Ankle-Brachial Index

The Ankle – Brachial Index (ABI) is a ratio of the systolic blood pressure measured simultaneously in the leg and arm. This test is done to screen for peripheral arterial disease (PAD) of the legs.

What the values mean:

• An ABI ratio less than 0.8 implies significant arterial obstruction.
• A ratio of 0.5 or less implies critical obstruction.
• A ratio of < 0.3 implies impending gangrene.
  

Patients with PAD should not wear compression stockings due to high risk of ischaemia.

References:

• Ankle-brachial index test, WebMD
  
• Facts about Intermittent Claudication, North Suburban Cardiology Group

Management of adult cardiorespiratory arresst

Geris tutorial with the Prof

The acute geriatric admission

Principle 1 - Atypical presentation

Geriatric giants:

• Confusion
• Falls
• Incontinence
• Failure to cope

The reasons that the geriatric syndrome exists and that older people don't present with simple complaints the way younger people would is due to a combination of their underlying medical conditions as well as decreased reserve from multi-system failure and inability to compensate.

Principle 2 - Comorbidity

• Multiple Dxes and complex issues in Dx and management plan.
• Drugs and bugs - common precipitants of acute hospitalisation.

Principle 3 - Complications of immobility

Seven sins of immobilisation:

1. pressure sores
2. constipation and urosepsis
3. deconditioning
4. depression
5. malnutrition
6. venous thrombosis
7. bronchopneumonia
   

Prinicple 4 - Function

• Level of function and independence.
• Discharge planning on admission.

Rules of prescribing

• Rule of halves (impaired drug clearance, increased adverse effects)
• Rule of fives (polypharmacy)
• Medication untrial (adverse drug reactions)
• Medication trial (careful medical management)

Falls

• Syncope (Stokes Adams, postural hypotension, aortic stenosis, cerebrovascular disease, epilepsy, diabetic hypoglycaemia SPACED)
• Acute - drugs and bugs etc
• Chronic - 4 causes: drugs and disorders of eyes, cognition and gait

Incontinence

• Post void residual for retention (obstruction or neurological disorder)
• 5 causes: drugs, UTI, atrophic vaginitis, faecal impaction, prostate

Delirium

• Acute and fluctuating, inattention, altered LOC
• Reversible causes (drugs and bugs etc)

Giant cell arteritis (GCA)

Giant cell arteritis is a vasculitis of large and medium size vessels. Although it can affect arteries in the neck, upper body and arms, it occurs most often in the arteries in the temples. For this reason, giant cell arteritis is sometimes called temporal arteritis or cranial arteritis.

Giant cell arteritis is also known as granulomatous arteritis — a reference to a particular type of inflammation it causes.

Epidemiology & Aetiology

• Adults older than age 50 are at greatest risk of giant cell arteritis.
• Women and caucasians are most commonly affected.
• The exact cause isn't known, but researchers believe that genetic, viral and environmental factors may play roles in the inflammation.

Clinical presentation

Giant cell arteritis frequently causes headaches, jaw pain, and blurred or double vision, but the most serious potential complications are blindness and, less often, stroke. These problems occur when swelling in the arteries impairs blood flow to the eyes or brain.

The onset of the symptoms tends to be gradual and includes low grade fever, fatigue, weakness and weight loss.

• A new headache, mild or severe, occurs in at least two-thirds of patients with the pain tending to be located over the sides of the head in front of the ears but may be frontal or other located.
• Nearly one-half of patients suffer from jaw claudication after chewing.
• Impaired vision is often an early manifestation of the disease.
• Permanent partial or complete loss of vision in one or both eyes has been observed in 15-20 % of patients. It is rare for patients to become completely blind in both eyes.
• Polymyalgia rheumatica, which is characterized by pain in the shoulders and hips, is closely linked to GCA, occurring in about 40-50 % of patients.
  

Investigations

• ESR – elevated in most patients with GCA.
• Temporal artery biopsy

Suggested in all cases of suspected GCA even if the diagnosis may appear "classic".

The biopsy is of low risk, causes very little pain, and often leaves little or no scar.

After the use of a topical numbing medication (the same one used by a dentist), a small part of the temporal artery from under the scalp is removed.

• Other ways to diagnose GCA include: ultrasonography, angiographic examination, CT scanning and MR angiography, high resolution MRI and position emission tomography (PET).

Management

• Although there's no cure for giant cell arteritis, immediate treatment with corticosteroid medications usually relieves symptoms and prevents loss of vision.
• Glucocorticoid treatment should be instituted immediately once the diagnosis of GCA is established.
• Daily dosing is more effective than alternate day dosing. The response usually occurs within two to four weeks after the institution of therapy.
• The diagnosis should be reevaluated in patients who are resistant to adequate steroid therapy.
• Steroid withdrawal can begin once clinical remission has been induced.
• Relapses are seen more frequently in the first year or two of the disease.
• Relapses often necessitate increased dosage or prolonged steroid treatment. Some researchers have suggested that the addition of methotrexate may be steroid-sparing while others have not demonstrated any benefit. However the routine addition of methotrexate to glucocorticoid therapy for GCA is not recommended. The efficacy of other cytotoxic drugs, dapsone, antimalarials, etanercept, and penicillamine has not been studied adequately although they have been reported to be helpful in some case reports.
• The finding of an increased risk of visual loss in patients with GCA and thrombocytosis (increase of the number of platelets in the blood), has led some to suggest the addition of drugs like aspirin for patients with high platelet counts, but there is not a lot of data to prove that this may reduce brain/skull problems.

References:

• “Giant cell arteritis”, mayoclinic.com, http://www.mayoclinic.com/health/giant-cell-arteritis/DS00440
• “Giant Cell Arteritis (Temporal Arteritis)”, Vasculitis Foundation, http://www.vasculitisfoundation.org/giantcellarteritis

Relationship between pulmonary embolism (PE) and atrial fibrillation (AF)

If PE and AF occur together it is most likely that the PE is the cause of the AF.

The mechanism of the AF is said to be acute right ventricular dilatation with "strain" due to the embolus in the pulmonary circulation creating backpressure into the right ventricle.

If a patient presents with unexplained AF, look for an accompanying PE as the cause.

It is postulated that AF can cause PE if a clot originates in the right atrium rather than the left, but this is less common than clots originating from the right ventricle and more studies need to be done in this area.

References:

• Flegel K., When atrial fibrillation occurs with pulmonary embolism, is it the chicken or the egg?, CMAJ 1999;160:1181-2

Tests for hearing loss

Rinne test

Normal hearing = POSITIVE. Air conduction is louder than bone conduction.
Conductive hearing loss = NEGATIVE. Bone conduction is better than air conduction.
Sensorineural hearing loss = POSITIVE because both bone air and bone conduction are equally reduced (NB: may need to mask normal ear to avoid a false negative from the opposite side).

Weber test

Normal hearing = sound comes from middle of forehead.
Unilateral conductive hearing loss = sound is loudest in AFFECTED ear because the ambient noise is picked up by the normal ear, masking the sound of the tuning fork on that side.
Unilateral sensorineural hearing loss = sound is loudest in UNAFFECTED (normal) ear.

References

• http://en.wikipedia.org/wiki/Weber_test
• "C:\Tam's docs\uni\Admin\year2\OSCE\Clinical skills summaries\ProcSkills\Procedural Skills.doc"
  

Sequestra

A sequestrum is a piece of dead bone that has become separated from normal/sound bone during the process of necrosis . It is a complication (sequelae) of osteomyelitis.

Pathological process of development of sequestra:

• infection in the bone -> inflammatory exudate -> increase in intramedullary pressure
• periosteum becomes stripped from the osteum -> vascular thrombosis
• lack of blood supply -> bone necrosis
• sequestra are formed

Due to the avascular nature of sequestra, antibiotics which travel to sites of infection via the bloodstream, poorly penetrate these tissues. Hence the difficulty in treating chronic osteomyelitis.

At the same time as sequestra are developing, new bone is forming (known as involcrum). Openings in the involcrum allow debris and exudates (including pus) to pass from the sequestrum via sinus tracts to the skin.

References:

• http://en.wikipedia.org/wiki/Sequestrum

• Image from http://www.steinergraphics.com/surgical/006_19.3.html