This is colloquially known as a ‘head rush’ or ‘dizzy spell’, and is unsteadiness or LOC on standing from lying in those with inadequate vasomotor reflexes. It is defined as a fall in systolic BP of 20mmHg+ or a fall of diastolic BP by 10mmHg+ when an individual assumes a standing position.

Those at risk include:

• The elderly
• Those with autonomic neuropathy
• Those on antihypertensive medications
• Overdiuresis
• Multi-system atrophy (MSA)

Postural hypotension is an important cause of falls and faints in the elderly.

Physiology

• The symptom of orthostatic hypotension results from the gravity-induced pooling of blood in the lower extremities following a change in posture.
• This pooling of blood compromises venous return, thus lowering cardiac output and subsequent arterial pressure.
• This ultimately leads to insufficient perfusion of the upper body with blood.
• In health, the blood pressure does not fall very much upon standing because the baroreceptor reflexis triggered.
• This process is mediated by the autonomic nervous system. Carotid sinus baroreceptors are innervated by CN IX and the aortic arch baroreceptors are innervated by CN X.
• Baroreceptors are stretch-sensitive mechanoreceptors. High blood pressure causes distension of blood vessel walls, which stimulates the baroreceptors to fire action potentials at a faster rate. This leads to inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system.
• In contrast, when blood pressure falls, blood vessel walls are less distended; this is recognised by the baroreceptors which stimulate sympathetic activation and parasympathetic inhibition, thereby triggering vasoconstriction and an increase in heart rate in order to elevate the blood pressure, press blood up into the body again, and avoid the ‘dizzy spells’ we have mentioned.
• Secondary factors which cause a greater than normal fall in blood pressure are often responsible for orthostatic hypotension; factors such as hypovolaemia, sepsis, systemic vasodilatation or diuretics mean that the sudden change in blood pressure cannot be compensated for by the reflex.
• Avoiding orthostatic hypotension relies on being able to maintain an adequate blood supply, which relies upon a heart strong enough to pump, arteries and veins which are able to constrict when necessary, and having enough blood and fluid within the vessels. Interruption in any of these can thus lead to problems.

Aetiology

• Hypovolaemia:
  • Dehydration (vomiting, diarrhoea, fever, heat stroke)
  • Blood loss
  • Excessive use of diuretics
  • Vasodilators
  • Prolonged bed rest
  • Anaemia
• Disease:
  • Addison’s disease
  • Atherosclerosis
  • Autonomic neuropathy
  • Diabetes (peripheral neuropathy may affect the autonomic nervous system and thereby interfere with the baroreceptor reflex)
  • Phaeochromocytoma
  • Parkinson’s disease
  • Heart disease
  • Hypopituitarism (low ACTH)
• Medication:
  • Beta blockers (block the beta-adrenergic receptors in the body and prevent the heart rate from increasing, the heart from contracting as forcefully as is possible, and the dilatation of blood vessels)
  • Sildenafil (Viagra – works by dilating blood vessels and its effects are magnified if taken in conjunction with nitrites, so beware in patients with Angina!)
  • Tricyclic antidepressants
  • Monoamine oxidase inhibitors

Clinical Features

Upon moving from a sitting or lying to a standing position:

• Lightheadedness
• Weakness
• Blurred vision
• Syncope/LOC
• Distortion in hearing
• Seizures

These are the consequences of inadequate cerebral perfusion as a result of the blood pressure being too low. This may lead to a vasovagal episode to be stimulated, otherwise known as vasovagal/ neurocardiogenic syncope.

Vasovagal Syncope

• Emotion, pain, fear, or standing for too long can stimulate reflex bradycardia +/- peripheral vasodilatation.
• Excess activation of the parasympathetic system causes the heart rate to slow and blood vessels to dilate.
• Onset is over seconds, and is preceded by nausea, pallor, sweating and closing in of visual fields (a phenomenon known as ‘pre-syncope’).
• Patients may lose consciousness for ~2mins. This, as well as symptoms of dizziness occur due to the lowering of blood pressure and decrease of blood flow to the brain.
• The vagus nerve that causes this response may also in some cases be triggered by micturition (especially in men) or by severe straining with constipation.
• Brief clonic jerking of the limbs may occur (reflex anoxic convulsion due to cerebral hypoperfusion) but there is no stiffening or tonic àclonic sequence, and it can thereby be distinguished from a typical epileptic seizure of that nature.
• Post-ictal recovery is rapid.

Diagnosis of Orthostatic Hypotension

• Ensure patient has been lying down for at least 5 mins and is relaxed
• Explain procedure and obtain consent
• Take sitting or lying blood pressure with the arm supported at heart level, e.g. on a pillow
• Leave the cuff in place and ask patient to stand
• Allow the patient to stand for three minutes
• Ensure their arm is once more supported at heart level and repeat blood pressure
• Record results

Diagnose orthostatic hypotension if there is a drop in systolic BP of >20mmHg or a drop in diastolic BP of >10mmHg after standing for 3 minutes vs lying down.

Management

Conservative:

• Lie down if feeling faint
• Stand slowly (with escape route, e.g. a chair to fall back on)
• Consider referral to a ‘falls clinic’
• Manage any autonomic neuropathy
• Increased water and salt ingestion can help
• Physical measures such as leg crossing, squatting, elastic abdominal binders/stockings (must check dorsalis pedis pulse is present) and careful exercise may help
• If prost-prandial dizziness, eat little and often and reduce carbohydrate and alcohol intake
• Head-up tilt of the bed at night increases renin release, so decreases fluid loss and increases standing blood pressure

Medical:

• Fludrocortisone (retians fluid). Monitor weight and beware if CCF or low albumin: oedema worsens.
• Sympathomimetics e.g. midodrine or ephedrine. Can give pyridostigmine if detrusor under-activity too.

References

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• women are more likely to be affected due to weakened pelvic floor / sphincter muscles, as a result of childbirth

Risk Factors

• Multiparity
• Hysterectomy
• Obesity
• Bowel Dysfunction
• Menopause
• Dietary factors (caffeine, alcohol)
• Drugs (TCA’s, diuretics)

Types

• Stress
• Urge
• Overflow
• Functional
• Bed wetting – see Incontinence in Children

Normal micturition

Stress incontinence

Treatment

Pelvic floor exercises – improves symptoms in 50% of cases
Intravaginal electrical stimulation may help, but many women find this unacceptable.
Ring pessary – this is rubber/metal/plastic ring in which the cervix of the uterus sits. It is usually used to prevent prolapse of the uterus. A prolapsed uterus is basically where the uterus slips downwards – it may move so far that is protrudes out of the vaginal orifice. This occurs due to dysfunction of the muscles that usually hold the uterus in place.
Duloxetine – is a SNRI (serotonin-norepinephrine reuptake inhibitor) that is usually used to treat depression. It will not cure the condition, but will relieve symptoms in about 50% of cases, but has significant side effects, including nausea, vomiting and abdominal pain
Surgery – if pelvic floor exercises are unsuccessful, another option is surgery. You can surgically alter the position of the bladder or the urethra to relieve symptoms of this condition:

• Sling procedure – this is about 85% effective and is the procedure of choice for most women. A sling is created, either from native body tissue (such as fibrous connective tissue from the rectum) or man-made materials (such as telfon – although these are not as effective as natural body tissue). The sling is attached to the abdominal wall, and lifts up the top part of the urethra thus increasing pressure around this region and reducing incontinence.
  • The procedure involves open surgery, and thus there is a recovery period of 2-4weeks, although patients may return home after 3-4 days.
  • There is a chance that the procedure will have to be redone within 10 years
• Tension-free vaginal tape (TVT)– this is a more modern procedure, and basically has fwere side-effects, and higher success rate than a sling procedure. It is does via the vagina under local anaesthetic, and can be done as an outpatient procedure.
• Cholposuspension – this is a large operation in which the bladder is attached to the posterior abdominal wall. It is more effective than a sling procedure, but is a much more serious operation. It also means you can’t have children after you have had it done. This has an 85% success rate. There is a 5% risk of incontinence or difficulty passing urine afterwards.

Urge Incontinence

Treatment

• Try limiting fluid intake and avoiding irritant foods
• Examine for spinal cord and CNS signs to determine if is it as a result of brain damage.
• Test for vaginitis (inflammation of the vaginal mucosa).If this is present, then treat with estriol. If there is a long history of vaginitis, and there has been no hysterectomy, consider treatment with cyclical progesterone, as this reduces the risk of uterine cancer.
• Basically, this is very hard to treat. Often it involves a disabled patient with a CNS condition. Try a toilet regimen (perhaps every 4 hours) – the aim being to keep the bladder volume below that which triggers the incontinence. It might also be necessary to try aids, such as pads.
• Drugs – there are several drugs available, although their efficacy is debateable. Often anticholinergic drugs may be used as these will reduce the activity of the autonomic nervous system (which will control bladder contraction in the lack of conscious control seen in conditions of brain damage).  Examples include oxybutynin and tolterodine. You should avoid giving these if there is a history of UC or glaucoma.
• Botox to the bladder neck may also be considered

Overflow Incontinence

• Urethral stricture – such as an enlarged prostate, and perhaps kidney and bladder stones.
• Detrusor weakness –this may be seen in multiple sclerosis, where signals from the bladder about bladder fullness are not transmitted properly. Diabetes may also cause an autonomic neuropathy in a similar manner.

Post-micturation dribble

Treatment of Overflow incontinence

• Identify and eliminate the obstruction
• Consider alpha-block for prostatic enlargement (e.g. doxasosin)
• Consider catheterisation

Functional incontinence

• Use of portable commode and pads can improve QoL, but risk of UTI and skin irritation.

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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• Osteoporosis means literally porous bone
• Refers to decreased bone density, which leads to an increase in fracture risk
• Risk factors
  • Bone density declines with age
  • Highest risk is in post-menopausal women
  • Use of corticosteroids
• In women over 65, fracture risk (of any bone) is 3-5x that of men
  • Hip fracture risk is 2x that of men
  • 30% of women aged 90 will have suffered a hip fracture
• Incidence has declined due to effective treatments, but since the acknowledged association between HRT and breast cancer, rates have crept up again
• May not present until it is complicated by fracture
  • Vertebral crush fractures / loss of height
  • Hip fracture (femoral neck)
  • Colles fracture
• Can be prevented with lifestyle factors:
  • Regular exercise
  • Sufficient dietary calcium
  • Sufficient vitamin D
• Usually a primary disorder – due to increased osteoclast activity
• Rarely can be secondary – e.g. endocrine disease, malabsorption, malignancy
• The primary aim of treatment is to reduce the risk of fracture – not just to increase bone density

Epidemiology and Aetiology

• Very common in elderly populations
  • Approx 50% of women over 80
  • Approx 20% of men over 80
  • Lifetime risk of osteoporotic fracture – 60% for women and 30% for men
• All low trauma fractures are associated with increased mortality
• Massively under-treated
  • <30% of women with post-menopausal fractures receive pharmacological treatment
  • <10% of men with osteoporosis receive pharmacological treatment

Risk Factors

• Age
• Female gender
• Post-menopausal
• Frequent falls
• Glucocorticoids
  • 30-50% of patients on long-term glucocorticoids will have a fracture
• Low body weight
• Diabetes
• Vit D deficiency
• Low physical activity
• Hypothyroidism
• CKD
• Chronic liver disease
• Organ transplant
• Coeliac disease or other cause of malabsorption
• Myeloma
• HIV
• Depression
• Drugs
  • SSRI
  • Anti-psychotics
  • PPI
  • Anti-epileptics
  • Glucocorticoids (as above)

Diagnosis

Diagnosis is confirmed by either:

• Low bone density on densiometry (T score <-2.5) OR
• A fragility fracture – a low impact fracture from standing height that would otherwise not be expected to cause a fracture – e.g. hip fracture, or spine fracture

Investigations

Only bone densiometry is diagnostic. Other investigations such as x-ray can help to support a diagnosis and address risk factors.

X-ray

• Osteoporosis only be detected on x-ray once >40% of bone has been lost
• Osteoporosis can be suspected incidentally on x-rays performed for another reason
• Not often useful, except to detect wedge fractures of the spine. Do spinal series x-rays if:
  • Loss of height >3cm
  • Kyphosis
  • Unexplained back pain
  • If this confirms a wedge fracture – then move on to DEXA scan to confirm diagnosis

Bloods

• Vitamin D
  • Often low
• Calcium, phosphate, Alkaline phosphatase and parathyroid hormone
  • Often normal
• TFTs

DEXA scan (bone densitometry)

• DEXA – Dual-energy X-ray absorptiomety
• Measures bone density in multiple locations – usually the spine and femoral neck
• Femoral neck density is the most useful diagnostic measurement – this is the gold standard test
• T score
  • This is the number of standard deviations from the mean bone density of a 30 year old adult
  • E.g. -2.5 represents 2.5 SD below the young adult mean
  • Treat if T score <-2.5
  • >1.0 – NORMAL
  • -1 to -2.5 – OSTEOPENIA
  • <-2.5 – OSTEOPOROSIS
  • <-2.5 + # – SEVERE OSTEOPOROSIS
• Z score
  • This is the number of SD from the mean bone density of and age and gender matched control
  • Frequently reported on DEXA scan results, but often not useful clinically
  • Useful when suspecting osteoporosis in younger patients
  • Score of <-2 should prompt urgent further investigation

When to perform a bone density scan

• Any patient age >70
• Age >50 in women (or age >60 in men) and any of
  • On glucocorticoids
  • Postmenopausal
  • Fracture after age 40 with minimal trauma
  • FHx osteoporosis
  • Smoker
  • BMI <18
  • Consider in other patients with minor risk factors (see risk factors in Epidemiology and Aetiology above)
  • After diagnosis – repeat every 2 years
• OR age >45 with low trauma fracture
• Post menopausal women or men over 50 with a vertebral fracture (e.g. “wedge fracture”)

Consider using a fracture risk assessment tool – such as FRAX to assess risk in all patients over 50, and postmenopausal women over 45, even if you don’t think they require a DEXA scan

• DEXA scan can be performed about every 2 years after diagnosis of osteoporosis – or every 12 months if there are major changes to treatment
  • In patients on long term glucocorticoids – consider DEXA annually
• In osteopenia or pre-osteopenia, there is no defined time at which to repeat the scan. You should try to estimate when the patient will need another scan based off their original T score. The average loss of bone density, without treatment, is equivalent to a decline in T score of about 0.1 per year in the absence of any other underlying bone disease. For example:
  • A 70 year old lady, with no risk factors for accelerated bone loss, has a T score of -1.5. You could consider repeating in 5 years, knowing then that on average, her T score would be -2.0 at that point

Treatment

The main aim of treatment is to reduce the risk of fracture by preventing further bone loss.

When to treat

Initiate treatment in any of the following scenarios

• Minimal trauma hip or vertebral fracture
• Minimal trauma fracture at any other site AND T-score of <-1.5
• Risk assessed and DEXA scan performed based on risk-assessment:
  • T score <-2.5
  • T score <-1.5 AND hip fracture risk score >3% OR any fracture risk score >20%, based on risk fracture assessment tools such as FRAX

No agents have been shown to effectively increase bone density. Treatment duration is not well defined. Consider continuing treatment for all patients whose T score remains less than -2.5, OR if they have any recent fractures. Consider cessation of treatment if bone density is greater than -2.5 and there are no recent fractures. Recent US guidelines suggested there was no benefit to treatment after 3-5 years, and treatment could be safely stopped after this period. There is no specific recommendation in UK or Australian guidelines for when to stop treatment.

Hormone Replacement Therapy

• The most effective osteoporosis treatment – but also carries largest side effect burden
• Weigh up risks vs benefits
• Long-term use is not usually recommended

Bisphosphonates

• Decrease bone absorption
• Proven to reduce fracture rates
• Can be used in combination with other agents
• Traditionally the mainstay of treatment but are being challenged by denosumab (Prolia®)
• Side effects
  • Risk of osteonecrosis of the jaw – sometimes called MRONJ – Medication related osteonecoris of the jaw
    • Thankfully, very rare – less than 10 cases per 10 000
    • Can be very debilitating
    • Risk is reduced with good oral hygiene and increased when dental surgery occurs whilst on treatment – try to treat any dental disease before starting treatment
    • There is not enough evidence to suggest cessation of treatment for minor dental procedures
  • Oesophagitis
• Contraindications
  • Hypocalcaemia
  • Uveitis
  • Disorders which delay oesophageal emptying (oral agents)
• Agents
  • Alendronate
    • 10mg daily OR
    • 70mg weekly
  • Risedronate
    • 5mg daily OR
    • 35mg weekly OR
    • 150mg monthly
    • +/- vitamin D and calcium
  • Zoledrone acid
    • Annual IV injection
• IV agents are easy to administer. Oral agents can be difficult, because they require:
  • To be taken first thing in the morning
  • To be taken on an empty stomach
  • Not to eat for 30 minutes afterwards
  • To remain sitting upright or standing for 2 hours after taking (to prevent oesophageal irritation from reflux)

Denosumab

• Monoclonal antibody
  • Binds to “RANKL” – a signaller released by osteoblasts and taken up by osteoclasts. By binding to it – osteoclast activity is reduced.
• 60mg SC every 6 months
• ONLY give when calcium and vitamin D levels are adequate
• Also carries risk of osteonecoris of the jaw
• Treatment usually recommended for 3 years – but many patients remain on it indefinitely
  • The guidelines are unclear as to the pros and cons of continuing after 3 years – however – beware of the rebound effect
  • Rebound effect – it has been shown that after denosumab is stopped (or a dose is missed) – there is a a very large increase in osteoclast activity which reduces bone density below pre-treatment levels. One study(1) showed that the medium number of vertebral fractures at 7-11 months post cessation of denosumab was 5 (!).

It is very important to remind patients of this rebound effect. In my own clinical practice I tend to keep patients on denosumab indefinitely and advise them to be careful about not missing or being late for a dose – and I use clinical software to send SMS reminders to the patient to attend for the next dose when it is due – Dr Tom Leach.

Strontium

• Dissociates bone reabsorption and bone formation
• 2g (powder) daily – usually taken before bed and at least 2 hours after eating
• Can cause vascular complications – use with caution in vascular disease and renal impairment
• Also associated with VTE, serious skin reactions, including Stephens-Johnson Syndrome
• Strontium binds to bone, and absorbs x-rays – and so may artificially increase bone mineral density scores

Teriparatide

• A synthetic parathyroid hormone
• Increases bonce formation
• 20mg SC once daily

Prevention

• Calcium intake 1200 – 1300mg daily
  • Low fat dairy products recommended
  • 500mls of milk contains 1000mg
  • Fish – particularly tinned fish
  • Citrus fruit
  • Sesame and sunflower seeds
  • Supplementation is recommended in all post-menopausal women
    • Calcium citrate is better absorbed than carbonate
    • Doses are equivalent to 500mg elemental calcium
    • 38g of calcium citrate OR
    • 5g calcium carbonate (with food)
• Vitamin D
  • Maintain serum levels >75nmol/L
  • Recommended sunlight exposure (regional guidelines vary)
  • Supplementation – cholecalciferol
    • 1000 – 2000 IU daily (25 – 50 mcg)
• Exercise
  • Low intensity, ‘leisurely’ exercise such as walking, swimming or cycling do NOT improve bone density
  • Prescribed, regular, varied and high-intensity exercise, including balance training is strongly recommended
    • In postmenopausal women with osteoporosis there is good evidence that exercise increases bone density
  • Walking / jogging or similar sports may prevent bone loss, but are unlikely to increase bone density
• Smoking cessation
• Limit alcohol to safe drinking limits
  • <2 standard drinks per day, x2 alcohol free days per week
• Weight – keep BMI >18 Kg/m2
• In elderly patients at risk of falls
  • Falls prevention
  • Hip protectors – unsurprisingly compliance is poor!

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Osteoporosis – RACGP Red Book
• Osteoporosis risk assessment, diagnosis and management – RACGP
• Osteoporosis – afp

1. How to manage the rebound effect at denosumab discontinuation and avoid multiple vertebral fractures? – Rev Med Suisse. 2019 Apr 17;15(647):831-835.

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• Sphincter weakness (following childbirth/surgery);
• Anal/rectal pathology e.g. fistulae, Crohn’s, proctitis;
• Neurological disease (chorda equine, pudendal nerve);
• Dementia and unconsciousness;
• Diarrhoea (infective or due to malabsorption);
• Constipation (common in the elderly, diabetes, hypothyroid);
• Drugs e.g. antibiotics, muscle relaxants, PPIs, metformin.

Investigations

• DRE/PE – assess sphincter function and rule out impaction. Check perianal sensation to rule out neurological cause.

Management

• Perianal exercises may be used in sphincter weakness.
• Surgical anal sphincter repair.
• Steroids or GTN gel – In the presence of anorectal pathology.
• Bowel training can be used to develop predictable pattern.
• Diarrhoea and constipation should be managed

References

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Falls are an incredibly common presentation. You will see them as GP referrals, A+E presentations, and countless times on the ward.

Exactly how you examine and manage the patient will depend on the situation. For example, a 16 year old presenting with a fall / seizure might be lot different to Doris, the 93 year old inpatient who keep falling over going to the toilet at night.

Regardless of this there are several things that you should rule out for everybody who has a fall.

The causes of fall can be divided into:

• Cardiac – e.g. arrhythmia
• Neurological – e.g. seizure, stroke, peripheral neuropathy
• Vasovagal
• Intoxication / alcohol / pharmacological
• BPPV (Benign Paroxysmal Positional Vertigo)
• Infection
• Environmental (poor lighting / uneven surface) – rare!

You will often see “Mechanical fall” written as a diagnosis in the notes. Be wary of this. I don’t fall over all the time. Do you? Probably not. There is almost always a cause, despite Doris adamantly saying she tripped over the carpet.

History Taking

As usual, probably the most important part. Try to differentiate from the possible causes. Ask about:

• Palpitations
• Dizziness
• Loss of Consciousness (LOC)
• Duration of LOC
• Tongue biting
• Incontinence
• Did they bang their head?
• Onset (sudden, gradual)
• Previous similar episodes
• Medications
• Alcohol / drug use
• Any injuries as a result

Examination and Investigations

EVERYBODY who falls over, as a bare minimum should have:

• Cardiovascular and respiratory exam – do the basics. Feel the pulse. Listen to the heart. Listen to the chest. Take the temperature. Do they have an arrhythmia? Signs of a chest infection? Are they dehydrated? Is the mouth dry? (Skin turgor is not a very useful sign, particularly in the elderly)
• Basic GALS examination – check the joints in all the limbs. Check for any signs of head injury. Particularly check the hips. Can they walk? Are they able to weight bear? Is one leg shortened and externally rotated? (Hip fracture!)
• ECG – check for arrhythmias. Most commonly AF.
• Lying and standing BP – make sure you know how to do this properly, and make sure the nurse knows how to do this properly. Ideally the patient should be lying down for 10 minutes. Take their blood pressure. Keep the blood pressure cuff on. Ask them to stand up. Take the BP again at 1 minute, 3 minutes, and 5 minutes.
• Significant postural drop is: >20 systolic or >10 diastolic from the lying position.
• Urine dipstick – UTI is very common cause of falls, especially in the elderly. Ketones in the urine can also be a sign of dehydration
• Neuro observations – anyone with a head injury should have ‘neuro obs.’ The nurses wont thanky ou for it as it can be time consuming. Your hospital should have a protocol for their frequency but it will be something like:
  • Every 15 minutes for 1 hour
  • Every half an hour for the next two hours
  • Every hour for the next two hours
  • After this time anything other than a subdural haematoma (which can take weeks to develop symptoms) will be unlikely.

Other tests

• Basic blood tests – U+Es (dehydration), CRP and WCC (any signs of infection), CK (creatinine kinase – can be used to diagnose rhabdomyolysis if patient has been immobile on the floor for a long time after the fall)
• X-rays – of any damaged parts as necessary
• CT / MRI head – if stroke is suspected you will need to do it urgently. If there is a head injury, you may do one if there are any new or late onset neurological signs.

Other fancy tests

• Short Synacthen Test (ACTH stimulation test) – tests for true postural hypotension secondary to adrenal insufficiency. Treated with fludrocortisone

References

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Delirium is defined as an acute and fluctuating disturbance in level of consciousness, attention and global cognition.

• Prompt treatment is required to avoid potential brain damage.
• The underlying mechanism is poorly understood, but believed to involve neurotransmitter abnormalities and inflammation.

Epidemiology

• It is predicted that 10% of patients over 65 show signs of delirium on admission to hospital.
• Affects 15% of in-patients.

Signs and symptoms

• Reduced level of consciousness;
• Psychiatric symptoms:
  • Disorientation (time/place/person);
  • Inattention;
  • Illusions/hallucinations;
  • Altered personality;
  • Mood disorders;
  • Speech disorders (slurred speech/aphasic error/chaotic pattern).
• Lacking insight.
• These symptoms fluctuate over the course of the day and tend to be worse at night. Patients may show signs of hyperactivity (typically in withdrawal states) or lethargy (common in hepatic encephalopathy).

Causes

Diagnosis

• A collateral history is needed to determine if the changes in mental status are recent and the patients normal level of functioning.
• This would be different in a patient with dementia, where the memory problems are more likely to be chronic with a gradual onset. Patients with dementia are also less likely to have inattention or impaired level of consciousness until the later stages of disease.

It is also important to take a drug history (consider any with CNS effects or new additions as a potential cause) and alcohol history.
A mini-mental state examination is likely to show deficits in attention (e.g. immediate repetition of 3 objects).
Diagnostic tools such as the Confusion Assessment Method (CAM) states that the following features are diagnostic:

• Acute change in cognition which fluctuates during the day;
• Inattention;
• Disturbance of consciousness;
• Disorganised thinking.

The patient should be examined to look for potential sites of infection or any focal neurological signs (suggesting a structural CNS disorder).

Treatment

• Treating the underlying cause or removing aggravating drugs is the principle treatment.
• Environmental management: nurse patients in a quiet and well-lit room.
• Minimise sensory deficits (check hearing aids/glasses etc.)
• Agitation can be managed with haloperidol (0.5-1.0mg PO) or lorazepam (0.5-1.0mg PO), however, they should be avoided as they may worsen or prolong delirium.

References

1. Mind disorders – Delirium
2. E-medicine – Delirium
3. The Merck Manual – Delirium and dementia
4. BNF

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Dementia is a progressive global decline cognitive function, without impairment of consciousness. It is typically defined as a syndrome secondary to one or more of multiple causes, rather than a diagnosis in its own right.

Mild Cognitive Impairment (MCI) is defined a decline in cognitive function which does not affect day to day functioning. It is often seen as a pre-cursor to dementia – 50% of those with MCI go on to develop dementia.

Dementia is associated with increased mortality, and has a large economic impact.

The DSM-IV criteria for the diagnosis of dementia include:

• Clear evidence of decline in memory and learning (e.g. MMSE or MOCA), PLUS
• At least one of:
  • Reduce language ability – aphasia
  • Reduced motor ability – apraxia
  • Reduced recognition – agnosia
  • Reduced executive function – e.g. planning and organising
• Symptoms interfere significantly with social or work functioning
• Gradual onset and continual decline
• No known organic cause
• Not due to delirium
• Not due to mental health disorder – e.g. depression

• Normal reduced cognition of advanced age
• Delirium (see below)
• Depression – sometimes termed pseudodementia in this context. In this case, the decline in cognitive function will usually resolve when the mood disorder is treated. There is also often a previous history of depression or other mental illness
• Drug abuse / side effect
• Medical disorders
  • Anaemia
  • Hypothyroidism
  • Other endocrine disorders
  • Cerebral tumours / metastases
  • Syphilis (neurosyphilis)
  • Amyloidosis
  • Creutzfeldt-Jakob disease (CJD)
  • Poor nutrition (often also a feature of dementia)

Differentials for acute confusion (delirium):

Pathogenesis

Alzheimer’s disease

• Is associated with reduced life expectancy
• The mean survival is 7 years
• Death usually results from bronchopneumonia
• There is a general atrophy of brain tissue, and the weight of the brain is usually reduced. The frontal and temporal lobes are particularly affected.
• There is often compensatory dilatation of the ventricles, resulting in hydrocephalus.
• The cerebellum and spinal cord are normal

Pathological processes

It is believed that there are two important underlying pathological processes:

• Formation of beta-amyloid plaques (extracellular)
• Formation of intracellular “tangles”

Beta-amyloid plaques

• There may be the excess deposition of beta-amyloid in the brain – leading to the formation of beta-amyloid plaques
  • Amyloid precursor protein – APP is found in the cell membrane of neurones. It is thought to be involved in the cell repair process. Over time, due to normal cell repair, these APPs breakdown
  • α-secretase and β-secretase are enzymes involved in the breakdown of amyloid plaques
  • α-secretase breaks down the protein into soluble remnants that are easily taken away by the blood and lymphatics
  • β-secretin produces non-soluble remnants the end up being deposited as beta-amyloid plaques
  • These plaques often accumulate between synapses and affect nerve transmission
  • They also trigger an immune response, causing localised inflammation
  • They can also deposit around blood vessels in the brain – amyloid antipathy – which weakens blood vessel walls and can increase the risk of haemorrhage
  • However – it is not entirely clear if these plaques cause dementia, or are just a result of some other underlying process which may be the true cause of dementia

Tangles

• Within neurones are microtubules which are used to move nutrients around the cell
• The Tau protein is integral in the structure of these microtubules
• It is thought that beta-amyloid plaques outside the cell, leads to increased activation of kinase within the cell
• Kinase transports phosphate groups to the Tau protein – which causes structural changes in Tau proteins, causing them to dissociate from the microtubule, and TANGLE with other similarly affected tau proteins within the cell
• The lack of tau proteins in the microtubules also weakness the microtubules and they breakdown
• As a result of tangles and non-functioning microtubules, some neurones can’t function and undergo apoptosis

Other pathological effects

• There is also atrophy of cholinergic fibres that run from the hippocampus to the cerebral cortex. Initially there is a reduction on cholinergic transmission, and later a reduction in the synthesis of acetylcholine, particularly in the cerebral cortex itself.
• The damage is variable, and can occur at different rates in different parts of the brain. Most likely to be affected are the Amygdala, temporal cortex, and a few selected brainstem nuclei.
• There is no change in the number of muscarinic receptors, but the number of nicotinic receptors is reduced.
• In very late stage disease there can be variable depletion of other neurotransmitters

Vascular dementia

• Pseudobulbar palsy
• Shuffling gait with small steps – marche a petits pas – sometimes called atherosclerotic Parkinson’s disease.

Lewy body dementia

• Deposition of Lewy bodies in the brain
• Often associated with Parkinsonism and visual hallucinations
• Mental state often fluctuates quite widely

Differentiating types of dementia

• Treating risk factors for cerebrovascular disease in vascular dementia
• Consider specific medical treatments for Alzheimer’s disease

Management

• Even mild dementia increases the risk of accident whilst driving
• Asses the patient’s ability to drive, like you would with any other patient – based on their function
• Many patients will be very reluctant to give up their driving license
• Patients diagnosed with dementia must inform the DVLA (in the UK). In Australia – most states require the roads authority to be informed

I can recall several stories of patients known to me – whom, despite no longer having a driving license (and in some cases not even their own car), have been found to go driving. On one occasion, a patient of mine took his old, unregistered vehicle for a 20km joyride to the next town, was given several tickets by police (unregistered vehicle, driving without a license) – and then was subsequently allowed to drive home! I have no idea how he managed to find his way back again. – Dr Tom Leach

Non-medical management

• Take a patient-centred approach
• Advanced care planning
  • Adults should be assumed to have capacity unless proven otherwise – see below
• Promote independence as much as possible
• Refer to local support services – e.g. special interest groups, social worker
• Consider elder abusive from relative or others

Advanced Care Planning and making a will

• Understand and retain the information involved
• Believe the information is true
• Demonstrate they are able to weigh up the pro’s and con’s of an argument and come to a decision based on these – this doesn’t mean that the decision needs to match what others might deem acceptable. Eccentric or apparently unwise decisions are still just as valid if all of the above factors can still be demonstrated

Where is patient is deemed not competent to make a decision, then decision makers must be seen to act in the patient’s best interest – e.g. in medical care – when deciding on a treatment option (or deciding not to treat).

Relatives and carers should be involved in management decisions wherever possible.

Alzheimer ’s disease

Drug therapy is controversial

• Drugs are expensive
• Offer a modest effect at best – some trials have shown no benefit of the drugs over placebos
  • Greatest effect is with larger doses, but generally these are less well tolerated
  • No benefit has been shown in severe dementia
• In many cases it is thought that they at least allow a few more months in a home care environment
• Drug therapy is usually only initiated by a specialist after discussion with family and carers

• Mechanism – these drugs work by inhibiting cholesterases, and thus increasing cholinergic transmission within the brain.
• Unwanted effects – anorexia, nausea, vomiting, diarrhoea, abdo pain, insomnia, confusion, agitation, headache
  • Note that some of these effects are similar to the clinical symptoms of Alzheimer’s!
• Clinical use – thought to delay the decline of cognitive impairment in 40% of patients – probably only by about 3-6 months. Probably more effective in those without the gene apoE4.
  • Usually initiated at a low dose and titrated upwards whilst monitoring for side effects
  • Important to assess efficacy, and to stop treatment in those who do not respond.
  • Rapid decline is seen when the drug is stopped in previously responsive individuals
  • Have functional benefits that may improve QOL
  • Not recommended in mild cognitive impairment or severe dementia
  • The MMSE score is not designed to differentiate the severity of dementia – it is a useful tool as part of this process, but absolute scores are not indicative of whether or not treatment should be considered
  • NOT useful for non-Alzheimer’s dementia

• Mechanism – an inhibitor of glutamate NMDA receptors. It binds selectively, depending on the voltage, and thus prevents excitotoxicity, without altering gluatamtes role in normal memory and learning.
• It can be given in combination WITH anticholinesterases
• Unwanted effects:
  • Diarrhoea, insomnia, dizziness, headache, hallucinations
  • Again, note that some of these are similar to symptoms of dementia!
• Clinical use
  • Usually more well tolerated than anticholinesterases, but probably not as effective
  • May provide some benefit in cognitive function, and may slow cognitive decline
• Not widely used

• Advanced disease beyond this stage is unlikely to benefit from medical management

This is mild to moderate dementia
NICE guidelines state:

• Treatment to be reviewed every 6 months
• Don’t treat if MMSE <12, as side effects of drug likely to outweigh benefits
• Treatment only to be administered and monitored by specialist centres
• Don’t rely on MMSE as your only tool for aiding prescribing, e.g. get collateral histories, assess function and behaviour

• May be required – particularly at night
• Many types are used
• Rivastigmine – an anticholinesterase drug (as above) often used for this purpose
• Olanzapine (are commonly) or quetiapine (less commonly) may also be used – these are atypical antipsychotics
• Oxazepam or other benzodiazepines may be used to control anxiety at night. They should be used with caution, and only for short duration (e.g. less than two weeks) as they can exacerbate the cognitive impairment of dementia

Vascular Dementia

• Aspirin or warfarin therapy – aspirin often quoted anecdotally, but there is little evidence that low dose (e.g. 100mg daily) therapy provides any benefit against vascular dementia. Some high risk patients may be put on warfarin therapy.
• Controlling BP
• Anticholinesterases and memantine – may have some benefit in vascular dementia.

• Some recent evidence suggests that engaging in cognitively taxing activities late on in life can protect against dementia!
• Vitamin E – has shown in some instances to protect against dementia

• Are commonly found in association
• Medication can be difficult to manage – refer to a specialist for advice
• A common combination is levodopa with quetiapine at night

Prevention

There is evidence that lifestyle factors reduce the risk of dementia. Correcting these factors can also slow the progression of dementia in patients who have already been diagnosed. Factors include:

• Controlling BP – the most important factor
• Regular exercise – 150 minutes of moderate intensity exercise weekly (e.g. brisk walk or similar intensity)
• Controlling hyperlipidaemia
• Healthy weight
• Alcohol consumption – drinking within safe drinking limits reduces the risk
• Diet – e.g. mediterranean diet – maximising intake of plant-based whole foods
• Preventing diabetes and controlling blood sugar
• Mentally stimulating activities

Other Types of Dementia

• Symptoms fluctuate
• Permanent memory dysfunction is not apparent in the early stages
• Associated with Parkinsonianism
• Associated with depression and sleep disturbance
• Causes visual hallucinations – often frightening and persecutory
• There may be transient LOC

• Whipple’s disease
• Parkinson’s disease
• Alcohol/drug abuse
• Huntington’s disease
• CJD
• HIV

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Dementia – patient.info
• Dementia – an update on management – afp

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