the vertical line, checking if you can visualise sclera above the iris
• Fluoroscein should be used to inspect the cornea where ulceration/abrasions etc are suspected.
• The lids should be everted to inspect the conjunctiva in conjunctivitis

Visual Acuity (NB This is a test done in almost every patient)

• With one eye at a time (with glasses on), test far sight with a Snellen chart at 6m.
  • If the patient cannot read to 6/6, a pinhole may be used to improve acuity (in an OSCE it is unlikely you will have to do this
  • If the patient cannot read the top line, bring the chart to 1m and ask again; If this is still difficult, ask to count fingers/hand movement/ light
• IF the patient is complaining of central loss, check close reading with appropriate charts

Visual Fields (NB should only really be tested if there is suspicion of a field defect.  This could be suggestive of a central (CNS) cause of visual loss or a vascular cause)

• To test for homonymous defects
  • With you sitting 1 metre away at the patient’s level, with both eyes open and the patient focusing on your eyes:
    • Hold both arms out and wiggle a finger of one hand.  Ask the patient to point to the one that moves.
    • Do this at 10/2 o’clock and 4/8 o’clock
  • For sensory inattention
    • Move both fingers at the same time and check the patient responds to both
• For peripheral fields
  • Test each eye separately (i.e. ask the patient to cover one eye while you cover your opposite (corresponding) eye)
  • With your finger at the corner of each quadrant moving centrally, ask the patient to say when they see your finger entering their vision
    • NB if you finger is equidistant from you and the patient, this should occur at the same time as your finger enters your visual field.
  • Repeat for the opposite eye
• For Central visual field and colour desaturation
  • Use a red hatpin to test each eye individually, again comparing to your own
  • With the hatpin as close to fixation as possible, ask what colour it is
    • e.g. pink/white (colour desaturation- e.g. optic neuritis)
  • Do a similar test as for peripheral fields but with the hatpin, asking at what stage does it go from black to red
• For Blind spot (in practice rarely actually done)
  • In the same configuration as the previous tests, find your own blind spot (slightly inferotemporally) and compare that of the patient’s

Strabismus and Cover tests/Diplopia AND Eye movements

• Inspect for a manifest squint/ obvious muscle weakness
• From about 1m away, ask the patient to look at your pen-torch and observe the reflection off the cornea (should be central- a weak eye will have an off-centre reflection)
• Ask the patient to follow your finger in a cross and an ‘H-shape’ and ask where diplopia is maximal, inspecting the eye movements for any problems.
  • On down gaze you may have to lift the lids up a bit
  • Look for nystagmus too and describe it if present e.g. direction and location, fast/slow/rotational etc
• Cover tests
  • Cover one eye with the patient fixating on your pen torch
  • Observe the non-covered eye the first time.  Repeat and observe the covered eye as it is uncovered.
    • If either eye has to move to fixate, a manifest squint is present (eso/exotropia)
  • Repeat with the other eye
  • Next, cover one eye, then move to cover the other and then continue alternating, observing any eye movement as you do so
    • If there is eye movement, a latent squint is present (eso/exophoria)

Pupillary Examination

• On shining a pen-torch into one of the eyes, look for both direct and consensual light reflexes
• Check convergence/accommodation by bringing your finger from a distance towards the patient’s nose while asking them to look at your finger.  (Pupils should constrict)

Colour vision(rarely done in clinic)

• Use ishihara slides.

Direct Ophthalmoscopy

Should be in a dimly lit room.  In general, use the same hand and eye as the patient’s eye you are examining.

1. Check the red reflex
   1. Standing 1m away, with the lens at 0 and the scope at largest diameter/full brightness, shine the light onto each eye, looking for the red reflection of the retina.
      1. Comment on clarity, brightness etc
2. Inspect the eye from front to back.  Ask the patient to look straight ahead on a fixed point.
   1. Dial the lens (clockwise) to the black 10 (+ve).
   2. Come towards the eye until the cornea (front of the eye) is in focus.  If done at roughly 45°, you should be able to see the optic disc most quickly.
   3. Inspect the cornea and conjunctiva briefly, commenting on any abnormalities seen e.g. FB, ulceration, abrasion, injection etc
   4. Dial down the lens and come closer to the eye until the retina is in focus
      1. In a ‘normal’ eye this is at lens 0.
      2. In a myopic eye, you may require to dial further into negative lenses (the reverse may be true for hypermetropic eyes)
      3. Similarly, you may have to adjust for any refractory error of your own eye.
   5. Examine the retina- 6-point examination
      1. Optic disc
         1. Cup
            1. the outer rim should normally be less than 50% of the diameter (a cup to disc ratio of 0.3 is normal and above 0.5 is pathological)
         2. Colour
            1. Normally orange/pink.  If pale, may be an optic neuritis? or other nervous pathology
         3. Contour
            1. Regular/irregular
      2. 4 vascular arcades- follow the vessels and describe any pathology e.g. hard/soft exudates; cotton wool spots; dot/blot haemorrhages; flame haemorrhages; drusen; laser scarring; detachment etc etc.  Start with superotemporal
      3. superonasal
      4. inferotemporal
      5. inferonasal
         1. NB it may be helpful for the patient to look in the opposite direction for you to have a better look at each corner of the eye.  Always ask in an exam.
      6. Macula
         1. traditionally viewed by asking the patient to look directly into the light, although, again, can often be viewed fairly well without this aid.
3. Repeat on the other eye.

Potential Causes

•  Acute
  • Ischaemic optic neuropathy
  • Retinal artery occlusion
  • Retinal vein occlusion
  • Retinal Detachment
  • Retrobulbar/Optic neuritis
  • Amaurosis Fugax
  • Vitreous Haemorrhage
• Chronic
  • Macular Degeneration
  • Glaucoma (Open/Closed)
  • Cataract
  • Diabetic Maculopathy
  • Refractive Error
  • Malignancy