Chest Imaging tutorial

Another great radiology resource - this time a tutorial on reading CXRs.

Popliteal fossa

Boundaries

• superior and medial: semitendinosus (semimembranosus is medial to the semitendinosus)
• superior and lateral: biceps femoris
• inferior and medial: medial head of gastrocnemius
• inferior and lateral: lateral head of the gastrocnemius

Contents

• popliteal artery (continuation of the femoral artery)
• popliteal vein
• tibial nerve
• common peroneal nerve
• popliteal lymph nodes embedded in the fat

References

• http://en.wikipedia.org/wiki/Popliteal_fossa
• Posterior Compartment of the Thigh, http://mywebpages.comcast.net/wnor/postthigh.htm
  

MedPix™

MedPix™ is a great radiology resource.

Focal neurological symptoms

A focal neurologic symptom is a problem that affects either:

• A specific location - such as the left face, right farm or even just a small area such as the tongue
• A specific function - for example, speech may be affected, but not the ability to write

The problem occurs in the brain or nervous system. The type, location, and severity of the change can indicate the area of the brain or nervous system that is affected.

In contrast, a non-focal problem is NOT specific - such as a general loss of consciousness.


References:

• MedLine Plus Medical Encyclopedia, http://www.nlm.nih.gov/medlineplus/ency/article/003191.htm
  

Asthma Hx

Things you need to ask someone with asthma:

• Sx: wheeze, dyspnoea, cough, disturbed sleep
• Exercise - quantify distance to breathlessness
• Days per week off work or school
  
• Diurnal variation
• Triggers - RTIs, cold, exercise, pets, emotions, drugs
  
• How & when they monitor their asthma e.g. peak flow meter
• Use of preventers and inhalers. Has there been any changes?
• For elderly people, ask if they've had Fluvax and Pneumovax vaccines (major RF for infective exacerbation)
• Any other atopic diseases like eczema, hay fever, allergy
• Previous attacks or hospitalisations
• Family history of asthma

References:

• http://www.aippg.net/forum/viewtopic.php?p=55254
  

T4 during infection

Metabolism of thyroid hormones is accelerated during acute infection in man and in experimental animals. The mechanisms for this is uncertain, but activated leukocytes of the infected host have been implicated as potentially important sites of hormone degradation.

Apparently T4 can go up in infection similar to an acute pahse reactant - but I couldn't find anything on the net really backing this up!!


References:

• DeRubertis, Accelerated host metabolism of L-thyroxine during acute infection, Journal of Clinical Endocrinology & Metabolism, Vol 40, 589-600
  

Nilstat

Actions

Anti-fungal.

Indications

Treatment of candida.

References:

• AMH
  

Lipodermatosclerosis (LDS)

• LDS literally means "scarring of the skin and fat" and is a slow process that occurs over a number of years.
• Occurs in patients with long-standing venous disease resulting in chronic venous insufficiency.
• Affects the skin just above the ankle, usually on the inside surface.
  
• Over time the skin becomes brown, smooth, tight and often painful.
  
• The precise mechanism of LDS is not fully understood, but we do know that it is caused by an excessively high venous pressure in the subcutaneous veins in the lower leg.

References:

• http://www.simondodds.com/Venous/LDS.htm
• http://www.bu.edu/woundbiotech/wounds/UncommonWounds%20Gallery/pages/19..htm
  

Chronic Venous Insufficiency (CVI)

Symptoms

• Varicose veins
• Ulceration or skin breakdown
• Lipodermatosclerosis
  
• Reddened or discolored skin on the leg
• Oedema

Risk factors

• Heredity
• Obesity
• Pregnancy
• Sedentary lifestyle
• Smoking
• Jobs requiring long periods of standing or sitting in one place
• Age and sex (women in their 50s are more prone to developing CVI)
• Incompetent valves
• previous DVT

Pathophysiology

• Increased venous pressure transcends the venules to the capillaries, impeding flow.
  

• Low-flow states within the capillaries cause leukocyte trapping.

• Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes.

• Plasma proteins,such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff.
  

• Interstitial fibrin and resultant oedema decrease oxygen delivery to the tissues, resulting in local hypoxia.
  

• Inflammation and tissue loss result. Ulceration may occur.
  

Management

• Leg elevation
  
• Elastic compression therapy - especially with older patients you need to ensure they are actually able to put the compression stockings on for themselves.
  
• Sclerotherapy - chemically scarring the veins from the inside out so that they can then no longer fill with blood. Blood that would normally return to the heart through these veins returns to the heart through others. The body eventually absorbs the veins that received the injection.
• Vein stripping
• Deep vein surgery - note that surgical treatment is reserved for those with discomfort or ulcers refractory to medical management.
• Valve repair

Great resource on hands

Handworld - the name says it all huh? :)

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