Clinical Teaching and Communication Skills Taking a Cardiovascular History

At the end of this session you should be able to: 1. 2. 3. 4. Take a detailed cardiovascular history from a patient. Complete a full history. Complete a systems review. Present and summarize the case.

Introduce yourself to patient and find out patients name, age and where they are from. Ask them what brought you to hospital.

Presenting Complaint Chest pain

Site of pain - central/retrosternal Radiation jaw, left arm Onset gradual/sudden Periodicity intermittent/constant Duration minutes, hours, days Character- crushing/heaviness Severity out of 10 Aggravating factors - exertion/stress, pain at rest may indicate unstable angina Relieving factors rest/GTN Associated features Nausea Vomiting Sweating [diaphoresis] Anxiety Dyspnoea Palpitations Syncope Fatigue Intermittent claudication Ankle swelling

With angina, pain may initially occur with exertion, getting progressively worse over time and eventually leading to pain at rest [Unstable angina], or myocardial infarction.

Canadian cardiovascular society (CCS) classification of angina Class I No angina/ mild angina at strenuous exertion. Class II angina with moderate exertion (walking > 2 blocks on level or climbing > 1 flight of stairs). Class III angina with mild exertion (walking 1-2 blocks on level or climbing 1 flight of stairs). Class IV angina at rest.

New York Heart Association (NYHA) functional classification - Class I no SOB with activity/ exertion. - Class II SOB at moderate activity/ exertion. - Class III SOB at mild activity/ exertion. - Class IV SOB at rest.

Cardiovascular Risk Factors 1. Hyperlipidaemia high cholesterol/triglycerides (? medication) 2. Smoking (duration/number per day) 3. Hypertension (? medication) 4. Family History of CAD 5. Diabetes mellitus (type/duration/medication) 6. Obesity [BMI] 7. Age 8. Gender 9. Physical activity Relevant background History of angina Previous myocardial infarction History of palpitations Previous cardiac investigations Previous cardiac surgery/interventional procedures Recent dental work [endocarditis] Rheumatic fever in past Ask all the relevant questions to presenting complaint (If chest pain ask all pain questions, etc.)

Other cardiovascular symptoms Shortness of breath (SOB)/ Dyspnoea

Exertional? Relieved by rest? Acute vs. chronic? Worsening? Associated wheeze (cardiac wheeze)? How many pillows at night when sleeping? Using more pillows lately? Characterise as 1,2, 3 or 4 pillow orthopnoea.

Orthopnoea

Paroxysmal nocturnal dyspnoea (PND)

patient wakes from sleep gasping for air Due to acute left ventricular failure.

Palpitations 1) Aim to get a good description of the palpitations

Describe the palpitation/ unexpected awareness of heart beat? Slow/fast; regular or irregular; sensation of a skipped beat or an extra beat? Ask the patient to try tapping out the rhythm When did they start? Increasing in frequency or the same? Duration of palpitations when they occur? Sudden onset/ termination? Or gradual onset? Associated symptoms with the palpitations? Eg pain, symptoms of heart failure

2) What is causing the palpitations? - Obvious triggering factors? Alcohol? Caffeine intake? Symptoms of hyperthyroidism? Known hyperthyroidism? Illicit drugs? Stress? - Previous cardiac history precipitating palpitations? - Family history of arrhythmia? - Medications causing palpitations eg salbutamol 3) Effect of the palpitations - Syncope 3

Heart failure etc

Syncope/ pre-syncope
Transient loss of consciousness due to cerebral anoxia. Is dizziness postural? Sudden onset vs. gradual? Warning signs? (Nausea, vomiting, sweaty, dizziness, palpitations, chest pain, headache, etc). Collateral history if loss of consciousness (LOC) - (seizure activity?). Length of LOC? Symptoms when recovered from LOC (palpitations, pain, etc.?).

Ankle swelling
Symmetric? Worsening?

Past Medical/Surgical History

Other medical/surgical problems. Mention dates of surgery and previous medical diagnosis (dates of bypass surgery? how many grafts?) Previous percutaneous coronary intervention? How many stents? Dates of procedure and where it was done?

Medication
Prescribed and over the counter. Always use generic names of medication. Mention dosing regimen (i.e. OD, BD, etc.). State type of drug and indication

Allergies
To any medication Document the reaction which occurred, e.g. nausea/ vomiting / rash/ wheeze/ bronchospasm/ loss of consciousness.

Social History
Marital status Children Employment Home situation Alcohol intake [count units] Smoking (quantity of cigarettes per day, and duration of smoking must be documented) o Activities of daily living? Home help? o o o o o o

Family History
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Relevant family history MI / PVD / stroke, Hypertension, Diabetes mellitus, High cholesterol/triglycerides. Onset of cardiovascular disease in first degree relatives? Age at initial diagnosis with CVD Family history sudden cardiac death?

Complete Systems Review

- Refer to Talley and OConnor for questions in systems review.

Summarize History
Refer to Talley & OConnor for further reading on cardiovascular history taking. The above notes are NOT intended as a replacement for the book. Practice makes perfect!

Clinical teaching - Cardiovascular Examination

To begin examination Student must introduce themselves to patient. Find out patients name. Explain to patient what they are going to do.

Exposing the patient

The patient must be put lying at 45 degree angle and be comfortable. Chest must be exposed [take off shirt/top/pyjamas/vest].

General inspection
For all systems initial inspection is done from the end of the bed Look at general state of health. Does patient appear ill? Rapid/laboured respiration (tachypnoea) Cachectic [severe loss of weight and muscle wasting]. Severe cardiac failure may have this

effect. Comment on chest asymmetry/scars/pulsations. Pacemaker Comment on intravenous lines/any equipment around bed

Hands
Ask patient to hold out their hands. Note if cold, clammy or well perfused. Check capillary refill.

Tar staining

Indicative of a history of cigarette smoking

Clubbing
Inspect for loss of nail angle between the nail bed and the finger. Grade 1: Fluctuation and softening of the nail bed This can be examined for by compressing nail bed with your fingers and rocking it. Grade 2: Loss of the nail-bed angle Grade 3: Increased curvature of the nail Grade 4: Fingertip develops a clubbed (drumstick) appearance Grade 5: Hypertrophic pulmonary osteoarthropathy (HPOA). Cardiovascular causes of clubbing 1. 2. 3. Cyanotic congenital heart disease Infective endocarditis Atrial myxoma

[The cause of clubbing is not known there are several theories]

Pallor - Pallor of the palmar creases/palm of hand

This may indicate underlying anaemia. Anaemia from any cause may result in cardiovascular symptoms eg chest pain due to lack of oxygen supply to the myocardium Anaemia related to cardiovascular disease is usually normochromic, normocytic anaemia Causes 1. Haemolytic anaemia ( prosthetic heart valves) 2. Infective endocarditis (chronic inflammation)

Splinter haemorrhages
Linear haemorrhages of the nail bed may be caused by infective endocarditis or vasculitis.

Osler Nodes
Red raised tender nodules on the pulps of the fingers, thenar and hypothenar eminences in infective endocarditis

Janeway Lesions
Non-tender erythematous maculo-papular lesions containing bacteria on palms or pulps of fingers in infective endocarditis

Xanthomata
Yellow deposits of lipid occur in hyperlipidaemia.

Arterial Pulse
Palpate radial pulse using pulp of forefinger and middle finger. Rate Normal pulse: 60-100 beats per minute [Bradycardia < 60/minute, Tachycardia > 100/minute] Rhythm Regular or irregular [Atrial fibrillation is an example of an irregularly irregular rhythm] Radio femoral Delay Palpate radial pulse and femoral pulse at the same time. A delay in the arrival of femoral pulse suggests coarctation of the aorta. Femoral pulse is located below the inguinal ligament one third of the way between the pubic tubercle and the anterior superior iliac spine Radial-radial inequality Palpate both radial pulses together Inequality in timing or volume usually due to large arterial occlusion or aneurysm Character and Volume Collapsing pulse of aortic incompetence. Otherwise character and volume better assessed at the carotid

Blood Pressure
Systolic BP - Peak pressure that occurs in the artery following ventricular systole Diastolic BP - Level to which arterial blood pressure falls during ventricular diastole

Face
Jaundice 8

Severe congestive cardiac failure leads to hepatic congestion, causing intra-hepatic jaundice. Xanthelasma Intracutaneous yellow cholesterol deposits around the eyes may indicate hyperlipidaemia.

Arcus senilis/Corneal arcus Cholesterol deposits in the corneal stroma result in a white/grey opaque ring surrounding the cornea. It is associated with hyperlipidaemia and with ageing.

Malar flush Rosey cheeks with a bluish tinge. Associated with pulmonary hypertension and severe mitral stenosis. Mouth High arched palate This is a feature of Marfan Syndrome. This is an autosomal dominant connective tissue disease. It is associated with cardiac complications, in particular, aortic regurgitation and dissection. Patients have a distinctive physical appearance tall and thin, with an arm span that exceeds height (arachnodactyly).

Tooth decay This may be a source of endocarditis infection.

Petechiae May be present in infective endocarditis Lips Peripheral cyanosis associated with cyanotic congenital heart disease. It affects the distal extremities and circumoral or periorbital areas. It is caused by increased tissue oxygen extraction.

Tongue Central cyanosis ask patient to open their mouth and look under their tongue. It is caused by decreased arteriolar oxygen saturation. Cyanosis is a bluish discoloration of the tissues that results when the absolute level of reduced hemoglobin in the capillary bed exceeds 3 g/dL.

The Neck
Carotid Arteries
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Medial to the sternomastoid muscles Provides information about aorta and left ventricular function Evaluate the pulse wave form [collapsing pulse of aortic regurgitation] o Anacrotic Aortic stenosis (small volume slow uptake) o Plateau Aortic stenosis (Slow upstroke) o Bisferiens Anacrotic and collapsing in AS and AR o Collapsing Aortic regurgitation Hyperdynamic circulation PDA Peripheral AV fistula o Small volume Aortic stenosis and Pericardial effusion

Jugular Venous pressure

Provides information regarding right atrial and right ventricular function Internal jugular vein is medial to sternomastoid muscle External jugular vein is lateral to sternomastoid muscle External jugular vein has more tortuous course, the internal jugular vein is more reliable The column of blood in the internal jugular vein extends into the right atrium The right atrium is about 5cm below the sternal angle It enables us to observe pressure changes in the right atrium The JVP is measured as the vertical distance between the sternal angle and the top of the venous column.

Gentle pressure at the base of the neck may abolish visible pulsations and may make a vein visible by causing distension above the occlusion 11

When the JVP is more than 3cm above the zero point then right heart filling pressure is raised.

Features of Jugular Venous Pressure It is a multi-wave form. It is visible, not palpable. It is occludable. It fills from above. It decreases with inspiration. It increases with pressure on the abdomen (hepatojugular reflux). Hepatojugular Reflux Abdominal compression increases venous return and pressure and facilitates analysis of the JVP Apply firm sustained pressure over upper abdomen It is a simple way of confirming the venous nature of a pulsation in the neck. Causes of elevated JVP Renal failure - fluid overload Right ventricular Failure Tricuspid regurgitation Tricuspid stenosis Pericardial effusion Constrictive pericarditis Cardiac tamponade Superior Vena Caval Obstruction

The Praecordium Inspection

Scars Sternotomy [A cut down the middle of the sternum - CABG and valve surgery]

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Thoracotomy [mitral valvotomy - a stenosed mitral valve is opened through an incision made in the left atrium] Skeletal abnormalities Marfans Syndrome may cause pectus excavatum/kyphoscoliosis. Severe deformity may cause distortion of the position of the heart and great vessels and also interfere with pulmonary function]

Visible apex beat Heaves/abnormal pulsations Pacemaker or Inmplanted Cardiac Defibrillator (ICD) Box [Under the left pectoral muscle easily palpable]

Palpation
Apex beat 1. Assess Position This is the most lateral, inferior point at which the palpating fingers are raised with each systole. Its normal position is in the fifth left intercostal space midclavicular line. 13

Begin palpation in axilla and move medially until apex beat is located. Once you have located the apex beat count down the number of intercostal spaces to confirm its position. The second intercostal space lies just below the manubriosternal angle. The apex beat may be displaced laterally or inferiorly or both. This usually indicates ventricular dilatation but may be due to chest wall deformity. The apex beat is best located with the patient in the left lateral position, in order to position the apex closer to the chest wall. Note any apical thrills (palpable murmurs) 2.Character Normal Heaving LV hypertrophy 2ry to pressure overload (hyperkinetic) 2ry to Systemic hypertension Aortic stenosis Coarctation of the aorta Thrusting LV dilatation 2ry to volume overload (hyperdynamic) 2ry to Aortic regurgitation Mitral regurgitation VSD Tapping mitral stenosis causing a loud & palpable S1 Double impulse HOCM Causes of an impalpable apex beat 1. 2. 3. 4. 5. Obesity Emphysema (hyperexpansion) Pericardial effusion Shock Dextrocardia

Causes of a displaced apex beat 3. 4. 5. 6. 7. Left ventricular dilatation Right ventricular dilatation Cardiomegaly Chest wall deformities Mediastinal mass

Parasternal heave may be palpable when the heel of the hand is rested just to the left of the sternum. The fingers can also be used. This is present in right ventricular enlargement/hypertrophy. Thrills Thrills are palpable murmurs. Palpate for thrills with the flat of the hand. Palpate over the apex, left sternum and base of the heart (sitting forward in full expiration for base of heart).

Percussion
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Little additional information is gained and therefore is not helpful.

Auscultation

1. Begin in the mitral area [over the apex beat] Listen with the bell (low pitch sounds such as diastolic murmur of mitral stenosis. Then listen with the diaphragm for mitral regurgitation. 2. Listen in tricuspid area with diaphragm [fifth left intercostal space] 3. Listen in the pulmonary area with diaphragm [second left intercostal space] 4. Listen in aortic area with diaphragml [second right intercostal space] The bell amplifies low pitched sounds i.e. mitral stenosis. The diaphragm is best for higher pitched sounds i.e. mitral incompetence. The bell must be applied lightly to the chest wall as forceful application will stretch the skin so it forms a diaphragm. NB. Palpation of carotid pulsation will indicate the timing of systole and allow heart sounds to be identified. The first heart sound - S1 Mitral and Tricuspid valve closure. The second heart sound - S2 Aortic and pulmonary valve closure Marks the end of systole Lower pitch The second heart sound has two components, the aortic (A2) and the pulmonary (P2). This occurs because the pressures in the pulmonary circulation are lower than those in the systemic circulation, leading to a delay in the closing of the pulmonary valve.

Cardiac Murmurs
Pansystolic Murmur: Audible throughout systole 15

Causes 1. Mitral regurgitation 2. Tricuspid regurgitation 3. VSD Ejection Systolic Murmur: Audible best at midsystole. Causes 1. Aortic stenosis 2. Pulmonary stenosis 3. Hypertrophic Obstructive Cardiomyopathy (HOCM) Early Diastolic Murmur: Loudest at the beginning of diastole. Causes 1. Aortic Regurgitation 2. Pulmonary Regurgitation Mid Diastolic Murmurs: begin later in diastole. Causes 1. Mitral Stenosis 2. Tricuspid Stenosis Continuous murmurs Causes 1. Patent Ductus Arteriosus 2. Arteriovenous fistula

Grade Murmurs 1-6

1/6: very soft 2/6: soft 3/6: moderate [no thrill] 4/6: loud, palpable thrill 5/6: very loud, thrill easily palpable 6/6: very, very loud (audible without stethoscope)

Extra heart sounds the third heart sound is a low pitched mid-diastolic sound that is best appreciated by listening for a triple rhythm. It is often called a gallop rhythm. A pathological S3 is due to reduced ventricular compliance so that a filling sound is produced even when diastolic filling is not rapid. Presentation of auscultation Heart sounds 1&2 Normal or abnormal? Loud, soft, splitting? Any extra heart sounds? Eg 3rd or 4th heart sounds 16

Any additional sounds? Friction rub, opening snap, clicks Any murmurs Timing Area of greatest intensity Grade Radiation Effect of dynamic manoevres o Systolic (early, midsystolic or pansystolic) o diastolic (early or late diastolic) o Continuous

Dynamic manoeuvres Lesions on the left side of the heart are best elicited on listening in full expiration. Lesions on the right side of the heart are best elicited on inspiration.
Mitral Stenosis: Listen over mitral area using bell with patient in left lateral position.

Aortic Regurgitation: Lean patient forward in full expiration and listen at lower left sternal border with diaphragm.

Mitral Regurgitation: Radiates to axilla, listen with diaphragm Aortic Stenosis: Radiates to carotid arteries, listen with diaphragm or bell if patient small/thin. Best heard leaning forward in full expiration| 17

We also listen over the carotid arteries for a bruit which will be audible with carotid stenosis

The Back
Auscultation of the lung bases for pulmonary oedema crackles/crepitations (often due to congestive cardiac failure) or pleural effusion may be identified Check for sacral oedema

The Abdomen
The liver may be enlarged [hepatomegaly] and/or tender due to congested hepatic veins caused by right-heart failure. A pulsatile liver is a feature of tricuspid regurgitation.

The Legs
Check for pedal oedema Palpate distal shaft of tibia. Compress the area for at least 15 seconds with the thumb. *Area often tender be gentle*

Pitting oedema - Skin is indented and only slowly refills. Note upper level of oedema, abdominal wall and scrotum may be involved.

Palpitations
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Palpitations are the perception of cardiac activity. They are often described as a fluttering, racing, or skipping sensation.

Differential diagnosis
1) Some patients simply have heightened awareness of normal cardiac activity, particularly when exercise, febrile illness, or anxiety increases heart rate. 2) Arrhythmia Common arrhythmias include

Premature atrial contractions (PACs) Premature ventricular contractions (PVCs)

Both usually are harmless. Other common arrhythmias include

Paroxysmal supraventricular tachycardia (PSVT) Atrioventricular nodal reentrant tachycardia Atrial fibrillation or flutter Ventricular tachycardia Bradyarrhythmias and heart block

May occur spontaneously or due to an underlying disorder. Cardiac Disorders Precipitating Arrhythmia myocardial ischemia, congenital heart disease, valvular heart disease, conduction system disturbances (eg, disturbances that produce bradycardia or heart block). Patients with orthostatic hypotension commonly sense palpitations caused by sinus tachycardia upon standing.

Noncardiac Disorders Precipitating Palpitations thyrotoxicosis pheochromocytoma anxiety anaemia hypoxia hypovolemia electrolyte abnormalities eg K+

Other Precipitants of palpitations 19

Stress/Anxiety Caffeine Nicotine Alcohol Medications o Salbutamol

Pathophysiology
The mechanisms responsible for the sensation of palpitations are unknown. Ordinarily, sinus rhythm at a normal rate is not perceived, and palpitations thus usually reflect changes in cardiac rate, rhythm, or contractility. It is the abnormal movement of the heart within the chest that is felt. In cases of isolated extrasystoles, the patient may actually perceive the augmented post-extrasystolic beat as the skipped beat rather than the premature beat itself, probably because the extrasystole blocks the next sinus beat and allows longer ventricular filling and thus a higher stroke volume. The clinical perception of cardiac phenomena is highly variable. Some patients are aware of virtually every premature ventricular beat, but others are unaware of even complex atrial or ventricular tachyarrhythmias. Awareness is heightened in sedentary, anxious, or depressed patients and reduced in active, happy patients. In some cases, palpitations are perceived in the absence of any abnormal cardiac activity. Consequences: Many arrhythmias that cause palpitations have no adverse physiologic consequences of their own (ie, independent of the underlying disorder). However, bradyarrhythmias, tachyarrhythmias, and heart blocks can be unpredictable and may adversely affect cardiac output and cause hypotension, heart failure or death. Ventricular tachycardia sometimes degenerates to ventricular fibrillation and cardiac arrest.

The History
3 tasks in presenting complaint and history of presenting complaint 1) Aim to get a good description of the palpitations - Describe the palpitation/ unexpected awareness of heart beat? - Slow/fast; regular or irregular; sensation of a skipped beat or an extra beat? - Ask the patient to try tapping out the rhythm - When did they start? - Increasing in frequency or the same? - Duration of palpitations when they occur? - Sudden onset/ termination? Or gradual onset?

20

Symptoms associated with the palpitations? Eg pain, symptoms of heart failure, syncope, light-headedness, tunnel vision, dyspnoea, and chest pain. Give clues regarding aetiology and potential seriousness.

2) What is causing the palpitations? (See above also) - Obvious triggering factors? Alcohol? Caffeine intake? Symptoms of hyperthyroidism? Known hyperthyroidism? Illicit drugs? Stress? Anaemia, Blood loss, etc - Previous cardiac history precipitating palpitations? - Recent chest pain/progressive dyspnoea suggesting ischaemia - Family history of palpitations, arrhythmia, sudden death or thyroid problems? - Medications causing palpitations eg salbutamol 3) What were the consequences of the palpitations? None Syncope Heart failure symptoms What was the trigger for presenting to the doctor?

Red flags: Certain findings raise suspicion of a more serious aetiology of palpitations:

Light-headedness or syncope (particularly if injury occurs from syncope) Chest pain New onset of irregularly irregular heart rhythm Heart rate >120 beats/min or < 45 beats/min while at rest Significant underlying heart disease Family history of sudden death

Suggestive Historical Findings with Palpitations

Finding Occasional skipped beats Possible Cause PACs, PVCs

Rapid, regular palpitations with sudden PSVT, atrial flutter with 2:1 onset and termination atrioventricular block, ventricular tachycardia Often history of recurrence Syncope following palpitations Sinus node dysfunction, atrioventricular bypass tract, such as in the WolffParkinson-White syndrome, congenital long QT syndrome

21

Palpitations during exercise or an emotional episode

Healthy person: Sinus tachycardia History of coronary artery disease: Ventricular arrhythmia from exerciseinduced ischemia

Palpitations following episodic drug use Drug-induced cause Sense of doom, anxiety, or panic Postoperative patient Recurrent episodes since childhood Suggests (but does not confirm) a psychologic cause Sinus tachycardia (eg, due to infection, bleeding, pain) Supraventricular arrhythmia (eg, atrioventricular nodal re-entrant bypass tract, Wolff-Parkinson-White syndrome) Congenital long QT syndrome (usually manifests during adolescence) Family history of syncope or sudden death Brugada syndrome, long QT syndrome, inherited dilated or hypertrophic cardiomyopathy

Peripheral Vascular Disease

History Presenting Complaint/History of Presenting Complaint Past Medical/Surgical History Medication Allergies Social History Family History Systems review Respiratory Cardiovascular Gastrointestinal Genitourinary Musculoskeletal Neurological Pain History 10 points that should be elucidated in taking a pain history 22

1. Time course 2. Mode of onset 3. Pattern 4. Site 5. Radiation 6. Character 7. Severity 8. Aggravating factors 9. Relieving factors 10. Associated symptoms Symptoms of peripheral vascular disease Gradual arterial obstruction, particularly in the lower limbs, presents as Intermittent Claudication Intermittent Claudication Ischemic cramp-like pain usually in the calves during exercise and relieved by rest. Pain may be in one or both calves but can also occur in thighs or buttocks.

Claudication distance Determine how long patient can walk prior to onset of pain. The distance they can walk prior to onset of pain is called the Claudication distance. The claudication distance may be shorter when patient is walking up a hill. Can they walk to shop? To local church? To bus stop? To the end of the garden? Across the room?

**Both limbs often affected, usually one more severely than the other** Rest pain Severe chronic arterial insufficiency may cause rest pain. This may be felt deep in the limb or superficially. Usually described in the dorsum of the foot. There may be altered cutaneous sensation and there may be a feeling of burning. The patient may attempt to relieve discomfort by letting the leg hang over the side of the bed at night, outside the bed clothes. In severe cases the patient may even report sleeping in a chair. Rest pain is indicative of severe peripheral vascular disease and of critical limb ischemia.

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Ulceration, gangrene and tissue loss In very severe cases, patients may actually present with ulceration and gangrene due to insufficient blood supply. These are also indicative of critical limb ischemia. Risk factors for vascular disease Smoking Diabetes mellitus Hypertension Hypercholesterolemia Family history of arterial disease

Differential Diagnosis 1. 2. 3. 4. 5. 6. 7. 8. 9. Spinal stenosis (pain on getting up, improves on walking) Sciatica Lumber spondylosis Arthropathy (osteo/rheumatoid/gout) Varicose veins DVT Compartment syndrome Infections / cellulitis Abdominal aneurysm

Acute Ischemic Limb Causes sudden onset of severe pain This can be the result of: 1. Embolism [sudden blockage of an artery by material brought to the site of the obstruction in the blood stream e.g. clot] 2. Thrombosis [clotting of blood within an artery so that the blood flow is reduced or impeded] 3. Injury. Peripheral arterial embolism usually arises from thrombus in the heart, where it is often secondary to, Myocardial infarction Atrial fibrillation Infective endocarditis

Acute arterial occlusion of a major peripheral limb artery results in the six Ps, Painful Pale Pulseless Paralysed limb Perishing Cold 24

 Venous Insufficiency Varicose Veins DVT Varicose Veins: Causes:

Paresthesia

Previous DVT Venous HTN from prolonged standing Pregnancy Uterine Fibroids Pelvic Malignancy Exam: Trendelenberg test Tourniquet test DVT Risk Factors: Immobility Surgery Pregnancy Malignancy OCP

Vascular examination of the lower limb

The lower limbs should be fully exposed. All examinations begin with inspection.

Inspection
Look for; Leg pallor Dry skin Absence of hairs Thickened atrophic toenails Ulceration Gangrene Students should comment of each of these findings when inspecting limb [presence or absence of].

Describe an ulcer
Site 25

Size Shape Surface Edge Base Surrounding skin Arterial ulcers Due to critical limb ischemia Painful Punched out Relatively deep [tendon may be visible] Occur where arterial supply poorest: Tips of toes Dorsum of foot Heel Middle of shin Venous Ulcers Superficial Painless Medial or lateral malleolus Can undergo malignant change Beer bottle leg Brawny oedema Dermatoliposclerosis (sub cut fat replaced by collagen)

Palpation
Feel for temperature of limbs. Compare temperature of limbs Capillary refill Oedema (Pitting or non-pitting if present)

Palpate for lower limb/peripheral pulses

Femoral Artery Femoral pulse is felt at the mid inguinal point which is halfway between the anterior superior iliac spine and the pubic symphysis The femoral artery lies halfway between the pubic symphysis and the anterior superior iliac spine. It cannot be felt satisfactorily through clothing. Examine both femoral arteries by palpating and then auscultating. A bruit may be heard if the artery is narrowed. [Bruit will not be heard over smaller arteries] 26

Popliteal Artery Popliteal pulse is felt in the popliteal fossa between the two heads of gastronemius against the tibial plateau Palpate for the popliteal artery behind the knee. The patient should be lying supine with the knee slightly flexed. Press with the finger tips [use both hands] in the middle of the fossa. The artery is one of the deepest structures in the fossa and lies the knee joint. With practice it can nearly always be detected unless there is proximal obstruction.

popliteal posterior to

Posterior Tibial Artery The Posterior Tibial pulse is felt in a groove half way between the medial maleollus and the Achilles tendon Palpate behind the medial maleollus. Dorsalis Pedis Artery The Dorsalis Pedis pulse is felt two thirds is the way along a line drawn from the midpoint of the two maleolli and the first interdigital cleft Palpate on the forefoot. Lateral to extensor hallucis longus tendon on the dorsum of the foot. In the elderly the Dorsalis Pedis artery and the posterior tibial artery may not be palpable. Buerger's test is used to assess the adequacy of the arterial supply to the leg. It is performed in two stages. With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes. Observe the color of the feet. Pallor indicates ischemia. It occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity. The poorer the arterial supply, the less the angle to which the legs have to be raised for them to become pale. Then sit the patient up and ask them to hang their legs down over the side of the bed at an angle of 90 degrees. Gravity aids blood flow and colour returns in the ischemic leg. The skin at first becomes blue, as blood is deoxygenated in its passage through the ischemic tissue, and then red, due to reactive hyperemia from post-hypoxic vasodilatation. Both legs are examined simultaneously as the changes are most obvious when one leg has a normal circulation. 27

Investigations Specific: ABPI 0.9 0.71 0.90 0.41 0.70 0.00 0.40 Doppler / Duplex Ultrasound Arteriogram MRA Others: FBC Renal Profile Fasting Glucose HbA1C Fasting Lipids ECG Management Must be able to identify acute limb ischemia. Requires heparin infusion if no absolute contraindications and seek expert help straight away. 6 hour window period from time of onset. Decrease risk factors Stop smoking Treat DM Treat Hypertension Lower cholesterol Weight loss Normal Mild Obstruction Moderate Obstruction Severe Obstruction

Regular exercise encourages development of collateral vessels. Care to avoid trauma/infection. Surgery Balloon dilatation/angioplasty/stenting Bypass grafts Amputation-severely ischemic/gangrene

Taking a Gastrointestinal History

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Presenting Complaint
Abdominal pain The following questions must be asked, when enquiring about any pain: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Site/radiation Ask the patient to point to the site of pain o Pancreatitis Back o Epigastric oesophagitis, gastritis, peptic ulcer disease, pancreatitis o Right Upper Quadrant gallstones, cholangitis, cholecystitis o Central Abdominal irritable bowel syndrome, inflammatory bowel disease o Suprapubic diverticular disease, irritable bowel syndrome, inflammatory bowel disease o Flank renal colic o Right Iliac Fossa appendicitis, hernia, ovarian cyst Ask about radiation of pain Appendicitis pain commonly begins in the periumbilical region, later radiating to and then localising in the RIF Pancreatitis pain can radiate from the epigastric region through to the back Gall bladder pain can radiate around into the flank and the back Renal pain can radiate down along the ureters and into the groin Pain associated with subdiaphragmatic irritation (gall stones, perforated ulcer) can also be felt in the right shoulder and tip of the scapula. 29 Site Radiation where the pain moves Character sharp/dull/ache Severity score from 1 to 10, 1 being very mild, 10 being worst pain ever experienced. Onset sudden/gradual Periodicity constant/intermittent Duration minutes/hours/days Aggravating precipitants/makes it worse Relieving eases Associations other symptoms that accompany the pain, e.g. nausea, vomiting, diarrhoea etc.

Onset/periodicity/duration Onset - When did the pain start? Sudden or gradual Periodicity - How often it occurs Duration How long does / did it last? Acute/chronic

Character and severity Sharp/burning/dull/gnawing Colicky pain comes in waves e.g. from obstruction of bowel

Associated features
Loss of appetite/weight Ask about any change in appetite Determine from patient how much weight loss has occurred, and over what period, i.e. 6 kg over two months Nausea and vomiting Acute - gastrointestinal infection e.g. Food poisoning [staphylococcus aureus] Ask about contents old food e.g. Gastric outlet obstruction Blood [haematemesis] gastric/oesophageal - ulceration/malignancy Other causes Small bowel obstruction Pregnancy Medications e.g. opioids, chemotherapy, antibiotics Infections gastrointestinal, any systemic sepsis Bulimia Pancreatitis Cholecystitis Peptic ulcer disease Heartburn/acid regurgitation Regurgitation of stomach contents into the oesophagus Heartburn burning or discomfort in retrosternal area Acid regurgitation Sour or bitter tasting fluid coming up into the mouth In reflux disease the lower oesophageal sphincter muscle is usually weak Dysphagia Difficulty swallowing, usually solids initially, progressing to dysphagia with liquids Causes 30

 Change in bowel habit

Oesophageal spasm Oesophageal stricture Oesophageal Carcinoma Mediastinal mass Neurodegenerative disorder

Diarrhoea Diarrhoea refers to a decrease in faecal consistency. It may refer to an increased volume or frequency, or change in consistency, of the stool. Constipation Constipation is generally understood as a delay or difficulty in defaecation, but the interpretation of the term "delay" varies broadly. Determine what patient means by constipation. Causes Hypothyroidism Hypokalaemia Anorexia Pregnancy Multiple sclerosis Low-fibre diet How often would your bowels normally move? How often are they moving now? How long has this been going on for? Alternating diarrhoea and constipation Suspicious for underlying colonic malignancy Gastrointestinal Bleeding Haematemesis: vomiting blood [bleeding from upper GIT] Melaena: passage of dark black tarry stools [bleeding from upper GIT/ right side colon/small bowel lesions] Bright red blood per rectum: usually indicates bleeding from lower GIT Causes of upper GIT bleeding Peptic ulcer disease Oesophageal varices Oesophageal/Gastric neoplasm Arteriovenous malformations Mallory-Weiss tears

Causes of lower GIT bleeding 31

 Jaundice

Cancers/polyps Colitis/ulcers (including Inflammatory bowel disease and infectious) Anorectal (hemorrhoids, fissures, and rectal ulcers) Diverticular disease

Yellow discoloration of the sclera or skin Due to the presence of excess bilirubin

Have you noticed your skin or your eyes looking a little yellow? Has anyone else commented on it? Has your urine been any darker (obstructive jaundice)? How about your stools are they paler than usual (obstructive jaundice)? Causes of jaundice 1. 2. 3. Increased bilirubin production Haemolysis [unconjugated bilirubin] Congenital hyperbilirubinaemia Gilberts syndrome [unconjugated bilirubin] Cholestatic jaundice Intra-hepatic (Liver disease) Viral Alcohol Drug Pregnancy Cirrhosis any type Extra-hepatic Common duct stones Carcinoma head of pancreas/ampulla/bile duct Pancreatitis/pseudocyst Biliary stricture Abdominal distension 32

Bowel obstruction Pregnancy Constipation Irritable Bowel Syndrome Liver disease (ascites)

History of Presenting Complaint

Previous diagnosis of: Peptic ulcer disease Irritable bowel syndrome Jaundice Hepatitis GIT malignancy Inflammatory Bowel Disease Previous abdominal surgery Previous OGD/colonoscopy

Past Medical/Surgical History

Other medical/surgical problems

Medication
Determine what medication patient is taking prescribed/over-the-counter Anti-diarrhoeal agents Laxatives Anti-emetics Analgesics, especially paracetamol (can cause liver damage) and Non Steroidal Anti-Inflammatory Drugs (cause peptic ulcer disease/GIT bleeds)

Allergies
To any medication ask about type of reaction

Social History
Married/children Employed Home situation Alcohol - Excessive alcohol use can cause liver problems [cirrhosis] Smoking High risk behaviour for Hepatitis transmission travel/sexual behaviour/Intravenous drug usage

Family History
Bowel cancer 33

Inflammatory bowel disease Liver disease, e.g. haemochromatosis

Complete Systems Review

CVS RESP GI GU Musculoskeletal Neuro

Preparation: 4Es Environment Warm and private Good light Explain that you are going to examine their abdomen and ask their permission. General Inspection From the end of the bed General Appearance Jaundice Yellow discoloration of the skin and sclera Cachexia and wasting GIT malignancy and malabsorption Malnutrition in alcoholic patients Mental state Hepatic encephalopathy due to decompensated liver disease Patients eventually become stuporous and comatosed

The hands Look at patients hands, initially palmar surface and then ask patient to turn hands over. Clubbing Cirrhosis Inflammatory bowel disease Coeliac disease

34

Leuconychia White discoloration of the nails due to hypoalbuminaemia

Koilonychia Thin, brittle, concave finger nails May result from iron deficiency anaemia

Palmar erythema Reddening of the thenar and hypothenar eminences Attributed to raised oestrogen Can also occur with pregnancy/thyrotoxicosis/polycythaemia/rheumatoid arthritis Anaemia Inspect palmar creases for pallor [blood loss/malabsorption B12 and folate] Dupuytrens contracture Thickening and contraction of the palmar fascia causing permanent flexion most often of the ring finger [associated with alcoholism, manual work also familial]

Hepatic Flap/Asterixis Ask patient to stretch out the arms in front, seperate the fingers and extend wrists Look for jerky, irregular flexion-extension movement at the wrist and metacarpophalangeal joints Also present with cardiac, respiratory and renal failure

35

The arms Bruising Absorption of vitamin k and therefore clotting factors 2, 7, 9 and 10 Scratch marks Obstructive or cholestatic jaundice may cause pruritis Commonly the presenting feature of primary biliary cirrhosis Petechiae [pinhead sized bruises] Excessive alcohol consumptionbone marrow depressionthrombocytopenia Splenomegaly [portal hypertension] hypersplenismthrombocytopenia Spider naevi Central arteriole from which radiates numerous small vessels. Distribution is in the area drained by the superior vena cavaarms, neck and chest wall More than 2 spider naevi is abnormal, attributed to oestrogen excess Acanthosis nigricans Brown/black velvety elevations of the epidermis due to confluent papillomas Usually found in the axillae and the nape of the neck Rarely associated with GIT carcinoma, lymphoma, acromegaly, DM

The face Eyes Sclerae For signs of jaundice and anaemia Kayser-Fleischer rings Brownish green rings at the periphery of the cornea Due to deposits of excess copper found in Wilsons diseasecopper storage disease which causes cirrhosis and neurological disturbances

Xanthelasma Cholestasis is associated with cholesterol Xanthelasma are common in patients with primary biliary cirrhosis

36

Parotids/Parotidomegaly Clench the teeth and palpate the masseter muscle Parotid is best felt behind the masseter muscle and in front of the ear Associated with alcoholism rather than liver disease The Mouth Ulcers Aphthous ulceration: Cause unknown Other causes of mouth ulcers: Crohns/Ulcerative colitis/Herpes Simplex/Autoimmune disorders Fetor hepaticus Rather sweet smell of the breath Indication of severe hepatocellular disease Leukoplakia White coloured thickening of the mucosa of the tongue and the mouth This condition is premalignant Macroglossia/Enlargement of the tongue Downs Syndrome/Acromegaly/tumour infiltration/Amyloidosis Candidiasis Creamy white curd-like patches in the mouth Associated with immunosuppressionsteroids/chemotherapy/AIDS May spread to involve oesophagus causing dysphagia Peutz-Jeghers Syndrome Freckle-like spots on the buccal mucosa, fingers and toes are associated with hamartomas of the bowel Incidence of GIT adenocarcinoma is increased Autosomal dominant condition

The Neck and Chest Palpate the cervical lymph nodes Particularly important to feel for supraclavicular lymph nodes especially on the left These may be involved with gastric and other GIT malignancy Troisiers sign Presence of a large left supraclavicular/ Virchows node in combination with carcinoma of the stomach Examination bed Patient flat with head at 15-20 degrees i.e. one pillow under head (abdominal muscles are not stretched and remain relaxed) Rest arm by the side 37

Exposure

Nipple to pubic symphysis

Gynaecomastia Occurrence in the male of breasts resembling those of the sexually mature female Sign of chronic liver disease Changes in the oestradiol to testosterone ratio may be responsible Spironolactone used to treat ascites is also a common cause Position of examiner: Clean warm hands Hand & forearm horizontal plane with abdominal wall Kneel beside the patient Inspection: Asymmetry Shape: Flat, distended, obvious mass, Scars, Sinuses, Distended veins, Pulsation, striae, Cullens, grey turners Cough impulse Scars: Previous surgery/trauma.

1 2 3 4 5 6 7 8 9 1. 2. 3. 4. 5. 6.
Subcostal/Kocher's Choleocystectomy Right Paramedian Laparotomy Midline Laparotomy Nephrectomy/Loin Renal surgery Gridiron Appendectomy Laparoscopic Choleocystectomy Appendectomy Colectomies Left Paramedian Anterior rectal resection Transverse suprapubic/Pfannenstiel Hysterectomy Other pelvic surgery

7. 8.

9. Inguinal hernia Hernia repair 38

Palpation: Ask for pain; go from non tender to tender region Light palpation in nine areas Deep palpation Hand held still during inspiration an advanced on expiration Eyes on pts face Guarding: contraction of abdominal muscles, tenderness or anxiety, voluntary or involuntary Rigidity: constant involuntary contraction of the abdominal muscles, associated with tenderness, indicates peritonitis Rebound tenderness: strongly suggests peritonitis, compress abdominal wall slowly and release rapidly, sudden stab of pain Abdominal mass: Any intra-abdominal mass must be carefully described. Site/Size [may be measured]/Shape/Surface [regular or irregular] Consistency [hard or soft] Tenderness Mobility [move with inspiration] Pulsatile or not Get above mass Liver: Begin RIF Hand parallel to right costal margin If the liver edge is identified surface of liver should be felt (hard, soft, tender, non tender, regular, irregular, pulsatile or non-pulsatile) Measure total liver span: percuss down along right mid clavicular line until the liver dullness is detected. The normal upper border is 5th rib and normal span is less than 12.5cm. Gallbladder: Murphys Sign: Hand at the right costal margin, on taking a deep breath the patient catches breath when inflamed gallbladder presses on examiners hand. Courvoisiers law: If the gallbladder is enlarged and the patient is jaundiced the cause is unlikely to be gallstones. Carcinoma of the pancreas of the pancreas or lower biliary tree is likely to be present. The gallbladder with stones is fibrosed and is incapable of enlargement. Spleen: Enlarges inferiorly and medially Begin RIF moving to left costal margin If not palpable move the patient slightly on to the right side towards the examiner and palpation with two hand technique. Splenomegaly is detectable if the spleen is one and half to two times enlarged Kidneys: Both kidneys move downward with inspiration Bimanual method: Left hand slides underneath the back in the area of renal angle, right hand is placed over the upper quadrant, fingers flex at metacarpophalangeal joints. Ballotting: press over the renal angle by flexing the fingers of the posterior hand, the kidney can be felt to float upward and strike the anterior hand. 39

AAA: Place two hands along the midline just above the umbilicus and feel expansile pulsation Hernial Orifices: At rest and when the patient coughs (inguinal, femoral & umbilical) Lymph nodes: Supraclavicular and inguinal External Genetalia: Scrotum, testes Rectal Exam: The abdominal examination is not complete without the performance of a rectal examination. It is covered in practical skills sessions in detail. Percussion Liver The right side of the abdomen should be percussed from the right iliac fossa to the right costal margin along the mid clavicular line. Dullness defines the livers lower border. Define the upper border of the liver by percussing along the mid clavicular line from above. Normally the upper level of liver dullness is the fifth rib in the right mid clavicular line. Kidneys We do not percuss the kidneys as there will usually be a resonant area due to overlying gas. Bladder Percuss from the umbilicus to the pubic symphysis. An area of suprapubic dullness may indicate the upper border of an enlarged bladder or pelvic mass. Ascites 2-3 litres of ascites are present before this is clinically detected. Usually the percussion note over the abdomen is resonant due to air in the bowel. When peritoneal fluid [ascites] collects, this accumulates in the flanks due to gravity in a supine patient. When 2-3 litres of ascites is present the abdomen will be dull to percussion in the flanks. As fluid accumulates abdominal distension and umbilical eversion occur. The dullness is then detectable closer to the midline. Shifting dullness: Percuss out to the left flank until dullness is reached. Keeping your finger over this area ask the patient to roll towards you. Gravity will cause the fluid to move to the right side of the abdomen [wait 15-20 seconds]. Percussion is repeated and shifting dullness is present if the area of dullness has changed to become resonant. Fluid thrill: This may be present when very large amounts of ascites are present. One of the examiners hands is placed flat on the patients flank. The other hand then flicks the other flank. A shock wave is transmitted to the palpating hand. The patient can be asked to help by placing a hand in the midline of the abdomen to prevent any ripple from passing through the fat of the anterior abdominal wall. Auscultation 40

Place the diaphragm of the stethoscope just below the umbilicus on the right and left side. Bowel sounds can be heard intermittently. They should be described as either present or absent. Normal bowel sounds are low pitched and gurgling occurring every 15-30 second period. No bowel over 30 seconds indicates paralytic ileus. Distension of the bowel leads to high pitched tinkling sounds caused usually by mechanical obstruction. Succussion splash: In pyloric stenosis or obstruction the stomach is distended with fluid and gas. Hold the patients from hips and shake the abdomen from side to side, splashing sounds are heard.

Clinical Teaching and Communication Skills Taking a Respiratory History

RESPIRATORY CURRICULUM SC2

CORE KNOWLEDGE The following topics must be known well. Also student should have taken at least one history from patient with each of following conditions.
Chronic Bronchitis Emphysema Asthma Resp Failure Sepsis Pneumonia Lung Ca Sarcoid TB Occupational Lung Disease DVT/PE Sleep Studies Pneumothorax Pleural Effusions Cystic Fibrosis Lung Transplant Clinical Criteria for ICU admission

SYMPTOMS (Student must be capable of taking directed history and exam and be able to order and interpret relevant investigations)
Cough (productive and non productive) Shortness of breath (acute and chronic) Wheeze Stridor 41

Haemoptysis Pleuritic chest pain Pyrexia Asymptomatic nodules found on routine Chest X Ray Pleural fluid on CXR At the end of this session you should be able to: 5. Take a detailed respiratory history from a patient. 6. Complete a full history. 7. Complete a systems review. Introduce yourself to patient and find out patients name, age and where they are from.

Presenting Complaint
Allow the patient to describe their problem in their own words and in their own way. Beginning the interview with an open question may bring valuable information, which will help in making a diagnosis: Do you want to tell me about the problem? Explore the presenting complaint fully, asking questions to ensure you are clear about all aspects of the problem. Many of the questions pertaining to pain may be adapted for any symptom, e.g. onset, periodicity, duration, aggravating factors, relieving factors, associations. Ask about all the respiratory symptoms remember that the patient may not realise the relevance of certain symptoms or the association between them.

Cough
Duration Nature of cough ( dry, barking etc) Change in character ( if chronic cough) When does the cough occur? ( Night, post meals) Associated symptoms (fever, wheeze) Sputum producton?

Some causes of Cough Acute cough 1. Infection 2. Allergy 3. Asthma/COPD Chronic cough 1. Smoking 2. Asthma/COPD 3. Post-nasal drip 4. Lung Carcinoma 42

5. TB

Sputum
How much are you bringing up in a day? (tsp, tbsp, cup etc) What colour is it? If chronic then how much would you usually produce and what colour is it normally? Vs How much are you producing now and what colour? Have you ever seen blood / pink discoloration in it? Can you comment on the taste / smell? Can you describe the consistency? (thick, sticky, watery, frothy) Do you have trouble getting it up? What time of the day is it worse classically much worse in early morning with bronchiectasis.

Sputum production Copious amounts of purulent sputum are characteristic of an infective exacerbation of COPD. Large amounts of frothy-white/pink sputum are seen in cardiac failure. Some causes of sputum production 1. 2. 3. 4. 5. 6. 7. Infection Smoking COPD Bronchiectasis Lung CA TB Pulmonary oedema

Haemoptysis
Have you ever coughed up blood / bloodstained sputum? Can you describe it? (blood flecks, bright / dark red, pink & frothy, clots) How long is this going on for? How many times has it happened? How much on each occasion?

Some causes of haemoptysis 1. 2. 3. 4. 5. 6. Lung carcinoma Pulmonary embolism TB Pneumonia Bronchiectasis Cystic Fibrosis

Dyspnoea
How long have you been feeling breathless? Is it getting worse? Severity What brings it on? How far can you run / walk / climb before it happens? 43

Are you ever breathless at rest? Do you ever feel breathless in bed? Timing of onset (acute, subacute, chronic) Duration and variability. Eg dry cough at night in asthma Ask about associated factors eg wheeze How is it affecting your life? Ask about baseline vs current level of dyspnoea.

Some causes of dyspnoea 1. COPD 2. Asthma 3. Pneumonia 4. Pneumothorax 5. Lung carcinoma 6. Pulmonary embolism 7. Pulmonary fibrosis 8. Cystic Fibrosis 9. Pleural effusiom 10. Left ventricular failure

Wheeze

What brings it on? (allergens, exercise, cold air, stress, smoke, dust) How often do you get an attack? Is this more often than usual? How do you relieve it? Does this help? How often do you take you inhaler (if on one)? Do you check peak flows at home? What is your average usually? What is it now? How is it affecting your life? Have you ever had to attend A&E with an attack? Were you ever ventilated? Some causes of wheeze Acute Respiratory infection Foreign body aspiration

44

Chronic Asthma Chronic infection Cystic Fibrosis Bronchiectasis Mediastinal masses Cardiac wheeze (LVF)

Chest pain
How long have you had this chest pain? Is it worse on taking a deep breath? Was it of gradual or sudden onset? Ask all the pain questions SOCRATES - Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating and relieving factors, Severity.

If pain is pleuritic in nature, it is usually localised, sharp and made worse by deep inspiration and coughing.

Fever
Is patient febrile? Are they getting chills or rigors? Are they checking their temperature? What is it?

Hoarseness
Is this a new problem? How long is it going on?

Night sweats
How long is it going on? Does it happen every night? Do they have to change their night clothes and bed sheets?

Weight loss
ASK If they were trying to lose weight? Is there a change in appetite? How much weight was lost and over what time period?

Weight loss may be associated with Respiratory neoplasm or Chronic infection, e.g. COPD/Cystic Fibrosis

History of Presenting Complaint

45

Previous respiratory illness [asthma, pneumonia, TB, COAD, Tumour] and all relevant details about that? o In COPD ask when diagnosed and how, smoker or not? History of recurrent chest infections? How many exacerbations per year requiring antibiotics, how many hospitalisations per year, when was the last exacerbation? Every in ITU or intubated?, Every do pulmonary rehabilitation? Baseline dyspnoea, exercise tolerance and sputum (colour and volume), effect on mobility and life in general. Home oxygen use or not. Nebuliser use or not. o In asthma when diagnosed and how, current control, how often attacks and what triggers, what inhalers, compliance and technique, what is baseline peak flow and what is current peak flow? Every hospitalised with asthma, every in ITU or intubated? Risk factors for respiratory disease eg smoking, family history, Abnormal CXR? Any chest problems as a child? Any allergies, hayfever, eczema or other atopy increase risk of asthma? Previous admissions? Previous operations? o o o o Video Assisted Thoracoscopy for biopsy Chest drain insertion Lobectomy Pneumonectomy

Past Medical/Surgical History

Other medical/surgical problems

Medication
Prescribed and over the counter Bronchodilators/inhalers Home nebuliser Home oxygen Antihistamines Antibiotics Steroids

Allergies
To any medication Document the reaction which occurred, e.g. true allergy or adverse reaction. nausea/vomiting/rash/wheeze/bronchospasm/loss of consciousness.

Social History
46

Marital status/children Employment effect of condition on employment status Home situation Independent or needs help with ADLs, any adjustments made to the home, how mobilise? home help? Meals on wheels? Who is at home? Are there people/family nearby who help? Alcohol intake [count units per week] Smoking history

a. b. c. d. e. f.

Do you smoke? / Have you ever smoked? How many cigarettes do you smoke in a day? Have you ever smoked more / less? Have you ever tried to give up? Were you successful? Passive smoking in work place/at home

Occupational History Exposure to dust in mining industry/factories [asbestos/coal] Exposure to mouldy hay [allergic alveolitis] Exposure to birds [psittacosis]

Family History
Any family history of respiratory disease Asthma Cystic Fibrosis Emphysema Alpha-1-anti-trypsin deficiency

Any other illness in family

Complete Systems Review

CVS RESP GI GU Musculoskeletal Neuro

Respiratory Examination
47

Exposing the patient

Patient should be undressed to the waist. Patient can be sitting in bed, over the edge of the bed or on a chair.

General Appearance/Inspection
All examinations begin with a general inspection of the patient and their immediate surroundings. This is done from the end of the bed. Is the patient comfortable? Dyspnoea at rest [shortness of breath] Tachypnoea - rapid respiratory rate, count respiratory rate [Should not exceed 14 breaths/min @ rest] Are accessory muscles of respiration being used? - Sternomastoid, scalenes, trapezius, platysma muscles increasing chest expansion - Abdominal muscles - Splinting may also be seen where the arms are fixed to allow use of the pectoral and other muscles to assist in breathing

Character of cough Productive Excess bronchial secretions pneumonia/chronic bronchitis Dry cough Asthma/bronchial Ca/LVF Sputum production Volume/purulent/blood Haemoptysis quantity/duration Wheeze On expiration Asthma/COAD 48

Stridor [obstruction of larynx, trachea, and large airways, rasping noise loudest on inspiration i.e. foreign body/tumour] Hoarseness [Listen to voice] Recurrent laryngeal nerve palsy, E.g. Carcinoma of the lung Laryngeal cancer Laryngitis

Comment on equipment O2 delivery, IV access, ECG monitor, and catheter bag Comment on bedside table inhalers, sputum pot Mobility walking frame, wheel chair Cyanosis Haemoglobin molecule changes colour from blue to red when oxygen is added to it in the lungs. Cyanosis is a blue coloration of the skin and mucous membranes due to the presence of greater than, or equal to, 5 g/dL of deoxygenated hemoglobin in blood vessels near the skin surface Peripheral Cyanosis Blood supply to a certain part of the body is reduced and the tissues extract more oxygen than normal i.e. the lips in cold weather may appear blue. Central Cyanosis Abnormal amount of deoxygenated haemoglobin in the arteries causes a blue discoloration in parts of the body with good circulation [the tongue]

Examination of the Hands

Clubbing Inspect for loss of angle between the nail bed and the finger. It can be graded: Grade 1 fluctuation and softening of the nail bed. This can be examined for by compressing nail bed with your fingers and rocking it [swelling of the subcutaneous tissues over the base of the nail] Grade 2 loss of the nail-bed angle Grade 3 increased curvature of the nail [swelling of the subcutaneous tissues involves the nail bed] Grade 4 fingertip develops a clubbed (drumstick) appearance [swelling of the pulp of the fingers in all dimensions] Early clubbing Increased sponginess of the proximal nail bed [There is fluctuation of the nail bed] This can be examined for by compressing nail bed with your fingers and rocking it. The next change is loss of the nail angle.

49

Late clubbing Eventually the distal phalanx becomes enlarged due to soft tissue swelling [drum sticking] [The cause of clubbing is not known there are several theories]

In a few cases Hypertrophic Pulmonary OsteoArthropathy [HPOA] may develop causing pain and swelling of the hands, wrists, knees, feet and ankles, with radiographic evidence of subperiosteal new bone formation Causes of clubbing Cardiovascular Cyanotic congenital heart disease Subacute infective endocarditis Atrial myxoma Respiratory Bronchial carcinoma [squamous cell] Bronchiectasis Lung abscess Cystic Fibrosis Empyema Pulmonary fibrosis [fibrosing alveolitis] Mesothelioma Asbestosis Gastrointestinal Cirrhosis Inflammatory bowel disease Coeliac disease Thyroid acropachy hyperthyroidism Familial

50

Idiopathic NB Chronic bronchitis and emphysema do not cause clubbing

**Clubbing is a sign that is looked for as part of the CVS, Respiratory, Gastrointestinal and Thyroid exam. It is frequently asked in exams. You must know the causes and stages of clubbing. ** Tar Staining Sign of cigarette smoking

Pulse Tachycardia is a common feature of infection, and is a side-effect of beta-agonist therapy for obstructive airway disease. Bradycardia may occur in very severe sepsis/asthma. Atrial fibrillation may be caused by pneumonia and lung carcinoma. Mention that you would also like to take the blood pressure. Wasting and weakness Compression and infiltration by a peripheral lung tumour of a lower trunk of the brachial plexus results in wasting of the small muscles of the hands Flapping tremor/Asterixis 51

Dorsiflex the wrists with the arms outstretched and spread out the fingers. With severe carbon dioxide retention a flapping tremor may occur.

Causes of Asterixis 1. CO2 retention Respiratory failure 2. Liver disease usually associated with hepatic encephalopathy in cirrhosis or acute liver failure 3. Acute renal failure Signs of CO2 Narcosis 1. 2. 3. 4. 5. Bounding pulse Asterixis Chemosis collection of fluid under the conjunctiva Altered consciousness Kussmauls breathing deep sighing respiration

Examination of the Face

Anaemia Examine conjunctiva anaemia/chemosis Horners Syndrome Ptosis, miosis, anhydrosis and enophthalmos [sunken eye]

Partial ptosis/Constricted pupil/Loss of sweating [ipsilateral] Interruption of the sympathetic innervation of the eye at any point

E.g. Apical lung tumour compressing sympathetic nerves in the neck

52

Abnormal right eye in right-sided Horners syndrome Central Cyanosis Examine tongue Upper Respiratory tract infection Reddened pharynx Enlarged tonsils Pus on tonsils

Tooth Decay Pneumonia Lung abscess

Sinusitis Tenderness over sinuses

Nose Note any obvious septal deviation or polyps. A nasal speculum can be used to inspect for polyps or engorged nasal turbinates Facial plethora/oedema Superior vena caval obstruction 53

Prominent veins in superior vena cava obstruction

Trachea Is the trachea central or is it deviated from the midline? Explain to the patient that you are going to press gently on their neck and that it may be a little uncomfortable. Use the forefinger of the right hand to palpate for the position of the trachea above and backwards from the suprasternal notch. If displacement of trachea is present its edge rather than its middle will be palpated and a larger space will be present on one side than the other.

Causes of tracheal deviation Towards the lesion 1. Upper lobe fibrosis 2. Upper lobe collapse 3. Pneumonectomy Away from the lesion 1. Tension pneumothorax 2. Massive pleural effusion Tracheal tug is present when the finger resting on the trachea moves inferiorly with each inspiration. This is a sign of gross overexpansion of the chest. Lymph node examination Cervical - Examine patient sitting up from behind for submental, submadibular, jugular chain, supraclavicular, posterior triangle, occipital, postauricular and preauricular. If enlarged comment on site, size, consistency, tenderness, fixation, overlying skin.

The Chest
54

Examine anteriorly and posteriorly by inspection, palpation, percussion and auscultation. Compare left and right sides. INSPECTION Is the chest moving with respiration? Is the movement equal and symmetrical on both sides? A large effusion, pneumothorax, area of collapse etc in one lung can cause asymmetrical movement. Kyphoscoliosis

Kyphosis-forward curvature of spine Scoliosis-lateral curvature of spine

Severe kyphoscoliosis may reduce lung capacity and increase the work of breathing. Pectus Excavatum Depression of lower end of sternum. A developmental defect. In severe cases lung capacity may be restricted.

Pectus Carinatum Prominence of sternum and costal cartilages. Can occur with chronic childhood respiratory illness and rickets.

Barrel-shaped Scars From previous thoracic operations. Chest drains. Thoracotomy scars. Traumatic scars. 55 Anteroposterior diameter is increased compared with the lateral diameter. This indicates hyperinflation. Severe asthma and emphysema

Thoracoplasty An operation performed in the past for tuberculosis. It involved removal of a large number of ribs on one side of the chest to achieve permanent collapse of the affected lung. No longer required due to antituberculous medication.

Radiotherapy Marks on chest wall. Skin may appear erythematous and thickened over irradiated area. Lung Cancer and lymphoma Subcutaneous emphysema Swelling of chest wall and neck due to tracking of air from lungs as in pneumothorax. May also be due to rupture of the oesophagus. It is felt as a crackling sensation on palpating the skin of the chest or neck.

Movement of chest wall Look for asymmetry of chest wall movement anteriorly and posteriorly. Unilateral reduction in chest wall movement may be due to consolidation/pleural effusion/pneumothorax. Bilateral reduction of chest wall movement indicates a diffuse abnormality such as COAD/diffuse pulmonary fibrosis.

Palpation
Chest expansion Measuring chest expansion provides information on a number of things. Is expansion equal on both sides? If the patient has a pneumothorax or an area of consolidation on one side, expansion will be decreased on that side. In patients with COPD, because their chest is hyperinflated, chest expansion is decreased overall. Expansion will also be decreased with diffuse pulmonary fibrosis. 56

 Place hands over upper anterior chest wall and get patient to take a deep breath in and out. Chest movement should be equal on both sides. This is checking anterior expansion. The hands can also be wrapped around the lower chest to measure outward expansion. Place hands on lower posterior chest wall with fingers extending around the sides of the chest. The thumbs are lifted slightly off the chest and should almost meet in the midline. On inspiration the thumbs should move symmetrically apart at least 5cm. This will assess lower lobe expansion. Take a breath in, and let it all the way out please. When they are in full expiration, place your hands over the lower ribs and stretch your thumbs out until they meet in the midline. Take a deep breath in please The distance your thumbs move apart is measured in centimetres Vocal fremitus

Palpate the front and back of the chest with the hand in two comparable positions as the patient repeats 'ninety-nine'. Differences in vibration on the chest wall can be detected. The causes of change in vocal fremitus are the same as those for vocal resonance [checked as part of auscultation] e.g. consolidation. Over consolidated lung the sound/vibration is transmitted better. This sign may be difficult to interpret. Compress the chest wall anteroposteriorly and laterally. Localised pain suggests a fracture.

Ribs

Percussion
Position the patient sitting up with the arms folded in front of the chest. Put left hand on the chest wall with fingers slightly separated and aligned with the ribs. The middle finger is pressed firmly against the chest. Other fingers are raised slightly off the chest wall With the pad of the right middle finger strike firmly the middle phalanx of the middle finger of the left hand. The percussing finger must be held slightly flexed and a loose swinging movement should come from the wrist. The percussing finger should be held off the middle phalanx at the end of percussion. Ending percussion with the percussing finger held on the middle phalanx will result in a falsely dull percussion note. Percussion of symmetrical areas of the anterior, posterior and axillary regions is necessary. 57

If the underlying structure contains air, the sound produced will be resonant. If the underlying structure is solid, the sound produced will be dull. As the lungs contain air, we expect to hear a resonant note throughout all lung fields.

Begin with percussion in the supraclavicular fossa over the apex of the lung. Percuss the clavicles directly. On percussion posteriorly, the scapulae should be moved out of the way by asking the patient to move their elbows forward. This rotates the scapulae anteriorly.

Dull Percussion over solid structure i.e. consolidated area of lung. Stony dull Percussion over fluid-filled area i.e. pleural effusion. Resonant Percussion over normal lung. Hyper-resonant Percussion over hollow structures i.e. pneumothorax

Auscultation
Start using the bell of the stethoscope applied above the clavicles to listen to the lung apices. Auscultate using the diaphragm over the anterior, lateral and posterior chest wall. 58

It is important to compare each side with the other and to listen over enough areas.

Ask the patient to Breathe in and out through your mouth please Listen over the same areas you percussed, again comparing right & left sides at each level. Listen for the quality and intensity of breath sounds and the presence of additional sounds. Quality of breath sounds Vesicular breath sounds Normal vesicular breath sounds are produced in the airways. There is no gap between inspiratory and expiratory sounds. Bronchial breath sounds Bronchial breath sounds are due to turbulence in the large airways. They have a hollow and blowing quality. Often a gap is present between inspiration and expiration. Heard over areas of - consolidation [pneumonia] - pleural effusion [above the fluid] - collapsed lung [i.e. adjacent to a pleural effusion] Intensity of breath sounds Normal or Reduced Causes of reduced intensity COAD [especially emphysema] Pneumothorax Pleural effusion Pneumonectomy Pulmonary fibrosis

Added sounds: Note the stage in the respiratory cycle at which the added sounds occur: inspiration/ expiration, early/mid/late/pan. Wheeze Wheeze may be heard on inspiration or expiration or both. They imply significant airway narrowing. They tend to be louder on expiration. An inspiratory wheeze implies severe airway narrowing. Usually the result of acute [asthma] or chronic [COAD] 59

Airflow limitation may be due to Bronchial spasm Mucosal oedema Excessive secretions Crackles/Crepitations Crackles [crepitations] are probably the result of small peripheral airways collapsing on expiration. Fine Crackles similar to hair rubbed between the fingers i.e. pulmonary fibrosis Medium Crackles i.e. LVF Coarse Crackles Characteristic of pools of retained secretions and have an unpleasant gurgling quality. They tend to change with coughing. i.e. bronchiectasis/pneumonia Pleural rub Due to thickened, roughened pleural surfaces rubbing together as the lungs expand and contract - grating sound. I.e. Pulmonary infarction/pneumonia Vocal resonance Auscultating while a patient speaks gives further information about the lungs ability to transmit sounds. Ask the patient to repeat 'ninety-nine' and listen over each part of the chest. Over consolidated lung the numbers are clearly audible while over normal lung the sound is muffled.

Whispering pectoriloquy Aegophony Consolidated lung tends to transmit high-pitched sounds so that speech heard through the stethoscope takes on a bleating quality. When a patient says 'e'[bee] it sounds like 'a' [bay]. Listen over each part of the chest as the patient repeats e, e, e Vocal resonance is increased to such an extent that whispered speech is distinctly heard. Ask the patient to whisper 'ninety-nine' and listen over each part of the chest.

To complete the examination 60

LOUD P2 If loud pulmonary component to 2nd heart sound [P2] heard in second left intercostal space pulmonary hypertension should be suspected. Pulmonary hypertensive heart disease [cor pulmonale] may be due to: COAD Pulmonary fibrosis Pulmonary thromboembolism

PEMBERTONS SIGN occurs in superior vena cava obstruction. Raise arms over head Facial plethora [redness] Inspiratory stridor Non pulsatile elevation of JVP

ABDOMEN Enlarged liver due to secondary deposits in cases of lung cancer FEET Oedema [right heart failure] DVT

Diabetic History and Examination

History Presenting complaint A diabetic patient can present in a number of ways. 1) Subacute symptoms of hyperglycaemia Polyuria Polydipsia/thirst Blurred vision Hyperphagia Weight loss Tiredness / fatigue Irritability / Difficulty concentrating Infections - genital candidiasis and cutaneous infections.

The classical symptoms of, polyuria, polydipsia and weight loss are more common in type 1 diabetes. 2) Acute diabetic emergency Diabetic Ketoacidosis : Type 1 Diabetes 61

DKA of cases.

Thirst Nausea and vomiting Abdominal pain Confusion / Drowsiness / Coma Blurred vision Weakness is the first presentation of a new diabetic in 20 %

In an established diabetic it usually occurs in the context of intercurrent illness such as infection (60%) or ommision of insulin dose (30 %). Non Ketotic hyperosmolar diabetic coma Marked drowsiness / coma Thirst Symptoms of hyperviscosity such as blurred vision, headache, stroke

Hypoglycaemia - FIRST: Adrenergic symptoms (sweating, tremor, palpitations, anxiety, nausea, weakness) - THEN: Neuroglycopoenic symptoms (speech difficulty, confusion, drowsiness, convulsions, coma).

WHY DOES IT OCCUR LIKE THAT? From Harrisons Principles Of Internal Medicine, 17th ed, 2008: TABLE 339-2. PHYSIOLOGIC RESPONSES TO DECREASING PLASMA GLUCOSE CONCENTRATIONS Response Glycemic Physiologic Role in the Prevention or Threshold, Effects Correction of mmol/L Hypoglycemia (Glucose (mg/dL) Counterregulation) Insulin 4.4-4.7 (80Ra ( Rd) Primary glucose regulatory 85) factor/first defense against hypoglycemia Glucagon 3.6-3.9 (65Ra Primary glucose 70) counterregulatory factor/second defense against hypoglycemia Epinephri 3.6-3.9 (65Ra, Rc Third defense against ne 70) hypoglycemia, critical when glucagon is deficient Cortisol 3.6-3.9 (65Ra, Rc Involved in defense against and growth 70) prolonged hypoglycemia, 62

not critical 2.8-3.1 (50- Recognition Prompt behavioral defense 55) of against hypoglycemia (food hypoglycemi ingestion) a Cognition <2.8 (<50) (Compromises behavioral defense against hypoglycemia) Note: Ra, rate of glucose appearance, glucose production by the liver and kidneys; Rc, rate of glucose clearance, glucose utilization relative to the ambient plasma glucose concentration; Rd, rate of glucose disappearance, glucose utilization by the brain (which is unaltered by the glucoregulatory hormones) and by insulin-sensitive tissues such as skeletal muscle (which is regulated by insulin, epinephrine, cortisol, and growth hormone). Copyright 2008 by The McGraw-Hill Companies, Inc. All rights reserved. In people with diabetes, hypoglycaemia occurs in the context of treatment and an accurate history of treatment, home circumstances and depression, should be taken. 3) Presentation with complications Microvascular disease Retinopathy: Visual loss is a late symptom, which is why screening is required. Neuropathy: Peripheral and autonomic Nephropathy: May progress to renal failure

hormone Symptoms

Macrovascular disease Peripheral vascular disease Cardiovascular disease Cerebrovascular disease

Infection 4) Detection on screening with little or no symptoms History of presenting complaint 1. When was diabetes first diagnosed? How? Symptoms? 2. Recent glycaemic control a. Symptoms of hyperglycaemia b. Home glucose reading diary? c. Recent HbA1C? Does patient knows what it is? 3. Diet carbohydrates? Portions? Fats? Sweets? 63

4. Exercise patients with diabetes should exercise for at least 30 min daily 5. Early signs of complications a. Macrovascular: Any chest pain/SOB when walking? Any calf pain when walking? b. Microvascular: i. Any vision deterioration? (retinopathy, cataracts) ii. Any pins/needles/numbness/pain/altered sensation anywhere? (peripheral neuropathy?) iii. Any change in bowel motions pattern/ diarrhoea/ constipation/ incontinence? Early satiety? Dysphagia? (GI autonomic neuropathy) iv. Any dizziness when standing up? (CVS autonomic neuropathy) v. Any urinary incontinence? (bladder neuropathy) vi. For men: any difficulty getting or keeping an erection? Any symptoms of retrograde ejaculation? 6. If on hypoglycaemics (sulphonylurea, insulin) a. Any symptoms of hypoglycaemia? How often? When? After exercise/not enough food/ insulin dose increase? Any serious hypoglycaemia (LOC) that required family to administer glucagon? 7. If type 1, any admissions for DKA? 8. If type 2, any admission for HHS (hyperglycaemic hyperosmolar state)? 9. Any recent infections (genital candidiasis trush, balanitis; UTIs, URTI & LRTIs)? Any skin infections? Glucometer reading

Medication / Diabetic treatment /Allergies Insulin pens

What treatment the patient is on for their diabetes (diet, oral hypoglycaemics, insulin), doses and any recent changes in treatment

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Modification of co-morbidities: ACE inhibitors, Angiotensin receptor blockers, Statins, Aspirin

It is important to assess if the patient is undergoing regular ophthalmic review and foot care Past medical/surgical history / History of co-morbidities 1. 2. 3. 4. 5. 6. 7. Hypertension Dyslipidaemia Obesity Pancreatitis Obstetric history of macrosomia Heart disease/ strokes/TIA/PVD In type 1, ask for other autoimmune conditions or their symptoms (thyroiditis with hypothyroidism or Graves' disease with hyperthyroidism, Addisons, primary hypogonadism, myasthenia gravis, celiac disease, pernicious anemia, alopecia, vitiligo, and serositis all components of autoimmune polyglandular syndrome II) Marital status/children

Social history Very important to assess home situation, especially in elderly with regards to compliance with treatment, dietary regulation, and emergency assistance in the event of a diabetic emergency Family history Diabetes Hypertension Ischaemic heart disease or stroke If type 1, any other autoimmune diseases (see above)? Occupation SMOKING !!! Alcohol consumption

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Review of systems - as in every systemic disease, should be done as part of HPC. Examination General inspection glucose load Dehydration osmotic diuresis caused by

[Dry mouth, loss of skin turgor, sunken eyes] Weight loss glycosuria Obesity NIDDM Level of consciousness- ask time person and place Endocrine facies such as Cushings syndrome/acromegaly Pigmentation: Yellow brown skin discolouration can be associated with haemochromatosis which can be associated with secondary diabetes Have a look at the patients surroundings and make note of medications by the bedside, urinalysis samples, IV fluids, insulin, antibiotics, diabetic drinks and diabetic diet sign. Vital signs possible metabolic acidosis Hyperventilation is a sign of

Blood pressure, check both lying and standing. Look for postural drops of more than 20/10 mmHg which is a sign of autonomic neuropathy, or severe dehydration, in an acutely unwell patient Hands: o Look for signs of carpal tunnel syndrome (median nerve entrapment) o Thenar wasting o Tinels sign o Phelans sign o Look for ulnar nerve entrapment signs o Hypothenar wasting Eyes (obligatory in annual review)

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 Check visual acuity which could be impaired in a diabetic due to retinopathy, temporarily disturbed because of changes in the shape of the lens associated with hyperglycaemia or permanently, due to cataracts Check 3rd, 4th and 6th cranial nerves. Diabetic third nerve palsy from ischaemia, usually spares the pupil Fundoscopy: Use the ophthalmoscope first at arms length, to check for o rubeosis iridis (new blood vessel formation in the iris which can lead to glaucoma)

o cataracts (due to sorbitol deposition in the lens) retina will be red and cataract black then come close to the eye, find optic disc and look in all four retinal quadrants, following four retinal arteries

Non proliferative changes: Caused directly by ischaemia Microaneurysms (appear as dot haemorrhages, they originate in the inner retinal layer. Blot haemorrhages (Occur more superficially in the nerve fibre layer) Soft exudates (cotton wool spots) Hard exudates (Due to lipid and protein deposition) Venous beading

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Proliferative changes: Changes in the blood vessels in response to retinal ischemia and are associated with new vessel formation (neovascularisation), scar formation and eventually retinal detachment.

Mouth Neck Auscultate the carotid arteries for bruits Chest Respiratory o Signs of infection Cardiovascular o Resting tachycardia (>100) sign of autonomic neuropathy o Beat-to-beat HRV (not done routinely in clinic, but described here FYI) With the patient at rest and supine (not having had coffee or a hypoglycemic episode the night before), heart rate is monitored by ECG or autonomic instrument while the patient breathes in and out at six breaths per minute, paced by a metronome or similar device. A difference in heart rate of >15 bpm is normal, <10 bpm is abnormal. 68 Check for ketotic fetor which smells like acetone (in DKA) Look for candida infection

Abdomen Hepatomegaly fatty infiltration or haemochromatosis If taking insulin, look for fat atrophy/ lipohypertrophy areas and advise avoiding them Legs Diabetic foot exam: Inspection Assessment of foot pulses Testing for loss of protective sensation Inspection: Hairless Atrophy [ischaemia] Calluses describe where, how thick; if present, podiatry referral needed Ulcers at pressure points (mixed vascular / neuro) Fungal infection (skin or nails or both) Cellulitis Make note of the following about ulcer, if present. It is good practice to include a drawing. o Site Always check between toes for even the slightest skin defect which can rapidly ulcerate in a diabetic with vascular compromise and poor wound healing.

o o o o

Size Base (? granulation) Edges (sloping, punched out, overhanging) Surrounding skin (cellulitis)

Thighs and shins:

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Necrobiosis lipoidica diabeticorum - red / brown / yellow, raised and often ulcerated patches usually on shins [rare]

Muscle: Check for wasting of quadriceps muscle due to femoral nerve mononeuropathy ( Diabetic amyotrophy) Vessels: Know how to palpate peripheral pulses a. dorsalis pedis and a. tibialis posterior Temperature of the feet Capillary refill ABI + toe pressures o If symptomatic or pulses not palpable o As screening - in patients over 50 years of age considered in patients <50 with PAD risk factors (e.g., smoking, hypertension, hyperlipidemia, or duration of diabetes >10 years) (ADA consensus 2003) Neurology: All patients with diabetes should be screened annually for DPN by checking any of the five tests (use of a 10-g monofilament, vibration testing using a 128-Hz tuning fork, tests of pinprick sensation, ankle reflex assessment, and testing vibration perception threshold with a biothesiometer), but usually: 10-g monofilament plus testing any one of: 70

o o o o

vibration using 128-Hz tuning fork pinprick sensation ankle reflexes vibration perception threshold

(Diabetic Neuropathy, American Diabetes Association Statement, Diabetes Care 2005.) Charcot joint is a medical emergency! : A severely distorted and deformed joint caused by recurrent unnoticed injury as a result of loss of proprioception and pain sensation

Urinalysis Examination is not complete without urinalysis for 1. microalbuminuria (albumin/creatinine ratio) for assessment of ?nephropathy 2. protein, glucose and ketones a. if present, urine culture and sensitivity Exercise within 24 h, infection, fever, CHF, marked hyperglycemia, and marked hypertension may elevate urinary albumin excretion over baseline values.

Examination of Thyroid
The aim of this tutorial is to complete examination of the thyroid gland. All students should get an opportunity to complete the exam and students should practice on each other during the class. The normal thyroid consists of 2 lateral lobes joined together by a central isthmus. The normal thyroid may be just visible in a thin young person below the cricoid cartilage The thyroid gland is ensheathed by the pretracheal fascia and moves on swallowing Look at the front and sides of the neck and decide if there is localised or general swelling of the gland. The lateral lobes of the thyroid should have a volume no greater than the patients terminal phalanges of the thumbs.

GOITRE: enlarged gland 71

Often noticed as a cosmetic defect by patient, relatives and friends Most are painless but pain/discomfort can arise in acute varieties [thyroiditis subacute or rarely suppurative] Goitres can produce dysphagia and difficulty in breathing, implying oesophageal or tracheal compression

Inspection The presence of a goitre is best observed with the neck slightly extended and identified by its movement when the patient swallows Look for scars, a thyroidectomy scar forms a ring around the base of the neck in the position of a high necklace

Ask the patient to swallow sips of water and watch the neck swelling carefully. Take a sip of water and hold it in your mouth Look at the neck Now swallow A goitre or a thyroglossal cyst [cyst formed in remnant of thyroglossal duct] will rise during swallowing Swallowing allows the shape of the gland to be seen Check whether the base of the gland can be seen as it rises [implying the absence of retrosternal extension] Gland is usually symmetrical Rarely redness of the skin over the gland occurs in cases of suppurative thyroiditis Look for prominent veins. Dilated veins over the upper part of the chest wall, often accompanied by filling of the external jugular vein. This suggests retrosternal extension of the goitre [thoracic inlet obstruction] Palpation Ask the patients permission to feel the neck and then approach patient from behind Slightly flex the head to relax the sternomastoids With the right middle and index finger feel for the cricoid cartilage Below this palpate the isthmus of the thyroid gland which lies over the trachea Then palpate the 2 lobes of the thyroid gland which extend laterally behind the sternomastoid muscle using the pulps of the fingers over the gland 72

Palpation: Posterior Approach Determine: Size feel for the lower border as its absence suggests retrosternal extension Tenderness [thyroiditis subacute or rarely suppurative] Whether it is soft [normal] / firm [simple goitre] / hard [carcinoma] Whether it is smooth, nodular or diffusely enlarged If a single nodule is present describe its location, size, consistency, tenderness and mobility. Determine if other nodules are present [multinodular goitre] Whether it moves on swallowing [carcinoma may tether the gland]

Ask the patient to swallow again while you palpate the thyroid; ensure the neck is slightly flexed to ease palpation If goitre/nodules palpated anterior approach can also be used

Lymph nodes Palpate laterally for lymph nodes, if you find lymph node enlargement in the neck check Supraclavicular nodes Submandibular nodes Postauricular nodes Suboccipital nodes

Enlarged lymph nodes near goitre will suggest the possibility of carcinoma of the gland particularly if they are firm or hard 73

Describe lymph node findings {Complete examination of lymphatic system to be completed later in semester 2} Percussion The upper part of the manubrium can be percussed A change from resonant to dull indicates possibility of a retrosternal goitre, but this is not a very reliable sign

Auscultation Auscultate over the thyroid for evidence of increased vascularity which may occur in hyperthyroidism Listen over each lobe for a bruit Differential diagnosis includes carotid bruit

Pembertons sign Ask the patient to raise both arms over their head Wait and then look for; Facial congestion [plethora] Facial cyanosis Respiratory distress Inspiratory stridor Dilated veins over the upper chest and filling of the external jugular vein Ask the patient to take a deep breath through the mouth and listen for stridor

These signs suggest restrosternal extension and thoracic inlet obstruction [also can be caused by any retrosternal mass] If there is any evidence of thyroid disease begin to examine for thyroid status Thyrotoxicosis/Hypothyroidism This is covered in clinical skills

The symptoms and signs of endocrine disease Hyperthyroidism

The commonest cause

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in young people Graves disease, an autoimmune disorder where circulating immunoglobulins stimulate TSH receptors on the surface of thyroid follicular cells in older people multinodular goitre

History Weight and appetite: weight loss despite normal or increased appetite Bowel habit: Diarrhoea Increased sweating, nervousness, irritability and anxiety Tremors Heat intolerance [preference for cooler surrounds] Palpitations (Atrial fibrillation) Change in facial appearance: Exophthalmos, Lid retraction with thyroid stare Amenorrhoea Muscle weakness Lump in neck: Toxic multinodular goitre with or without a dominant nodule, Graves disease (diffuse enlargement), toxic adenoma or carcinoma

Examination General Inspection Check for agitation, anxiety, irritability Weight loss

Vital signs Heart rate: Thyrotoxicosis is a cause of sinus tachycardia and atrial fibrillation (an irregularly irregular heart rhythm) Blood pressure: Hypertension is common in thyrotoxicosis

75

Hands Check for a fine resting tremor [due to sympathetic overactivity]. It is often useful to ask the patients to stick their hands out palms down and place a sheet of paper on the back of the hands. This will make even the slightest tremor very obvious.

- Thyroid Acropachy (clubbing): Specific to Graves disease [This looks like clubbing and is clubbing, rarely seen in Graves disease but not with other causes of thyrotoxicosis]

Onycholysis [Plummers nails] separation of the distal nail from the nail bed

Palmar erythema - [Also in RA, liver disease, pregnancy] Feel the palms for warmth and sweatiness sympathetic overactivity Arms - Proximal Myopathy (Proximal muscle weakness) [Ask the patient to raise arms over head] - Reflexes may be brisk. Face Eyes and periorbital region

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Examine the eyes for exophthalmos protrusion of the eyeball out of the orbit It occurs only in Graves diesease Due to inflammatory infiltrate of the orbital contents not the globe If not obvious look at the sclerae which in exophthalmus are not covered by the lower eye lid Next look from behind over the patients forehead. If exophthalmus is present, the eye will be visible anterior to the superior orbital margin Examine for complications of proptosis, conjunctivitis, chemosis [oedema of the conjunctivae], corneal ulceration [due to inability to close eye lids], and opthalmoplegia [paralysis of eye muscles] as well as pain on eye movement Thyroid opthalmopathy Related to sympathetic overactivity and not specific to graves disease

Thyroid stare - frightened expression Lid retraction sclera visible above the iris Lid lag ask patient to follow your finger as it descends from the upper to the lower part of the visual field, descent of the upper lid lags behind descent of the eyeball

** Note: Must look for exophthalmos/proptosis from above

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Neck Examination of the Thyroid gland

Chest Legs - Pretibial myxoedema bilateral firm elevated dermal nodules and plaques caused by mucopolysaccharide accumulation 78 Auscultate the heart for systolic flow murmur

Occurs only in Graves disease

Proximal myopathy (Ask patient to squat) Reflexes which may be brisk

Hypothyroidism
Primary disease of the thyroid or secondary due to pituitary/hypothalamic failure Myxoedema implies a more severe form of hypothyroidism; mucopolysaccsaccharides accumulate in the ground substance of tissues including the skin.

History Lethargy, physical and mental slowing Weight gain Bowel habit: Constipation Cold intolerance - preference for warmer weather Skin and hair changes: Dry pale skin with thinning hair Decreased pigmentation: Hashimoto thyroiditis [autoimmune mediated] Lump in neck: Goitre (thyroiditis, non functioning adenoma) Change in facial appearance: Puffy face swelling of eyelids [oedema] Hoarseness of voice Menorrhagia/amenorrhoea Symptoms and signs of heart failure in severe cases due either to bradycardia or pericardial effusion: Shortness of breath, ankle swelling Symptoms of anaemia: chest pain, shortness of breath 79

Examination Inspection Mental and physical sluggishness General CNS slowing is common with stupor or coma in severe cases Weight gain Hoarse voice

The hands/ arms Cyanosis due to reduced cardiac output Palmar crease pallor anaemia due to: Chronic disease Folate deficiency bacterial overgrowth in bowel Vitamin B12 deficiency due to pernicious anaemia [associated autoimmune disorder] Iron deficiency menorrhagia

Pulse small volume and slow bradycardia (slow heart rate below 60 beats per minute)

Tinels sign tap over flexor retinaculum, carpal tunnel thickened in myxoedema, this may cause paraesthesia in the distribution of the median nerve Blood pressure: Hypotension Proximal Myopathy Reflexes hung up or slow to relax Face 80

Skin may be thickened Alopecia hair loss Vitiligo - associated autoimmune disorder

Skin but not sclera may appear yellow due to hypercarotenaemia [due to slowing of hepatic carotene metabolism] Periorbital oedema Loss/thinning of outer third of eyebrows Xanthelasma due to associated hypercholesterolaemia Ask the patient to speak and listen for coarse, croking, slow speech

Neck Observe patient for any surgical scars in the neck (often concealed by wrinkles) 81

Chest Legs

Examination of the Thyroid gland: Goitre Check for an elevated JVP: Right heart failure can be associated with hypothyroidism specifically in relation to pericardial effusion.

Check for pleural or pericardial effusion.

Ask the patient to kneel on a chair with the ankles exposed. Tap the Achilles tendon with a reflex hammer. There is normal contraction followed by delayed relaxation of the foot Reflexes are hung up or slow to relax Proximal myopathy (Ask patient to squat) Peripheral oedema: Sign of right heart failure

Acromegaly
Acromegaly is caused by excessive secretion of growth hormone from the pituitary gland most often due to an adenoma. Gigantism is the result of growth hormone hypersecretion occuring before puberty and fusion of the epiphyses. It results in massive skeletal and soft tissue growth. Acromegaly occurs when the growth plates have fused, so that only soft tissue and flat bone enlargement is possible.

History Symptoms due to local mass effects of the tumor 82

Symptoms depend on the size of the intracranial tumor. Headaches and visual field defects are the most common symptoms. Visual field defects depend on which part of the optic nerve pathway is compressed. The most common manifestation is a bitemporal hemianopia due to pressure on the optic chiasm. This often presents with a patient bumping into things accidentally due to loss of temporal peripheral vision. The pituitary mass may cause headaches by direct invasion of adjacent structures. Headache may also be caused by interruption of the flow of cerebrospinal fluid. Pituitary tumours may also promote vascular headaches such as migraines. Headache may also be caused by hypertension, which is a very common finding in patients with acromegaly. Loss of end organ hormones is due to diminished anterior pituitary secretion of corticotropin (ie, adrenocorticotropic hormone [ACTH]), gonadotropins (luteinizing hormone [LH], follicle-stimulating hormone [FSH]), and thyrotropin (thyroid-stimulating hormone [TSH]). Hyperprolactinaemia may also occur and in this setting oligomenorrhoea / amenorrhoea and galactorrhoea may occur in females while impotence may occur in males Symptoms due to excess of GH Soft tissue swelling and enlargement of extremities Increase in ring and/or shoe size. Symptoms of carpal tunnel syndrome including pain and parasthesia in the hands. Hyperhydrosis (Increased sweating) Coarsening of facial features with frontal bossing and prognathism (protrusion and squaring of the jaw). Patients often notice this themselves or have it commented to them by someone else. Old photographs are very useful in highlighting these changes. Macroglossia (enlargement of the tongue) Arthritis (particularly osteoarthritis of the knees) Symptoms of heart failure including exertional dyspnoea, and peripheral oedema. This occurs due to uncontrolled hypertension which is very common in patients with acromegaly and due to cardiomyopathy attributable to excess growth hormone.

Examination
General Inspection Hands 83 Blood pressure: Hypertension is a very important sign in acromegaly The facial and body habitus features of acromegaly mentioned below may be quite obvious on initial inspection from the end of the bed

Large / wide / spade like / Doughy hands. This is due to soft tissue and bony enlargement. Check if any finger rings have been moved to a smaller finger or cut to a new fit. The hands are often notably warm and sweaty. This is due to increased metabolic rate.

Wrist Test for carpal tunnel syndrome using Tinels sign. The symptoms of pain and parasthesia are reproducible by tapping on the flexor retinaculum. Arms Axilla Skin overgrowth skin tags (molluscum fibrosum) Greasy axillary skin Acanthosis nigricans: Velvety discoloration Proximal Myopathy (weakness of the proximal upper limb muscles) Check the BP for hypertension

Face 84

Frontal bossing, large supraorbital ridge, squaring of jaw (progmathia) Mouth: Large tongue/Splayed and separated teeth Eyes: Examine visual fields: Bitemporal hemianopia may be noted if the pituitary tumour is large. Fundoscopy: Hypertensive or diabetic changes: Hypertension and diabetes are common in patients with acromegaly. Papilloedema: Due to increased intracranial pressure with large tumour Optic atrophy: Due to nerve compression

Chest Signs of heart failure, cardiomegaly Abdomen Legs Back Kyphosis Proximal myopathy (Ask patient to squat) Foot drop due to peroneal nerve entrapment Signs of osteoarthritis especially of the knees and hips Hepatic, splenic, renal enlargement Testicular atrophy: Gonadotrophin deficiency which can be associated with an enlarging pituitary tumour

Test the urine for glucose as GH is diabetogenic [glycosuria]

Cushings syndrome
Features Change in body form, particularly central obesity, weight gain in the face that is referred to as moon like facies (never mention moon face in front of a patient!) Limbs appear thin 85 Due to chronic excess of glucocorticoids Cushings disease is specifically pituitary ACTH overproduction Cushings syndrome is due to excessive steroid hormone production from any cause It is very important to enquire about a history of steroid therapy

Skin changes with easy bruising [due to loss of perivascular supporting tissue], purplish stretch marks, called stria, and red cheeks (plethora). Acne is also common.

Look for excessive pigmentation on the extensor surfaces [because of MSHlike activity in the ACTH molecule] Buffalo hump due to fat deposition over interscapular area (but never call it that in front of a patient!!!) Bony tenderness due to crush fractures of the vertebral bodies from osteoporosis [steroid effect on bone] Excess hair growth on face, neck, chest, abdomen and thighs Overall weakness and fatigue 86

Loss of muscle bulk ask the patient to squat to test for proximal myopathy [due to mobilisation of muscle tissue or excessive urinary potassium loss] Menstrual disorders/decreased fertility and/or libido Hypertension including headache, chest pain, symptoms of heart failure Symptoms of diabetes which is common in patients with Cushings syndrome Depression with wide mood swings as well as steroid induced psychotic features.

Examination
General Inspection Face The patient should be undressed to underpants. Look for bruising Look for poor wound healing Look for increased pigmentation: Primary adrenal insufficiency or Cushings disease where the excess ACTH has MSH-like activity. Moonlike facies: Due to disproportionate fat deposition in the upper part of the face

tumour -

Plethora Acne and hirsutism can be observed if androgen production from the adrenal glands is also increased. Eyes: Examine visual fields: Bitemporal hemianopia with large pituitary in Cushings disease.

Fundoscopy: Hypertensive and diabetic changes may be present.

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Optic atrophy and papilloedema where there is an increase in intracranial pressure in cases of Cushings disease due to a pituitory tumour.

Axilla and Chest Acanthosis nigricans Note supraclavicular fat pads Buffalo hump - Fat deposition

Abdomen Legs Proximal myopathy Bruising, poor wound healing. Peripheral oedema [salt and water retention] Purple striae: These are caused by weakening of collagen fibres in the dermis leading to exposure of vascular subcutaneous tissue Central obesity: Due to marked disproportionate fat deposition Palpate for an adrenal mass, which may rarely be detected in cases of adrenal carcinoma.

Urinalysis Test the urine for sugar [as steroids are diabetogenic] Hypertension Hypertension is common due to salt and water retention

Primary Hyperparathyroidism
Due to excess parathyroid hormone which results in increased serum calcium, loss of phosphate in the urine and increased formation of 1, 25dihydroxycholecalciferol. Hyperparathyroidism causes problems with stones, bones, moans and abdominal groans Symptoms of hypercalcaemia (hyperparathyroidism) Kidney stones Osteopenia, leading to an increased risk of fractures Abdominal pain (Due to peptic ulcer disease, stone disease, pancreatitis and constipation) Increased thirst and urination due to increased excretion of calcium in urine (hypercalciuria)

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Nausea, vomiting or loss of appetite Confusion or poor memory Severe hypercalcaemia may cause coma or convulsions Muscle weakness or fatigue

Examination General Inspection Mental status: Hypercalcaemia-reduced level of consciousness if severe Hydration status: Dehydration due to hypercalciuria Face Band keratopathy (Calcium corneal deposition usually at the 3 or 9 oclock positions relative to the iris):

Body and limbs Palpate shoulders, sternum, ribs, spine and hips for bony tenderness, deformity or evidence of fractures Test for proximal muscle myopathy Test blood pressure as hypertension may occur Test for blood in the urine - haematuria [renal stones]

Hypoparathyroidism
Symptoms of hypocalcaemia (hypoparathyroidism) This results in hypocalacemia with neuromuscular consequences [tetany]. It is usually a postoperative complication following throidectomy.

Trousseaus sign with a blood pressure cuff on the arm, raise the pressure above the systolic pressure. Contraction of the hand occurs within 2 minutes when hypocalcaemia has caused neuromuscular irritability

Positive trousseaus sign

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Chevsteks sign - tap gently over the facial nerve [seventh cranial nerve] below the ear. The nerve is hyperexcitable in hypocalcaemia and a brisk muscular twitch occurs on the same side of the face.

Hyper-reflexia due to neuromuscular irritability Nails fragile and monilial infection Dry skin Deformity of the teeth Tingling (paresthesias) in the fingers, toes and lips Muscle aches or cramps affecting the legs, feet, abdomen or face Fatigue or weakness Anxiety or nervousness Always enquire about a history of thyroid surgery

Blood pressure: Hypertension is a very important sign Observe for general features of hypothyroidism (post thyroidectomy)

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General inspection 1. Non physiological asymmetry 2. Skin changes - Dimpling 97

o Tumor pulling on skin directly o Or close to coopers ligament - Gross edema- peu dorange 3. Nipple changes - Abscesses in or around nipple - Eczema rash around the nipple- pagets disease - Discharge Palpation - Most tumors in the upper outer quadrant- feel axillary tail of Spence The patient history- book Renal History Presenting Complaint
Infection Acute renal failure Chronic renal failure Dialysis Post transplant Not all of the questions outlined below will be relevant in all cases but use your judgement as to which are appropriate. Renal stones, GU tumours and prostate will be covered by surgeons.

General symptoms Change in urinary appearance Red discolouration:

Haematuria Haemoglobinuria (due to haemolysis) Drugs such as Rifampicin

Note: With suspected haematuria ask about whether the patient means frank distinct blood in the urine or a general tea coloured urine, whether it is painful or painless (more sinister). Is the blood totally mixed in? (from bladder or above). Also ask if the patient has noticed if the haematuria occurs early or late in the urinary stream or if it is uniform throughout. The later in the stream the higher up the urinary tract the pathology is likely to be. Are there blood clots? (cannot be from the kidney) Causes of haematuria Colour (Bloody, coca cola, frothy, cloudy). Cloudly in infection (may also be foul smelling). Concentrated in dehydration and some type of renal failure. Very light colour and large volume in recovery phase of acute tubular necrosis or in other states of impaired renal concentrating capacity. Changes in urinary volume

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Polyuria (over 3 L of urine per day): Can be a feature of acute renal failure due to acute tubular necrosis, diabetes mellitus, diabetes insipidus, psychogenic polydipsia - Oliguria (less than 400 ml of urine per day): Due to renal failure or dehydration. - Anuria (less than 50 ml of urine in 24 hours) You must rule out urinary retention by asking about suprapubic pain/discomfort feeling of needing to pass urine. In some patients urinary retention is asymptomatic apart from anuria particularly in neurological conditions and is retention is chronic. In these patients a palpable bladder will be present and if still concerned, do a bedside bladder scan. Frequency o (Identify the patients norms)
o o o How often passing urine and how much on each occasion. How much is the patient drinking? (alcohol or otherwise) Caffeine can also cause bladder irritation and lead to frequency.

Nocturia Does the patient wake frequently at night to pass urine? Clarify how many times per night and volume of urine passed each time Urinary obstruction Common symptom in elderly men [prostatism] Hesitancy - difficulty starting micturition Poor stream - cannot hit wall Post micturition dribbling Double voiding/ Incomplete emptying (needing to pass urine soon after micturition) Nocturia - an objective increase in the frequency of waking up at night to void urine Frequency urine passed more often without increase in volume Complete obstruction/Overflow incontinence Retention inability to pass urine with suprapubic discomfort and pain. Pain
SOCRATES

Dull/continuous renal angle pain due to tumour or large polycystic kidneys Renal colic is severe pain radiating down to groin [renal calculus/clot] Kidney - Loin or lower back - Renal angle pain due to pyelonephritis is associated with fever/rigors/dysuria [pain passing urine]
Ureter - Upper abdo, groin or genitals Renal stone colic classically radiates loin to groin. Bladder - Central & suprapubic Timing of the day, (worse day, afternoon, night?) Dysuria (Painful micturition) Causes inflammation cystitis, stones, trauma, bladder Ca

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 Prostatitis [inflammation of prostate e.g. bacterial infection] Remember full pain questionnaire - onset, site, radiation, severity, character, time course, aggravating and relieving factors, associated symptoms

Incontinence Stress incontinence - when sneezing, laughing [multiparous female] Urgency - strong desire to pass urine may be followed by incontinence [Gynaecological prolapse or bladder instability] Overflow incontinence Spinal cord lesion, bladder will fill and then empty reflexly Pneumaturia Passing bubbles in the urine [vesico-colic fistula e.g. crohns disease] Oedema Ankle oedema, ascites, puffy face and eyes (nephrotic syndrome results in large amounts of protein loss in the urine and loss of fluid into the tissues). Dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea from fluid overload due to failure of the kidneys to excrete enough fluids. Symptoms of urinary tract infection
Fever, general malaise, poor appetite, nausea and vomiting. Dysuria (pain/stinging passing urine suggestive of a bladder or urethral infection) Foul smelling cloudy urine, Haematuria may be present, Loin pain and rigors suggestive of pyelonephritis (infection of the kidney itself). Previous or recurrent infections including in childhood. If so any previous imaging and any anatomical abnormalities found. In men any prostatic symptoms or any symptoms of bladder outlet obstruction as stagnation of urine in the bladder leads to increased risk of infection. Sexual history. Any urethral discharge?

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Hygiene - Pass urine after intercourse reduces UTIs in women. Wiping from front to back after using the toilet? Double voiding to ensure bladder fully empty? Volume of water drinking Symptoms of infection

Acute renal failure/Acute kidney injury: Sudden and often reversible loss of renal function developing over days to weeks How it presents?
Asymptomatic or minimally symptomatic discovered on routine blood test. (eg noted post op) Urine o o o o Anuria - failure to pass more than 50mls of urine daily Oliguria - < 400mls urine daily Less frequent urination with dark coloured urine Polyuria, nocturia and frequency inability of kidneys to concentrate urine normally (urine usually pale)or nocturia and frequency may be due to bladder outflow obstruction such as in prostatism. Colour Haematuria Foamy or bubbly urine if high protein concentration.

o o o

Fatigue, Generally unwell Fluid overload or hypoalbuminaemia o Oedema, dyspnoea, PND, Orthopnoea o Facial, periorbital and limb oedema classically in nephrotic syndrome with resultant hypoalbuminaemia Symptoms of uraemia o Fatigue, Lethargy o Weight loss o Hiccuping o Nausea and vomiting tends to be worse in the morning o Pruritis o Easy bruising and bleeding due to uraemia interfering with haemostatic mechanisms. o Chest pain and fever from uraemic pericarditis

o o o o

Headache. Weakness. Restless legs Poor concentration 101

o o o o

Poor sleep, Drowsiness, Seizures Coma.

Hyperkalaemia o asymptomatic o vague symptoms including: o nausea, o fatigue, o muscle weakness, o tingling sensations.

More serious symptoms of hyperkalemia include slow heartbeat and weak pulse (may manifest with palpitations or sensation of skipped beats). Severe hyperkalemia can result in fatal cardiac arrest. Generally, a slowly rising potassium level (such as with chronic kidney failure) is better tolerated than an abrupt rise in potassium levels.

Ask about symptoms of potential causes of acute renal failure The first thing to rule out is a post renal cause such as urinary retention as this is an easily reversible cause. Then rule out prerenal causes and then consider intrinsic renal causes. Pre renal Impaired renal blood flow due to
Fluid loss o Blood (Haemorrhage) o Plasma (Burns) o Water and electrolytes (diarrhoea, vomiting and dehydration) Hypotension o MI o Heart failure o Septicaemic shock o Drugs Increased renal vascular resistance o liver failure (hepatorenal syndrome) Renovascular disease o renal artery occlusion embolism, dissection, atheroma o ACE inhibitors precipitating renal artery stenosis

Intrinsic Renal Failure

Acute tubular necrosis o Hypovolaemia leading to ischaemia o Toxins and drugs

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o o

Aminoglycosides Contrast media Heavy metals and many more Rhabdomyolysis Haemoglobinuria

Glomerular disease Interstitial disease- drugs (sulphonamides,ciclosporin A), poisoning, component of systemic multisystem disease Vasculitis or scleroderma Myeloma

Post renal
Always consider urinary retention as a cause of renal failure and rule it out immediate. Urethra o Calculus o Blood clot o Phimosis or paraphimosis Bladder neck o Calculus o Blood clot o Prostatic hypertrophy or cancer o Obstruction by stones, prostate or tumour Urethers o Intrauretheric Clot Pyogenic Debris Calculi Extraureteric Retroperitoneal fibrosis Pelvic tumour or surgery Uterine prolapsed

A thorough medication history is extremely important including any medications taken over the past few weeks that may have precipitated renal failure. It is also important as any nephrotoxic drugs that are currently being taken should be stopped and drugs which are excreted by the kidneys may need to be dose adjusted or changed to other medications. Chronic renal failure Irreversible deterioration in renal function which develops over a period of months to years. Initially manifests as only as a biochemical abnormality. Most often asymptomatic at diagnosis and progresses insidiously.

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When diagnosed? How and by who? Cause if know

o o o o o o o o o o o o o Diabetes Hypertension Glomerular disease Interstitial disease Renal artery stenosis Chronic urinary retention Nephrolithiasis Systemic Inflammatory Diseases Polycystic kidney disease Amyloid and myeloma Vasculitis Medications very important to take a thorough history as outlined above. And many others

Ask about symptoms of possible causes. Ask about urine symptoms, overload, uraemic symptoms and hyperkalaemia as in acute renal failure above. In addition ask about

Bone disease (Secondary hyperparathyroidism), Bone pain due to renal bone disease caused by secondary hyperparathyroidism which is compensating for vitamin D deficiency caused by the renal failure. Fractures? Osteomalaecia (vitamin d deficiency) or osteoporosis (also important as depending on condition patients may be on steroids. On alfacalcidol, calcium supplements, phosphate binders? Low phosphate diet? Symptoms of anaemia (Due to declining erythropoietin levels) Healthy kidneys produce the hormone erythropoietin which stimulates the bone marrow to make oxygen-carrying red blood cells. As the kidneys fail, they produce less erythropoietin, resulting in decreased production of red blood cells to replace the natural breakdown of old red blood cells resulting in anaemia. On EPO? On iron? Hypertension Symptoms, Do they check it regularly. How good is control? Hypertension can be both a cause a result of renal failure. Any known parathyroid problems? Hypercalcaemia (Tertiary hyperparathyroidism) o Bones, stones, groans, psychic moans

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o o o o o o o o

Abdomen pain Vomiting Constipation Anorexia Weight loss Tiredness Weakness Hypertension

o o o o o o o

Depression Confusion Pyrexia Renal stones Renal failure Polyuria Polydipsia

Cardiovascular disease and stroke o o o Much higher incidence in renal disease Patients with chronic renal failure have tendency to hypercholestrolaemia particularly hypertriglycerideaemia in nephrotic syndrome Caution with statins as many are renally excreted

Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys and sometimes the liver, can cause pain in the back or side Abnormally dark skin Gout Myopathy Peripheral neuropathy Low level of sexual interest and impotence
Menstrual periods stop (amenorrhea) Sleep problems, such as insomnia, restless leg syndrome, and obstructive sleep apnoea Clotting problems due to platelet dysfunction due to uraemia. In dialysis platelet dysfunction can be due to the process of dialysis itself also. Also anticoagulation with heparin is used during dialysis which transiently increases bleeding risk. Dehyration, sodium loss and hypotension due to loss of renal concentrating ability in some cases (usually recovery phase of acute tubular necrosis but can also occur in others) Metabolic acidosis due to failure of renal excretion of acids o o Kausmall breathing Confusion

In nephrotic syndrome

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Increased risk of thromboembolism Increase in clotting factors and platelet abnormalities

Hyperlipidaemia Particularly hypertriglyceridaemia Thought to be due to hepatic lipoprotein synthesis in response to low oncotic pressure

Increased susceptibility to infection Loss of immunoglobulins in urine

Diet - Renal failure patients must be questioned about diet - Protein, fluid and salt restriction, low phosphate diet and use of phosphate binders. Diet tailored to individual patient needs. Ask about Renal replacement therapy (see below) Are they on the transplant list? If on dialysis
When started on dialysis? What was cause of renal failure? Summary of symptoms on presentation and how the renal failure progressed as above. Still producing urine or not and how much? Method of dialysis currently o o Haemodialysis fistula (needle or button) or line Peritoneal dialysis

Previous methods of dialysis and why changed? Previous fistulas or catheters. For haemodialysis o o o o o How many times per week dialysed and for how many hours each session? What is your dry weight? (ie The weight that is aimed for post dialysis) How much weight do you gain between dialysis sessions and how much fluid is taken off on dialysis? Are you on fluid restriction? Every considered for home haemodialysis?

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Intraperitoneal dialysis o o CAPD or APD? How many exchanges per day in CAPD?

HIV, CMV Hepatitis status checked prior to dialysis patient may or may not know this. Have they had their hep B vaccine and annual flu vaccine? Previous methods of dialysis and why changed? Previous fistulas or catheters. Diet restrictions Phosphate binders, calcium and alfacalcidol? EPO? IV iron? Line infections or blockage or line falling out. Fistula o thrombosis, aneurysms, stenosis, infections, ischaemia, steal syndromes

Ask about complications of haemodialysis

Hypotension due to excess fluid removal or in some patients it becomes chronic due to failure of BP control mechanisms. Ask about dizziness on standing or during dialysis. Disequilibrium syndrome o Nausea, vomiting, headache, altered consciousness and rarely seizures or coma due to rapid changes in in placma osmolality and cerebral oedema on initial dialysis

Pulmonary oedema due to fluid overload Dyspnoea, Orthopnoea, PND. Cardiac arrhythmia due to potassium shifts palpitations or collapse. Paplitations may also be due to haemodynamic shifts. Haemorrhage due to anticoagulation Dialyser hypersensitivity (allergy to dialysis membrane) Air embolism Systemic sepsis Cardiovascular

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o o o o

IHD Stroke Cardiac failure ar all more common in dialysis patients Hypertension persists in 25-30% on dialysis

Anaemia o o o Combination of underlying condition and dialysis Treated with EPO and iron if also iron deficient. Iron given IV at time of dialysis. Transfusions avoided if possible if on transplant list as antibodies would be produced reducing the possibility of successful transplant.

Renal bone disease as above B2 microglobulin amyloidosis o o o Carpal tunnel syndrome Arthralgia Fractures

Acquired renal cysts which may lead to bleeding and haematuria Peritonitis fever, rigors, unwell, abdomen discomfort or pain. Problems with tenchkoff catheter placement. Can become blocked if moves high in the peritoneal cavity. More likely if patient becomes constipated so ask about bowel habit. Tenchkoff exit site infections Hernias Back pain Feeling of bloating

Ask about complications of peritoneal dialysis

How it affects life? Job? Study? Finance? On transplant list? Any previous transplants? Post transplant patient What was primary diagnosis? Were you on dialysis prior to transplant and for how long? Ask about complications of chronic renal failure eg bone disease. 108

When was transplant? Cadaveric, living related donor, living unrelated donor? After the operation
Did you produce urine immediately or was production delayed? What volume of urine was produced? What was your Creatinine post op and what is it now? Most patients will know this. Did your creatinine normalise quickly? What immunosuppressant, anti-fungals and antibiotics were you on initially and what regime are you on now? Any post op complications such as infections (wound, urine or systemic), haematomas, urine leaks from the newly anastomosed urether with formation of a urocele around the new kidney. Any episodes of rejection post transplant? Any renal biopsies needed? Did you need any dialysis after the transplant? (suggestive of delayed function) When the first transplant was? Cadaveric or living related donor or unrelated living donor? How long did the kidney function for? If known what was the cause of the rejection?

Was it the first transplant? If not the first transplant ask

CMV status may or may not know this Transplant compatibility may or may not know this Any opportunistic infections? Eg candida. Any UTIs? Any other infections If it has been some time since the transplant ask about any skin lesions that have appeared or if there have been any skin lesions removed? High risk of skin malignancy post transplant due to immunosuppression. Have they had the flu vaccine? Medications Immunosuppressant
Tacrolimus side effects of tremor and renal impairment Cyclosporin Steroids

Antifungals Antibiotics

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Past medical history Ask about conditions predisposing to renal failure and pre-existing renal conditions, Bladder Ca, surgery, dialysis, catheters, UTI as a child, stones, gynae/obs history. Hypertension. Hypercholestrolaemia, heart disease, stroke Drug History & Allergies A very careful drug history is important to screen for potential nephrotoxic medications that may have causes the renal failure. It is also important to stop nephrotoxic drugs even if they were not the original culpit as they may worsen the situation. Drugs which are renal excreted may need to be dose adjusted or changed to a different medication. Rifampicin discolours the urine turning it orange. Diuretics can result in pre renal renal failure and polyuria and frequency. Family History Family history of prostate Ca or kidney stones, heart disease, diabetes or high blood pressure, polycystic kidneys or any other renal problems Social History Smoking. Alcohol. Travel. Effects of symptoms on ADL, work and finances. Renal disease can have devastating effect on peoples lives and this is an important consideration. Review of systems A full review of all systems should be carried out

The genitourinary examination

If renal disease is suspected or known to be present then certain signs must be sought. The purpose of clinical examination is to assess clinical status as well as trying to elucidate the cause of the renal failure. Inspection General inspection remains crucial. Hyperventilation underlying metabolic acidosis Hiccupping can be a sign of terminal uraemia Sallow complexion dirty brown appearance in chronic renal failure [impaired excretion of urinary pigment] 110

Anaemia of chronic disease/poor nutrition/erythropoietin deficiency/haemolysis/bone marrow depression (pallor, palmar crease pallor, conjunctival pallor) Terminal renal failure Level of consciousness - drowsy/coma - due to nitrogen/toxin retention Muscle twitching/tetany/epileptic seizures due to low serum calcium level and to nitrogen retention The hands Leuconychia white transverse opaque lines in hypoalbuminaemia [nephrotic syndrome]

Terrys lines/ half and half nails distal brown arc occurring in 20% of renal failure patients

Anaemia palmar crease pallor Asterixis may be present in terminal chronic renal failure [Dorsiflex the wrists with the arms outstretched and spread out the fingers, a flapping tremor may occur as in liver failure] Hydration dehydration can cause acute renal failure over hydration can result from intravenous infusion of fluids to correct renal failure fluid overload can result from renal failure [pedal oedema/pulmonary oedema] Fluid balance and hydration can be assessed from BP, postural BP drop, pulse, skin turgor, mucous membranes, eyes, daily weight, level of oedema, is the patient thirsty?

The arms
1) Arteriovenous fistula used for haemodialysis [Make sure this is palpated for thrill and auscultated for bruit to assess function of the fistula] 111

Brachio-cephalic, radio- cephalic?

Bruising nitrogen retention causes abnormal platelet aggregation Skin pigmentation failure to excrete urinary pigments Scratch marks pruritis due to uraemia and calcium deposition Blood pressure hypertension may be the cause of renal disease or a complication Peripheral neuropathy/ myopathy

The face
Anaemia conjunctival pallor Jaundice nitrogen retention can cause haemolysis Uraemic fetor due to breakdown of urea to ammonia in the saliva Mucosal ulcers underlying connective tissue disease i.e. SLE Gingival hyperplasia due to immunosuppressant therapy [cyclosporin] Rash - underlying connective tissue disease i.e. SLE

The neck
Central line for dialysis Jugular venous pressure to assess hydration [elevated JVP in fluid overload/CCF] Carotid artery bruits there may be generalised atherosclerosis [renal artery stenosis]

The chest
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Cardiac - CCF due to fluid retention in chronic renal failure - Hypertension sodium and water retention and excess renin production - Pericarditis due to retained metabolic toxins and can cause a pericardial rub Lungs - Pulmonary oedema [volume overload] - Percuss for effusions - Infection due to immunosuppression in renal transplant patients

The abdominal examination

As done previously but particular attention must be paid to the following; Peritoneal dialysis scar- either on right or left next to the umbilicus Inspection Nephrectomy scar - look at loin and lumbar regions Nephrectomy tube - draining wound Nephrostomy tube - draining urine directly from kidney into a bag

Renal transplant scar right or left iliac fossa Transplanted kidney bulge under scar in RIF/LIF Catheter for peritoneal dialysis Small scars from catheter placement near midline or the lower abdomen Suprapubic catheter to allow drainage of urine directly from bladder Distension polycystic kidneys/ascites [nephrotic syndrome]/dialysis fluid Palpation The kidneys bimanual method

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To palpate the right kidney the examiners left hand is placed underneath the back. The left fingers flex at the metacarpophalangeal joints in the area of the renal angle. The examiners right hand is placed over the RUQ. The kidneys are felt by balloting, the renal angle is pressed by the flexing fingers of the posterior hand and the anterior hand is used to palpate the kidney. To palpate the left kidney the left hand is stretched over the abdomen and placed posteriorly over the renal angle. The right hand feels for the left kidney anteriorly. Deep palpation in the renal angle can elicit tenderness suggesting pyelonephritis. To distinguish a large left kidney from splenomegaly: 1. Spleen has no palpable upper border 2. Spleen has a notch 3. Spleens moves inferomedially on inspiration, kidney moves inferiorly 4. Spleen is not ballottable unless gross ascites present 5. Percussion note is dull over the spleen resonant over kidneys 6. Friction rub may be heard over the spleen but never over the kidney as it is too posterior Unilateral renal mass Renal cell carcinoma Hydronephrosis Polycystic kidneys [asymmetrical enlargement] Acute pyelonephritis Abscess Bilateral renal mass Polycystic kidneys Bilateral hydronephrosis Bilateral renal carcinoma Early diabetic nephropathy Infiltrative disease i.e. lymphoma/amyloid Transplanted kidney palpable in LIF or RIF. Note size, tenderness, presence of any bruits. Hepatomegaly - from hepatic cysts may be present in PCKD Bladder empty bladder is impalpable. If there is urinary retention the full bladder may be palpable above the pubic symphysis. It is typically regular, smooth, firm and oval shaped. It may reach as high as the umbilicus or even higher in severe urinary retention. It must be differentiated from any swelling arising from the pelvis. The bladder can be emptied by insertion of a urinary catheter. Percussion Ascites shifting dullness [nephrotic syndrome] Enlarged bladder percuss down from the epigastrium towards the pubic symphysis. Dullness will be heard over the bladder Auscultation 114

Renal bruits best heard just above the umbilicus about 2 cms to the left or right of the midline. Listen with the diaphragm of the stethoscope. Its presence suggests renal artery stenosis due to atherosclerosis or fibromuscular dysplasia. The absence of hypertension makes a diagnosis of renal artery stenosis less likely. Rectal and pelvic examination Examination of external genitalia for evidence of STI Prostatomegaly in males and Frozen pelvis from cervical cancer in females: These may cause urinary tract obstruction and renal failure The back Sacral oedema fluid overload/CCF Bony tenderness strike the vertebral column gently and may elicit tenderness. This may be due to renal osteodystrophy or secondary hyperparathyroidism The legs Oedema Pigmentation Scratch marks Gouty tophi in feet Peripheral neuropathy The fundi Diabetic changes Hypertensive changes Male genital examination and per rectum examination will be covered by the surgeons. Female genital examination will be covered in gynaecology next year. Renal replacement therapy background information For patients with end-stage renal disease, renal replacement therapy is achieved by dialysis (haemodialysis or peritoneal dialysis) or renal transplantation. Although true replacement of renal function is not provided by dialysis, this modality is lifesustaining since it removes metabolic wastes and excess body water. The guidelines for instituting renal replacement therapy in renal failure are as follows: Urea > 30 mmol/l [2.5-8.5 mmol/L] Creatinine > 600 umol/L [50-120 umol/L] Hyperkalaemia: K > 6 mmol/L [3.2-5.2 mmol/L] Metabolic acidosis PH [7.35 - 7.45] HCO3 [23.0 31.0 mmol/L] - Fluid overload and pulmonary oedema - Uraemic encephalopathy or pericarditis In acute renal failure haemodialysis is used for renal replacement therapy. 115

In chronic renal failure preparation for renal replacement therapy is begun usually about a year before predicted start date of dialysis as GFR begins to decline below 30 ml/min [Normal GFR is approximately 100 ml/min]. The options for renal replacement in chronic renal failure are haemodialysis (70%), and peritoneal dialysis (30%). All patients are considered for renal transplantation unless there is a contraindication such as an active malignancy, active vasculitis or severe ischaemic heart disease. Haemodialysis:Haemodialysis takes place usually over three to four hours, three times a week. To perform this type of dialysis it is necessary to gain access to the blood stream so that the blood can be taken and given back. The type of access used will depend upon the patient and how long the dialysis will be needed. AV fistulas are typically constructed with an end-to-side vein-to-artery anastomosis between an artery and vein. The most commonly used fistulas are created by anastomosing the radial artery and cephalic vein (radiocephalic or wrist fistula). This requires an operation. Although some fistulas mature within weeks, others require up to six months before they provide reliable haemodialysis access.
AV fistulas

Double-lumen tunneled cuffed catheters Alternatively, a special catheter may be used which is placed into one of the large veins in the neck and hidden under the skin so that only the end is exposed on the chest. Needles are not required for haemodialysis or blood sampling with this catheter. Catheters are most commonly placed in the internal jugular vein and tunneled superficially to exit on the upper, anterior chest. The catheter should be positioned under fluoroscopy such that the tip rests in the right atrium.

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Tunneled cuffed venous catheters are primarily used as intermediate-duration vascular access to allow maturation of grafts. Central venous catheters can also provide chronic dialysis access when haemodialysis is required for less than one year, arteriovenous access is contraindicated, and when patients refuse permanent access. The primary advantage is the ability to provide immediate access, while the main disadvantages are the risk of infection and malfunction. The preferred type of access is a fistula because they have the lowest risk of complications, lowest need for intervention, and the best long-term patency. 117

Peritoneal Dialysis
An alternative to haemodialysis is peritoneal dialysis where the patient's peritoneum acts as a blood filter. A catheter is surgically inserted into the patient's abdomen. During treatment, the catheter is used to fill the abdominal cavity with dialysate. Waste products and excess fluids move from the patient's bloodstream into the dialysate solution. After a waiting period, the waste-filled dialysate is drained from the abdomen, and replaced with clean dialysate. Peritoneal dialysis: Does not take blood from the body to be filtered Uses the lining of the abdomen (peritoneum) to filter blood Is flexible as can be done almost anywhere

Peritoneal dialysis works by using the patients peritoneum as a filter. There are three stages to a dialysis cycle (or exchange): The abdomen is filled with dialysis fluid (dialysate). The amount of fluid varies but is usually 2 litres The dialysis fluid stays in the abdomen for a period of time. During this time, waste products and chemicals pass into the fluid. The 'used' dialysis fluid is drained from the body and discarded.

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Types of peritoneal dialysis There are two main types of peritoneal dialysis: Continuous Ambulatory Peritoneal Dialysis (CAPD) Automated Peritoneal Dialysis (APD).

CAPD - This is the most commonly used form of peritoneal dialysis and works by using gravity. It is carried out manually throughout the day. A bag of fluid is warmed to body temperature (using a special heating machine) and placed at a high enough level to allow the fluid to drain into the abdomen through a tube. When it has filtered the blood of waste products, chemicals and water, an empty bag is placed at a low enough level to allow the fluid to drain out of the abdomen through the tube. It takes around 30 to 40 minutes to carry out a 'bag change' as above and patients can stick to their normal routine between bag changes. Between bag changes dialysate is left in abdominal cavity for several hours. Between 3 and 5 exchanges are usually required every day. APD - This system is used during the night, so that patients do not have to change bags during the day. A machine warms the fluid and delivers it through the tube. The machine leaves the fluid in the abdomen for a specified time and then drains it out of the abdomen through the tube. This 'cycle' is then repeated according to a pre-set programme. In the morning patients can disconnect from the machine and go about their normal routine. Before dialysis a procedure is required to insert a soft tube (catheter) into the abdomen. In many cases, the catheter can be placed with just a local anesthetic, but for some people, surgery is necessary.

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Peritoneal dialysis has the advantage of being carried out in the patients home.

Haemofiltration
This can be used to treat ARF patients in ITU setting. Haemofiltration is less likely than haemodialysis to cause acute hypotension in patients with septicaemia or with poor myocardial function. Large volumes of plasma water are removed and replaced by a sterile electrolyte solution. Although like haemodialysis it can be carried out intermittently using a machine it is usually performed as CAVH continuous arteriovenous haemofiltration. Its main advantage is in controlling fluid and electrolyte balance. Continuous venovenous haemofiltration [CVVH] can be carried out using central venous lines but requires a blood pump for circulation. A further variation is to combine continuous dialysis with continuous haemofiltration [CAVHD]. In this blood is ultrafiltered and dialysed. For CAVH and CAVHD cannulas are inserted into a major artery [usually the radial artery] and a vein to form an AV shunt. Frequent assessment of fluid balance is required.

The Genitourinary History

Pain
Questionnaire: 11. 12. Site Radiation where the pain moves

Renal Pain: felt in the Loin Renal Angle (angle between the 12th rib & the edge of erector spinae muscle) Ureteric Colic: felt along the line of the ureter loin to groin (starts in the loin & radiates down around the waist just above the inguinal ligament to the base of penis, scrotum or labia) Bladder pain: Dull suprapubic ache worse by micturation

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Prostatic pain: felt deep in the pelvis, between the legs in the perineum patient often thinks the pain is coming from rectum 13. 14. 15. 16. 17. 18. 19. 20. Character sharp/dull ache/colicky Severity score from 1 to 10, 1 being very mild, 10 being worst pain ever experienced. Onset sudden/gradual Periodicity constant/intermittent Duration minutes/hours/days Aggravating precipitants/makes it worse Relieving eases Associations other symptoms that accompany the pain, e.g. nausea, vomiting, diarrhoea, urinary symptoms etc.

Associated Features:
1. 2. 3. 4. Anorexia Weight loss Nausea & Vomiting Fever and chills

Do you feel feverish or sweaty?

Simple urinary tract infections generally dont lead to a pyrexia, however if left for some time, the patient may develop pyelonephritis resulting in fever, malaise and occasionally vomiting. Also an obstructing renal calculus may lead to pyrexia, rigors and vomiting due to obstruction of the ureter lead to superimposed infection, an emergency. A RCC may present as pyrexia of unknown origin, beware!

5. Changes in urinary appearance 6. Changes in urinary volume 7. Symptoms suggesting Urinary Obstruction

Change in urinary appearance

Haematuria: Frank distinct blood in the urine or a general tea coloured urine) Painful or painless (more sinister) If the haematuria occurs early or late in the urinary stream or if it is uniform throughout. The later in the stream the higher up the urinary tract the pathology is likely to be. Kidney/bladder tumour, Bleeding from prostate, Infection Calculi Other causes of red discolouration of urine: Haemoglobinuria (due to haemolysis) Drugs such as Rifampicin When did you first notice passing blood in the water? 121

Essential to establish whether this is an acute or chronic presentation. Acute presentations with large volumes of blood can lead to acute urinary retention secondary to clot formation in the bladder, which could be from a bladder neoplasm. Many older men may give a history of many months or even a couple of years of blood loss. New onset haematuria in the younger person is generally a UTI a renal calculus, or trauma.

Is the blood bright red or dark coloured?

Bright red blood is a fresh bleed, from either inflammation, trauma, infection or the sloughing of some tumour in the renal tract. Dark blood is possibly from a ruptured renal cyst into the collecting system and will appear as altered stale blood with some flecks of bright red.

Is the blood at the start of the stream or at the end?

Urethral inflammation, trauma or, prostatic disease can cause haematuria at the beginning of micturition which then clears, or haematuria only at the end of micturition.

Do you have any pain?

Painless haematuria raises the question a renal tract neoplasm. In the younger person pain resulting in frequency and urgency points towards a urinary tract infection and cystitis suprapubic pain/discomfort, or a renal calculus, which gives a colicky type pain mainly in the flank.

Changes in urinary volume

Do you need to pass water more often than usual?
Urethritis, Cystitis of any cause, UTI, prostatitis and heavy blood loss leading to clot retention can give symptoms of frequency and urgency and also dysuria.

Polyuria (over 3 L of urine per day): Acute renal failure due to acute tubular necrosis, Diabetes mellitus, Diabetes insipidus, Psychogenic polydipsia Oliguria (less than 400 ml of urine per day): Renal failure Dehydration. Anuria (less than 50 ml of urine in 24 hours): Renal failure Dehydration

Urinary obstruction
Common symptom in elderly men [prostatism] Hesitancy - difficulty starting micturition Poor stream - cannot hit wall

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Post micturition dribbling stream is weak and dribbles down to nothing as it finishes Straining - to push or strain to begin urination Double voiding/ Incomplete emptying - needing to pass urine soon after micturition Nocturia - an objective increase in the frequency of waking up at night to void urine Frequency urine passed more often without increase in volume Retention inability to pass urine

Urinary Incontinence
Urgency/urge incontinence urge to pass urine as soon as desire arises Overflow incontinence uncontrollable leakage and dribbling of urine from urethra Stress incontinence - when sneezing, laughing [multiparous female]

Pneumaturia
Passing bubbles in the urine [vesico-colic fistula e.g. crohns disease]

Urethral Discharge
Colour Consistency Quantity Painful or burning micturition Fever Chills Perineal fullness

Sexual problems in the male

Erectile dysfunction / impotence (inability to maintain an erection adequate for satisfactory sexual intercourse) Premature Ejaculation Loss of libido Haemospermia (trauma/infection)

Sexual problems in the female

Frequency, regularity and duration of menses, LMP Blood loss, clots suggest menorrhagia, heavy menstrual loss Dysmenorrhoea Primary/secondary amenorrhoea Post menopausal or post coital bleeding OCP/HRT Dyspareunia 123

History of Presenting Complaint

Have you had any kidney or bladder problems in the past?
As transitional cell carcinoma of the renal tract represents field change, meaning the entire urothelium has potentially been affected by TCC and strict surveillance is mandatory. A previous cautery or resection of a TCC ( transurethral resection of a bladder tumour (TURBT)) again raises suspicion of recurrence. Those with a history of renal calculi may have multiple recurrent episodes through their life time. Past transurethral resection of the prostate (TURP) does not exclude the prostate as the origin of haematuria as remaining tissue may undergo neoplastic change.

Vaginal/urethral discharge STD [e.g. gonorrhoea] Pregnancies number and complications Infertility

- History of recurring UTIs or renal calculi - Previous haematuria or proteinuria - History of DM/gout - Hypertension may cause renal impairment and is a complication of renal disease - Previous renal biopsy - Childhood UTIs/VUR, childhood GU surgery (congenital anomalies, e.g ureteric aplasia

Past Medical/Surgical History

Other medical/surgical problems

Medication
Do you have any medical problems? Are you taking any medication?
Recent treatment with Rifampicin can colour the urine red similar to haematuria. Radiation to the pelvis may lead to radiation cystitis and haematuria, which still needs to be investigated. Many patients with longstanding atrial fibrillation or valvular disease may not volunteer anticoagulants as medications: Its imperative that you ask! Any anticoagulant, aspirin, plavix, warfarin can lead to haematuria, and may in fact be the only cause. Any coagulopathies should be asked about also.

Steroids/immunosuppressants NSAIDS (Analgesic nephropathy) Anticoagulant: aspirin, plavix, warfarin

Allergies Social History

Do you smoke? What type of work do/did you do?
Transition cell carcinoma has a very strong association with smoking, 4 fold increase in urothelial tumours; it is important not only to illicit current smoking habits but also previously. Work such as coal mining, dye factories, and those working with benziolene and naphthylamine are associated with a 20

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60 fold increase in development of tumours as they are renaly excreted and result in prolonged exposure of the urothelium.

Marital status/children, employment, alcohol [count units], smoking If patient has chronic renal failure ask how they are coping with illness/dialysis. If the patient is on dialysis ask about travel times and expenses, effect on quality of life, home management of polypharmacy

Family History
Is there any family history of problems with the water, or any cancers in the family?
Family history of urological malignancies is important. Also benign pathology such as renal cysts and polycystic kidney disease may direct you to the cause.

Some forms of renal disease are inherited ie polycystic kidney disease is autosomal dominant Renal stones Other relevant family history diabetes/hypertension

Complete Systems Review Important questions to be asked in history

When did you first begin noticing urinary symptoms? Have your urinary symptoms been continuous, or occasional? Have your symptoms gradually worsened over time, or did they come on suddenly? How bothersome are your symptoms? How often do you urinate during the day? How often do you need to get up at night to urinate? Do you start and stop when urinating, or feel like you have to strain to urinate? Do you have difficulty starting urination? Do you ever leak urine? If so, when? Do you have a frequent or urgent need to urinate? Do you feel you arent able to completely empty your bladder? 125

Do you ever have blood in your urine? Have you had urinary tract infections? Is there any burning when you urinate? How do you know when you have a urinary tract infection? Do you have type 2 diabetes? Do you have any problems getting and maintaining an erection (erectile dysfunction) or any other sexual problems? Do you feel pain in your bladder area? Have you ever had surgery or another procedures that involved insertion of an instrument through the tip of your penis into the urethra? Do any of you blood relatives (such as your father or brother) have a history of enlarged prostate, or prostate cancer, or kidney stones? What medication do you take, including any over the counter medications or herbal remedies? Are you on any blood thinners such as aspirin, warfarin (Coumadin) or clopidogrel (plavix)?

The Genitourinary History and examination

Presenting Complaint

Change in urinary appearance Red discolouration: - Haematuria - Haemoglobinuria (due to haemolysis) -Drugs such as Rifampicin

Note: With suspected haematuria ask about whether the patient means frank distinct blood in the urine or a general tea coloured urine, whether it is painful or painless (more sinister). Also ask if the patient has noticed if the haematuria occurs early or late in the urinary stream or if it is uniform throughout. The later in the stream the higher up the urinary tract the pathology is likely to be. Kidney/bladder tumour, Bleeding from prostate, Infection Calculi Changes in urinary volume Polyuria (over 3 L of urine per day): Can be a feature of acute renal failure due to acute tubular necrosis, diabetes mellitus, diabetes insipidus, psychogenic polydipsia Oliguria (less than 400 ml of urine per day): Due to renal failure or dehydration. Anuria (less than 50 ml of urine in 24 hours)

Urinary obstruction Common symptom in elderly men [prostatism] 126

Hesitancy - difficulty starting micturition Poor stream - cannot hit wall Post micturition dribbling Double voiding/ Incomplete emptying (needing to pass urine soon after micturition) Nocturia - an objective increase in the frequency of waking up at night to void urine Frequency urine passed more often without increase in volume Complete obstruction/Overflow incontinence Retention inability to pass urine Pain Renal angle pain due to pyelonephritis is associated with fever/rigors/dysuria [pain passing urine] Dull/continuous renal angle pain due to tumour Renal colic is severe pain radiating down to groin [renal calculus/clot]

Prostatitis [inflammation of prostate e.g. bacterial infection] Remember full pain questionnaire - onset, site, radiation, severity, character, time course, aggravating and relieving factors, associated symptoms. Incontinence Stress incontinence - when sneezing, laughing [multiparous female] Urgency - strong desire to pass urine may be followed by incontinence [Gynaecological prolapse] Overflow incontinence Spinal cord lesion, bladder will fill and then empty reflexly

Pneumaturia Passing bubbles in the urine [vesico-colic fistula e.g. crohns disease] Symptoms of renal failure Anuria failure to pass more than 50mls of urine daily 127

Oliguria < 400mls urine daily Nocturia/Polyuria inability of kidneys to concentrate urine normally Anorexia/vomiting/fatigue/hiccup Pruritis general itchiness of the skin Oedema due to fluid retention Symptome of hyperkalaemia (muscle weakness, cardiac arrhythmia) Bone pain due to renal bone disease caused by secondary hyperparathyroidism which is compensating for vitamin D deficiency caused by the renal failure. Symptoms of anaemia (Due to declining erythropoietin levels) Altered level of consciousness( drowsy/forgetful/coma), in acute renal failure Dyspnoea, due to pleural effusions/ pericardial effusions / cardiac failure

Renal failure patients must be questioned about renal replacement therapy:Dialysis:What type, how long, urinary output, weight gain between sessions, fluid restriction Haemodialysis:-

Peritoneal dialysis

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Renal transplant Ask about function of graft, rejection episodes Other renal transplants Complications of drugs such as steroids and other immunosuppressants

129

Renal failure patients must be questioned about diet:Protein, fluid and salt restriction Sexual problems in the male Lack of libido/inability to achieve or maintain an erection/trouble with ejaculation Penile discharge/STD Sexual problems in the female Frequency, regularity and duration of menses, LMP Blood loss, clots suggest menorrhagia, heavy menstrual loss Dysmenorrhoea Primary/secondary amenorrhoea Post menopausal or post coital bleeding OCP/HRT Dyspareunia Vaginal/urethral discharge STD [e.g. gonorrhoea] Pregnancies number and complications Infertility History of Presenting Complaint - History of recurring UTIs or renal calculi - Previous haematuria or proteinuria - History of DM/gout - Hypertension may cause renal impairment and is a complication of renal disease - Previous renal biopsy - Childhood UTIs/VUR, childhood GU surgery (congenital anomalies, e.g ureteric aplasia Past Medical/Surgical History

Other medical/surgical problems Medication

Prescribed and over the counter Steroids/immunosuppressants NSAIDS (Analgesic nephropathy) Allergies

To any medication Social History

Marital status/children, employment, alcohol [count units], smoking 130

If patient has chronic renal failure ask how they are coping with illness/dialysis. If the patient is on dialysis ask about travel times and expenses, effect on quality of life, home management of polypharmacy) Family History

Some forms of renal disease are inherited ie polycystic kidney disease is autosomal dominant Other relevant family history diabetes/hypertension Complete Systems Review The genitourinary examination If renal disease is suspected or known to be present then certain signs must be sought. Inspection General inspection remains crucial. Hydration dehydration can cause acute renal failure over hydration can result from intravenous infusion of fluids to correct renal failure fluid overload can result from renal failure [pedal oedema/pulmonary oedema]

Hyperventilation underlying metabolic acidosis Hiccupping can be a sign of terminal uraemia Sallow complexion dirty brown appearance in chronic renal failure [impaired excretion of urinary pigment] Anaemia of chronic disease/poor nutrition/erythropoietin deficiency/haemolysis/bone marrow depression Terminal renal failure Level of consciousness -drowsy/coma - due to nitrogen/toxin retention Muscle twitching/tetany/epileptic seizures due to low serum calcium level and to nitrogen retention The hands Leuconychia white transverse opaque lines in hypoalbuminaemia [nephrotic syndrome]

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Terrys lines/ half and half nails distal brown arc occurring in 20% of renal failure patients

Anaemia palmar crease pallor Asterixis may be present in terminal chronic renal failure [Dorsiflex the wrists with the arms outstretched and spread out the fingers, a flapping tremor may occur as in liver failure]

The arms
2) Arteriovenous fistula used for haemodialysis [Make sure this is palpated for thrill and auscultated for bruit to assess function of the fistula]

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Bruising nitrogen retention causes abnormal platelet aggregation Skin pigmentation failure to excrete urinary pigments Scratch marks pruritis due to uraemia and calcium deposition Blood pressure hypertension may be the cause of renal disease or a complication Peripheral neuropathy/ myopathy

The face
Anaemia conjunctival pallor Jaundice nitrogen retention can cause haemolysis Uraemic fetor due to breakdown of urea to ammonia in the saliva Mucosal ulcers underlying connective tissue disease i.e. SLE Gingival hyperplasia due to immunosuppressant therapy [ciclosporin] Rash - underlying connective tissue disease i.e. SLE

The neck
Central line for dialysis Jugular venous pressure to assess hydration [elevated JVP in fluid overload/CCF] Carotid artery bruits there may be generalised atherosclerosis [renal artery stenosis] 133

The chest
Cardiac - CCF due to fluid retention in chronic renal failure - Hypertension sodium and water retention and excess renin production - Pericarditis due to retained metabolic toxins and can cause a pericardial rub Lungs - Pulmonary oedema [volume overload] - Infection due to immunosuppression in renal transplant patients

The abdominal examination

As done previously but particular attention must be paid to the following; Inspection Nephrectomy scar - look at loin and lumbar regions Nephrectomy tube - draining wound

Renal transplant scar right or left iliac fossa Transplanted kidney bulge under scar in RIF/LIF Catheter for peritoneal dialysis Ileostomy connection from bladder to abdominal wall, to allow drainage of urine directly from bladder to stoma bag. Small scars from catheter placement near midline or the lower abdomen Distension polycystic kidneys/ascites [nephrotic syndrome]/dialysis fluid Palpation

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The kidneys bimanual method

To palpate the right kidney the examiners left hand is placed underneath the back. The left fingers flex at the metacarpophalangeal joints in the area of the renal angle. The examiners right hand is placed over the RUQ. The kidneys are felt by balloting, the renal angle is pressed by the flexing fingers of the posterior hand and the anterior hand is used to palpate the kidney. To palpate the left kidney the left hand is stretched over the abdomen and placed posteriorly over the renal angle. The right hand feels for the left kidney anteriorly. Deep palpation in the renal angle can elicit tenderness suggesting pyelonephritis. To distinguish a large left kidney from splenomegaly: 7. Spleen has no palpable upper border 8. Spleen has a notch 9. Spleens moves inferomedially on inspiration, kidney moves inferiorly 10. Spleen is not ballottable unless gross ascites present 11. Percussion note is dull over the spleen resonant over kidneys 12. Friction rub may be heard over the spleen but never over the kidney as it is too posterior Unilateral renal mass Renal cell carcinoma Hydronephrosis Polycystic kidneys [asymmetrical enlargement] Acute pyelonephritis Abscess

Bilateral renal mass Polycystic kidneys Bilateral hydronephrosis 135

Bilateral renal carcinoma Early diabetic nephropathy Infiltrative disease i.e. lymphoma/amyloid

Transplanted kidney palpable in LIF or RIF Hepatomegaly - from hepatic cysts may be present in PCKD Bladder empty bladder is impalpable. If there is urinary retention the full bladder may be palpable above the pubic symphysis. It is typically regular, smooth, firm and oval shaped. It may reach as high as the umbilicus. It must be differentiated from any swelling arising from the pelvis. The bladder can be emptied by insertion of a urinary catheter. Percussion Ascites shifting dullness [nephrotic syndrome] Enlarged bladder Auscultation Renal bruits best heard just above the umbilicus about 2 cms to the left or right of the midline. Listen with the diaphragm of the stethoscope. Its presence suggests renal artery stenosis due to atherosclerosis or fibromuscular dysplasia. The absence of hypertension makes a diagnosis of renal artery stenosis less likely. Rectal and pelvic examination Examination of external genitalia for evidence of STI Prostatomegaly in males and Frozen pelvis from cervical cancer in females: These may cause urinary tract obstruction and renal failure The back Sacral oedema fluid overload/CCF Bony tenderness strike the vertebral column gently and may elicit tenderness. This may be due to renal osteodystrophy from osteomalacia or secondary hyperparathyroidism The legs Oedema 136

Pigmentation Scratch marks Gouty tophi in feet Peripheral neuropathy The fundi Diabetic changes Hypertensive changes

The Neurological History

A thorough neurologic history allows the clinician to define the patient's problem and, along with the result of physical examination, assists in making a diagnosis. Solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. The history of the presenting illness or chief complaint should include the following information:

Symptom onset: Acute onset symptoms (minutes to hours) suggest vascular or convulsive problems and may be preceded by an aura. Subacute onset (hours to days) occurs with inflammatory pathology such as that associated with meningitis, Guillian-Barre syndrome. Chronic onset (weeks to months) may indicate malignant aetiology; and onset in the order of months to years is associated with degenerative disease. Duration Course of the condition (eg, static, progressive, or relapsing and remitting) Associated symptoms, such as pain, headache, nausea, vomiting, weakness, and seizures Symptoms may be localized or diffuse and a logical assessment of the nervous system level of pathology can be made on this basis. Is the pathology occurring at the level of the cerebral hemispheres, posterior fossa, spinal cord, peripheral nervous system?

Important miscellaneous factors of the history include the following:

Results of previous attempts to diagnose the condition Any previous therapeutic intervention and the response to those treatments

A complete history often defines the clinical problem and allows the examiner to proceed with a complete but focused neurologic examination

Presenting symptoms
1) Headache Obtain details on all 10 characteristics of pain (outlined below). 137

The typical symptoms of the commonest causes of headaches are outlined. These are the commonest features, but every patient is different.

Tension Site Generalised neck(occasional ) Ache subjective Gradual variable Hours stress/posture rest/analgesia

Migraine Unilateral/ near eyes

Cluster Over one eye

SAH Local,then generalised

Radiations Character Severity Onset Periodicity Duration Aggravating Relieving

variable sharp or ache subjective gradual variable hours light rest/analgesi a Nausea/aura vomiting

forehead/cheek ache subjective gradual recurring bouts intermittent pollen/allergens decongestant Lacrimation rhinorrhoea

Neck thunderclap worst ever sudden persistent

Associations
Other causes of headache Meninges meningitis Intra- cranial

neck stiffness

Trauma Tumour / abscess / congenital malformation

(Any space-occupying lesion, which can cause raised intra-cranial pressure)

Systemic Asociated with infection, connective tissue disease, etc Vascular Acute cerebral artery/vein thrombosis Temporal arteritis Carotid aneurysm 138

Sinuses, middle or inner ear 2) Faints Syncope is defined as a transient loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness. Dizziness (faintness) is the symptom which precedes syncope. Causes of syncope

Cardiac syncope:

Vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction

Noncardiac syncope: Vasovagal syncope is the most common type in young adults but can occur at any age. It usually occurs in a standing position and is precipitated by fear, emotional stress, or pain (eg, after a needlestick). Autonomic symptoms are predominant. Classically, nausea, diaphoresis, blurred or faded vision, epigastric discomfort, and light-headedness precede syncope by a few minutes. Syncope is thought to result in decreased peripheral vascular resistance. It is not life threatening and occurs sporadically. Dehydration and decreased intravascular volume contribute to orthostasis. Orthostatic syncope describes a causative relationship between orthostatic hypotension and syncope. Situational syncope is essentially a reproducible vasovagal syncope with a known precipitant. Micturition, defaecation, and carotid sinus syncope are types of situational syncope. These stimuli result in autonomic reflexes, ultimately leading to transient cerebral hypotension. Neurologic syncope may have prodromal symptoms such as vertigo, dysarthria, dysphagia, diplopia, and ataxia. Syncope results from preexisting bilateral vertebrobasilar insufficiency with some superimposed acute process. Consider a transient ischemic attack as an alternative diagnosis.

A detailed account of the event must be obtained from the patient. The account must include the circumstances surrounding the episode: the precipitant factors, the patient's activity involved in prior to the event and the patient's position when it occurred.

Physicians should specifically inquire to identify symptoms, such as chest pain, dyspnoea, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event. 139

Patients should be asked to estimate the duration of their loss of consciousness. Syncope is associated with patient estimates ranging from seconds up to 1 minute in most cases. To discriminate from seizures, patients should also be asked if they remember being confused about their surroundings after the event or whether they have oral trauma [tongue biting] or incontinence. A detailed account of the event must also be obtained from any available witnesses. Witnesses can aid the clinician in differentiating among syncope, altered mental status, and seizure.

3) Fits Seizure: a sudden change in behaviour that is the consequence of brain dysfunction. Epileptic seizures: sudden change in behaviour due to abnormal electrical activity in the brain (cerebral cortex). Electrical activity can be measured using an EEG. Non epileptic seizures: sudden change in behaviour, without abnormal electrical activity in the brain. Characteristics of seizure Altered/loss of consciousness Involuntary movements jerking Incontinence Tongue-biting Preceded by an aura (abnormal visual/auditory/olfactory sensation) Weakness following fit (Todds paralysis)

Types of Epileptic Seizures Simple no loss of consciousness Complex loss of consciousness Generalised abnormal activity widespread in brain Partial abnormal activity in focal part of brain

Causes of Epileptic Seizures (damage to CNS) Brain injury( trauma/haemorrhage) Stroke Intracranial infection Congenital malformation Tumour

Causes of Non Epileptic Seizures (These are generalized seizures) Metabolic hypo/hyperglycaemia, hypothyroidism, hypercalcaemia, hyponatraemia. 140

Hypoxia infection, blood loss, cardiac dysfunction Renal failure/ Liver failure Drugs/medications alcohol, sedatives

4) Dizziness/vertigo Vertigo is an illusion of movement, caused by disease of the inner ear, the eighth cranial nerve, or the central connections of the eighth cranial nerve. In true vertigo, there is a sensation of rotation Associations: Nausea, vomiting, unsteadiness, pallor, weakness. Causes of Vertigo Inner Ear Causes Otitis interna Acute labyrinthitis CN 8 Causes Acoustic neuroma (tumour of CN 8) Central Connection Causes ( disease in the pons, origin of CN 8) Tumour Vascular disease Multiple Sclerosis (demyelination) 5) Deafness Impaired hearing can be due to damage/ obstruction of the ear canal, or due to damage to the nerve supplying the ear. (CN 8, vestibulocochlear nerve) Ear Canal Causes Middle ear infection ( otitis media) Wax (cerumen)

Nerve Causes Noise exposure Trauma (skull fracture) Drugs (alcohol) Congenital infections (rubella)

6) Visual disturbances 141

Diplopia double vision

Weakness of intra-ocular muscles or damage to nerves/blood supply of intra-ocular muscles Amblyopia blurred vision Photophobia light intolerance (migraine/ meningitis) Visual field loss These patterns are discussed in the clinical tutorials Visual loss a) Acute visual loss damage to the eye/ nerve supply/blood supply/brain Stroke Haemorrhage Multiple Sclerosis Retinal vascular occlusion b) Chronic progressive visual loss damage to the eye/nerve supply/blood supply/brain 7) Gait Many neurological conditions can impair walking. Gait can be abnormal due to disease of brain/ spinal cord (CNS) nerves to the leg muscles (PNS) leg muscles joints systemic disease Cataracts (ageing/DM/glaucoma/steroids) Diabetes Mellitus (damages blood supply and nerves and causes cataracts) Ageing (macular degeneration)

Types of impaired gait Cerebellar disease unsteady, reeling Stroke hemiplegic gait , dragging of one side Parkinsons disease- small steps, shuffling, slow

8) Disturbed sensation 142

With regards to temperature sensation, patients can be asked whether they have any problems detecting water temperature. Failure to notice cuts, wounds after injury due to lack of sensation. For fine touch discrimination, patients can be asked whether they have problems pulling the correct coin or other objects out of their pockets. Position sense can be explored by asking whether patients have problems knowing where their feet are on the car accelerator and brake pedals. One should also inquire about pins and needles which can result from nerve entrapement or peripheral neuropathy Causes of Sensory Neuropathy include Diabetes Mellitus Chronic renal failure Vitamin B12 deficiency Hereditary syndromes

9) Weakness Weakness may be local one arm or leg, or may be generalised. Enquire as to whether it is constant or intermittent. Causes Central Nervous System Following CVA Cerebral tumour Spinal cord injury Peripheral nervous system DM Toxins Anterior horn cell Motor Neuron Disease Neuromuscular junction Myasthenia gravis Muscle Alcohol Medications (steroids) Connective tissue diseases (SLE) 143

Endocrine (thyroid disease, Cushings, acromegaly) 10) Tremor and Involuntary movements Distinguish between resting (visible at rest), postural (present throughout movement) and intention (increases toward target). Causes of Tremor include Parkinsons disease Cerebellar disease Hyperthyroidism Anxiety Medications (inhalers, e.g. Ventolin)

11) Speech Dysarthria difficulty with articulation Causes of dysarthria Cerebellar disease ( slurred speech) Local oral disease mouth ulcers, cleft palate Dysphasia difficulty with communication Caused by disease of the dominant cortical hemisphere Receptive dysphasia: where the patient cannot understand the spoken or written word. Speech is fluent but disorganised. Ask patient to follow commands, unable to do so. Expressive dysphasia: the patient understands but cannot answer appropriately. Ask to name objects, repeat words. Nominal dysphasia: patient cannot name objects. Point to your pen, watch and ask patient to name them.

Other Higher Centre Functions include: Frontal lobe personality Temporal lobe memory, speech Parietal lobe performing tasks, speech Occipital lobe vision

Past Medical and Surgical history

Start with the OPEN ENDED enquiry first. Have you ever been admitted to hospital for any reason? is a good way to start. Follow this with Do you have any medical 144

conditions or health problems of any kind? and Have you ever had any operations no matter how minor before? In this part of the history it is helpful to ask the open ended question in a number of ways because what you and the patient consider a past medical history does not always coincide. Then you can focus on specifics. If the answer is yes to any of these, ask what the treatment has been, any changes in treatment and how successful any treatment has been. History of trauma / injury History of meningitis / encephalitis History of epilepsy / convulsions History of Diabetes If no, ask whether blood sugars have actually been checked History of high cholesterol Also ask if this has been checked specifically. History of hypertension Again, ask if it has been checked recently History of heart disease or peripheral vascular disease History of Atrial fibrillation or any other arrhythmia History of rheumatic fever or endocarditis

Medications/Allergies
Are you on any medications? How about over the counter medications Any herbal remedies?

Enquire about allergies and whether any medication has made the patient unwell before. Ask what the patient means by allergy? Relevant specifics: Anticoagulants and / or anti platelet agents Anti convulsants Antihypertensive agents Treatment for high cholesterol Oral contraceptive pill

Social History
Home circumstances: Including who is with the patient at home and the general health of that person, home modifications and home layout. Occupation Smoking (how much and how long?). Alcohol intake (Long term alcohol use is associated with dementia, neuropathy, cerebellar degeneration, encephalopathy) 145

Family History
Again, OPEN ENDED enquiry first. Are there any medical conditions that run in the family? Then more specific if suitable (i.e. not in an 85 year old patient): Are your parents still alive? How is their health? or What was the cause of their passing? The same for siblings Then Any relatives with a neurological condition? Family history of heart disease, stroke, hypertension, diabetes, high cholesterol, epilepsy

Systems review
Start with Is there anything else you would like to add or Do you have any other symptoms to report Then ask about general wellbeing, weight and appetite. Then 4-5 questions about each body system in quick point form.

WARD TUTORIAL Cranial nerve examination The aim of this tutorial is for students to begin examination of the cranial nerves. A student should volunteer for demonstration and then students should work in pairs Position the patient sitting over the edge of the bed Look at the head, face and neck

Inspection
Craniotomy scars Ptosis drooping of the upper eyelid Proptosis abnormal protrusion of the eyeball

The first [Olfactory] Nerve

Purely sensory nerve This nerve is not tested routinely, ask patient have they any difficuty with their sense of smell. If the answer is no, move to the second cranial nerve. If patient c/o loss of smell [anosmia] test each nostril separately with bottles containing essences of familiar smells such as coffee.

The second [Optic] Nerve

Purely sensory nerve which begins in the retina Visual acuity is tested with the patient wearing his or her glasses 146

Ask patient do they have any difficulty with their vision Can you see the clock on the wall? Can you read the newspaper? Each eye should be tested separately A portable Snellens chart will enable you to perform a more formal test A patient who is having visual problems should be asked to count fingers held up in front of each eye in turn, and if this is not possible then perception of hand movement should be assessed. Failing this light perception only may be present. Visual fields are assessed by positioning yourself in visual confrontation about a metre away. Always remove the patients glasses. Test the visual fields of your patient against your own. Ask patient to cover his right eye with his right hand and close your left eye Ask patient to keep looking at my eye Test his left temporal vision against your right temporal vision by moving your wagging finger from the periphery towards the centre Tell me when you see my finger move The temporal field should be tested in the horizontal plane and in the upper and lower temporal quadrants. Change hands and repeat on the nasal side Any areas of field defect are mapped out The visual fields of his right eye are assessed in the same way. Bitemporal hemianopia: optic chiasm lesion, pituitory tumour Unilateral field loss: optic nerve lesion, tumour/vascular Homonymous hemianopia: optic tract to occipital cortex, vascular/tumour The blind spot there is a small area close to the centre of the visual fields where there is no vision. This is the area where the optic disc is seen on fundoscopy and is the point where the optic nerve joins the retina. The blind spot enlarges with papilloedema eg raised intracranial pressure with brain tumour Central scotoma or loss of central macular vision is tested for with a redheaded hat pin. As before move the red-headed pin from the temporal periphery through the central field to the nasal periphery, asking the patient can you see the head of the pin? Eg demyelination of the optic nerve in multiple sclerosis can cause loss of central vision Colour vision Tests of colour vision are not carried out routinely They may reveal subtle defects of the retina or optic nerve Ishihara plates are used. Checking patients eyes separately plates made up of coloured dots containing numerical shapes are presented to patient who is asked to discern the numbers shown in each pattern. Fundoscopy Use the right eye to look in patients right eye and vice versa Look first at the cornea, iris and lens. Then look at the fundus. Search first for the optic disc then look at the four quadrants of the retina

147

The Third [Oculomotor], Fourth [Trochlear] and Sixth [Abducens]

The pupils The size of the pupils depends on a balance of parasympathetic and sympathetic innervation. The parasympathetic innervation of the eye is supplied by the EdingerWestphal nucleus of the third nerve [stimulation causes pupillary constriction] The pupillary reflexes depend on the optic nerve for their afferent limb Ask the patient to look at an object at an intermediate distance Examine the pupils for size, shape, equality and regularity Light reflex: with a pocket torch shine the light from the side [so the patient does not focus on the light and accomadate] into one of the pupils to assess its reaction to light Normally the pupil into which the light is shone constricts briskly this is the direct light reflex Simultaneously the other pupil constricts in the same way, this is the consensual light reflex Repeat this procedure on the other side Afferent pupillary defect/Marcus Gunn pupillary sign: Move the torch from pupil to pupil If an eye has optic atrophy or severely reduced visual acuity from another cause the affected pupil will dilate paradoxically after a short time This occurs because afferent impulses are reduced so the light reflex is markedly reduced in the eye with decreased acuity Accomodation: Ask the patient to look into the distance and then to focus on your finger held near the patients nose There is normally constriction of both pupils, the accomodation response Absent light reflex with an intact accomodation reflex occurs in Argyll Robertson pupil in syphilus affecting the nervous system Eye movements Assess for eye movement, diplopia [double vision] and nystagmus Look at my finger; follow it with your eyes Ask the patient to look laterally left and right, continue moving the finger to complete H pattern. The third nerve supplies all the ocular muscles except; Superior oblique fourth nerve Lateral rectus sixth nerve The lateral rectus and medial rectus abduct and adduct the eyes When the eye is abducted the elevator is the superior rectus [third nerve] while the depressor is the inferior rectus [third nerve]. 148

When the eye is adducted the elevator is the inferior oblique [third nerve] while the depressor is the superior oblique [fourth nerve] Third nerve also supplies Levator palpebrae superioris Tell the patient to inform you if they see double images [diplopia] Diplopia is an early sign of ocular muscle weakness The false image is usually paler, less distinct and more peripheral than the real one Features of a third nerve lesion 1. Complete ptosis 2. Eye down and out 3. Dilated pupil which is not responsive to light and accomadation Features of fourth nerve lesion Usually associated with a third nerve palsy Double vision going down stairs Ask patient to turn the eye in and then to look down Superior oblique paralysis Features of sixth nerve lesion Failure of lateral movement Nystagmus Ask patient to follow your finger to each side The direction of nystagnus is defined as that of the fast [correcting] movement Vestibular lesion nystagmus away from the side of the lesion Cerebellar lesion nystagmus to the side of the lesion Internuclear ophthalmoplegia abducting eye has greater nystagmus than the adducting eye. There is dissociation of conjugate eye movements. It suggests MS with a lesion in the medial longitudinal bundle WARD TUTORIAL Cranial nerve examination The aim of this tutorial is for students to complete examination of the cranial nerves. A student should be asked to volunteer and students should work in pairs.

The fifth [trigeminal] nerve

This nerve contains both sensory and motor fibres There are 3 sensory divisions 149

Ophthalmic: supplies forehead, cornea and conjunctiva Maxillary: supplies the middle of the face Mandibular: supplies the lower jaw

Facial sensation
Test in the three divisions of the nerve comparing each side with the other FOREHEAD - Ophthalmic MAXILLA - Maxillary LOWER JAW Mandibular Test for pain using sharp object. Ask patient does it feel sharp or dull. Test for light touch using cotton wool The patient should be instructed to say yes each time the touch of the cotton wool is felt. Do not stroke the skin touch it.

Motor division
Inspect for wasting of the temporal and masseter muscles Ask patient to clench their teeth and palpate for contraction of the masseter muscles Ask patient to open their mouth and hold it open while the examiner attempts to force it shut [pterygoid muscles]. A unilateral weakness of the motor division causes the jaw to deviate towards the weak side. If weakness is suspected patients should be asked to move the jaw laterally against resistance. The jaw can be moved towards the affected muscle but cannot move towards the normal side.

Jaw jerk
The afferent and efferent pathways are supplied by the fifth nerve The patient lets his mouth fall open slightly The examiners finger is placed on the jaw The finger is tapped lightly with a tendon hammer The reflex response comprises brisk closure of the jaw It is often not visible and can be difficult to determine if it is present

Corneal reflex
The afferent part of the reflex arc is the first division [ophthalmic nerve] of the fifth nerve The efferent arc is supplied by facial nerve Each fifth nerve communicates with both seventh nerves and therefore both eyes close when each cornea is stimulated Lightly touch the cornea with a wisp of cottonwool Reflex blinking of both eyes is a normal response

The seventh [facial] nerve

Supplies: The muscles of facial expression 150

Stapedius muscle Chorda tympani contains taste fibres from anterior two-thirds of the tongue Inspection: for facial asymmetry Unilateral drooping of the corner of the mouth Smoothing of the wrinkled forehead Smoothing of the nasolabial fold Muscle power Ask patient to look up and wrinkle his forehead Feel for muscle strength by pushing down on forehead This movement is preserved on the side of an upper motor neurone lesion [a lesion which occurs above the level of the brainstem nucleus], because of bilateral cortical representation of these muscles The remaining muscles of facial expression are usually affected on the side of an UMN lesion. In a LMN lesion all muscles of facial expression are affected on the side of the lesion. Ask the patient to shut the eyes tightly Observe and try to force open each eye Ask the patient blow out cheeks Ask the patient to show their teeth Compare the nasolabial grooves which are smooth on the weak side If a lower motor neuron lesion is detected [weakness on one side of face], check for ear and palatal vesicles of herpes zoster of the geniculate ganglion the Ramsay Hunt syndrome Examining for taste of the anterior two-thirds of the tongue is not usually required **Left upper motor neurone seventh nerve lesion leads to drooping of the corner of the mouth, flattened nasolabial fold, and sparing of the forehead on the left side**

The Eighth [Vestibulocochlear] nerve

There are two components: Vestibular containing afferent fibres for balance Cochlear with afferent fibres for hearing Examination for hearing Ask the patient do they have any problems with their hearing Cover one of the patients ears with your hand and whisper into the other ear 151

If deafness is suspected perform Rinnes test and Webers test Rinnes test A vibrating tuning fork is placed on the mastoid process behind the ear. When the sound is no longer heard it is placed in line with the external meatus. Normally the sound is audible at the external meatus. With nerve deafness the note is audible at the external meatus, as air and bone conduction are reduced equally, so that air conduction is better as is normal. This is termed Rinne-positive. With conduction [middle ear] deafness no note is audible at the external meatus. This is termed Rinne-negative. Webers test A vibrating tuning fork is placed on the centre of the forehead. Normally the sound is heard in the centre of the forehead. With nerve deafness the sound is transmitted to the normal ear. With conduction deafness the sound is heard louder in the abnormal ear. Audiometry Patients with defective hearing should be referred for audiometry. This measures the degree of hearing loss at different sound frequencies. Examination of vestibular function This cannot effectively be evaluated at the bedside.

The ninth [Glossopharyngeal] and Tenth [Vagus] nerves

Get the patient to open their mouth and inspect the palate with a torch. Note any displacement of the uvula. Ask the patient to say Ah. If the uvula is drawn to one side this indicates a unilateral tenth nerve palsy. The uvula is pulled towards the normal side. Now test gently for the gag reflex Ninth is the sensory component Tenth is the motor component Touch the back of the pharynx on each side with a spatula. Ask the patient if the touch of the spatula is felt each time. Normally there is reflex contraction of the soft palate. The ninth nerve supplies taste from the posterior two-thirds of the tongue this is not routinely tested for.

The eleventh [Accessory] nerve

It supplies motor fibres to the trapezius and sternomastoid muscles 152

Ask the patient to shrug their shoulders and feel the bulk of the trapezius muscles and attempt to push the shoulders down. Ask the patient to turn their head against resistance and feel the bulk of the sternomastoids. Feel for the sternomastoid on the side opposite to the turned head. There will be weakness on turning the head away from the side of a muscle whose strength is impaired.

The twelth [Hypoglossal] nerve

It is the motor nerve for the tongue Inspect for wasting and fasciculations. These indicate a lower motor neurone lesion Ask the patient to stick out their tongue. It will deviate towards the weaker side if there is a unilateral lower motor neuron lesion. Having completed the cranial nerve examination complete a full examination from 1-12 getting all students to participate Inspection: take a good general look at the patient; in particular the face. [1] Do you have any difficulty with your sense of smell? [2] Visual acuity Do you have any difficulty with your vision? Can you see the clock on the wall? Can you tell me what time it is? [Glasses should be worn and test each eye seperately] Can you read this line of your newspaper/book? Check visual fields and check for central scotoma with red-headed hat pin Fundoscopy [3, 4, 6] Check direct and consensual light reflex and accomadation Eye movements Nystagmus [5] Facial sensation Masseter, temporal and pterygoid muscles Corneal reflex Jaw jerk [7] Facial movement [8] Hearing/Rinnes/Webers test 153

[9, 10] Inspect/Check gag [11] Trapezius and sternomastoid muscles [12] Tongue

Gait, cerebellar function and MMSE

At the end of this session students should be able to examine gait, examine cerebellar function and complete MMSE

Gait
Ability to stand and walk normally is dependent on input from several systems, including: visual, vestibular, cerebellar, motor, and sensory. A lot of information about neurological (and other) disorders can be gained from simply watching a patient stand and then walk. Ask the patient to stand. If they are very weak or unsteady, make sure that you are in a position and capable of catching and supporting them if they fall. Enlist the help of a colleague if you need an extra pair of hands. If you are still unsure as to whether standing/walking can be performed safely, skip this area of testing. No test result is worth a broken hip! Have the patient stand in one place. This is a test of balance, incorporating input from the visual, cerebellar, proprioceptive, and vestibular systems. If they are able to do this, have them close their eyes, removing visual input. This is referred to as the Romberg test. Loss of balance suggests impaired proprioception, as it is this pathway which should provide input that allows the patient to remain stable with eyes closed. Romberg test is positive when unsteadiness increases with eye closure. Ask the patient to walk across the room, turn around quickly, and come back towards you. Pay particular attention to: a. Balance: Do they veer off to one side or the other as might occur with cerebellar dysfunction? Disorders affecting the left cerebellar hemisphere (as might occur with a stroke or tumor) will cause patients to fall to the left. Right sided lesions will cause the patient to fall to the right. Diffuse disease affecting both cerebellar hemispheres will cause a generalized loss of balance. b. Rate of walking: Do they start off slow and then accelerate, perhaps losing control of their balance or speed (e.g. as might occur with Parkinsons disease)? Are they simply slow moving secondary to pain/limited range of motion in their joints, as might occur with degenerative joint disease? c. How do they hold their arms and legs? Is there loss of movement and evidence of contractures as might occur after a stroke? 154

Heel to Toe Walking: Ask the patient to walk in a straight line, putting the heel of one foot directly in front of the toe of the other. Difficulty with this can be a sign of a midline cerebellar lesion. This may be difficult for older patients (due to the frequent coexistence of other medical conditions) even in the absence of neurological disease. Ask the patient to then walk on the toes [an S1 lesion will make this impossible] and then walk on the heels [an L4 or L5 lesion causing footdrop will make this impossible]. Test for proximal myopathy by asking the patient to squat and then stand up, or sit in a low chair and then stand. Gait disorders Hemiplegia - The foot is plantar flexed and the leg is swung in a lateral arc. Spastic paraparesis Scissors gait Parkinsons disease Hesitation, shuffling, freezing Cerebellar Wide based; the patient staggers towards the affected side Footdrop High stepping gait Proximal myopathy Waddling gait

The cerebellar examination

Causes of cerebellar disease Alcohol: Characteristically spares the upper limbs Unilateral cerebellar signs: Space occupying lesion (Tumour, abscess) Ischaemia (Vertebrobasilar disease) MS Trauma

Bilateral cerebellar signs: Drugs (Phenytoin) Alcohol Friedreichs ataxia Hypothyroidism Paraneoplastic syndrome MS Large space occupying lesion

Midline

155

 Paraneoplastic lesion Midline tumour Examination for cerebellar signs The cerebellum provides an important feedback loop for coordination of muscle activity by integrating the functions of the cortex, basal ganglia, vestibular apparatus, and spinal cord. Midline cerebellar dysfunction results in ataxia of gait with abnormal heel-toe walking and difficulty in maintenance of upright posture. Cerebellar hemispheric lesions result in additional signs outlined below. General inspection Patients level of consciousness Abnormal posture or gait Asymmetry (limbs, face) Involuntary movement Scars Skin (Rash Vasculitis, neurofibromas, caf au lait spots) Hearing aid Walking aid

Head and neck Check for nystagmus usually jerky horizontal nystagmus This occurs in the direction of the cerebellar lesion (toward the lesion). Assess speech for cerebellar dysarthria (scanning speech)

Keep in mind that dysarthria is not a disorder of speech content or language (dysphasia dominant hemispheric deficit) but difficulty with speech articulation. Dysarthria is usually a sign of diffuse involvement of the cerebellum. Cerebellar dysarthria is jerky, slurring, explosive and loud with irregular separation of syllables. Test for dysarthria by asking the patient to say British constitution or west register street. Upper limbs - Upper limb drift: When the arms are extended they drift upwards due to hypotonia. - Upper limb rebound: The patient is asked to raise the arms quickly from their sides and stop suddenly mid motion. Inability to stop is called rebound and it is caused by loss of coordination between agonist and antagonist muscular action 156

- Test tone Finger to nose testing: a. With the patient seated, position your index finger at a point in space in front of the patient. b. Instruct the patient to move their index finger between your finger and their nose. c. Reposition your finger after each touch. d. Then test the other hand. The patient should be able to do this at a reasonable rate of speed, trace a straight path, and hit the end points accurately

Interpretation: You need to look for the following which are signs of ipsilateral cerebellar disease: Past-pointing: Overshooting the target (the examiners finger) Intention tremor as the patients finger approaches the examiners Rapid Alternating finger Movements: a. Ask the patient to touch the tips of each finger to the thumb of the same hand. b. Test both hands. Interpretation: The movement should be fluid and accurate. Inability to do this, known as dysdiadochokinesis, may be indicative of cerebellar disease ipsilaterally. Rapid Alternating Hand Movements: a. Direct the patient to touch first the palm and then the dorsal side of one hand repeatedly against the palm of the other hand. b. Then test the other hand. Interpretation: The movement should be performed with speed and accuracy. Inability to do this, known as dysdiadochokinesis, may be indicative of cerebellar disease ipsilaterally.

157

Lower limbs Test tone Heel to Shin Testing: a. Direct the patient to move the heel of one foot up and down along the top of the other shin. b. Then test the other foot.

Interpretation: The movement should trace a straight line along the top of the shin and be done with reasonable speed. Failure to do this indicates loss of lower limb coordination and suggests ipsilateral cerebellar disease. Ask the patient to lift the big toe up to touch the examiners finger. Look for intention tremor and past pointing

The cerebellar gait and station When walking the patient staggers toward the side of the cerebellar lesion if the lesion is unilateral. These patients preferentially adopt a wide spaced gait to avoid falling to one side. Difficulty with heel to toe walking is a sign of balance loss and suggests a midline cerebellar lesion. The station is the ability to stand still upright with the feet pushed in together. Cerebellar disease is suggested if the patient is unable to do this with the eyes open or closed. Loss of this ability only on closing the eyes suggests a proprioceptive deficit. Truncal ataxia is a station abnormality characterized by an inability to maintain upright position with a tendency to fall backwards. It is due to a midline cerebellar lesion. Students must realise that other organ system problems can affect performance of any of these tests. If, for example, the patient is visually impaired, they may not be able to see the target during finger to nose pointing. Alternatively, weakness due to a primary muscle disorder might limit the patients ability to move a limb in the fashion required for some of the above testing. Thus, other medical and neurological conditions must be taken into account when interpreting cerebellar test results. 158

Dementia
Definition Evidence from the history and mental status examination that indicates major impairment in learning and memory as well as at least one of the following: - Impairment in handling complex tasks - Impairment in reasoning ability - Impaired spatial ability and orientation - Impaired language The cognitive symptoms must significantly interfere with the individual's work performance, usual social activities, or relationships with other people This must represent a significant decline from a previous level of functioning The disturbances are of insidious onset and are progressive, based on evidence from the history or serial mental-status examinations The disturbances are not occurring exclusively during the course of delirium The disturbances are not better accounted for by a major psychiatric diagnosis The disturbances are not better accounted for by a systemic disease or another brain disease

Diagnosing Dementia Patients and close family/friends are often uncertain about the onset of symptoms since the appearance of dementia is insidious. Useful questions for the patient and family/friends are, "When did you first notice the memory loss?" and "How has the memory loss progressed since then?" The physician can ask when the patient stopped driving or managing finances. Spouses, relatives, and friends take care of people with dementia. As symptoms progress care of patients in the home becomes more difficult and 24 hour care in a nursing home may be necessary. Students must be aware of the impact such a diagnosis has on family and friends.

Mental Status Examination

Level of alertness

No special testing is required to determine the level of alertness. While taking the history and examining the patient, observe whether the patient is alert, attentive, sleepy, or unresponsive. orientation Person what is your name? Place - where are you/do you know where you are? Time what day/date/month/year is it? Delirium: acute and reversible confusional state [infection in the elderly] 159

Dementia: chronic and irreversible confusional state [Alzheimers disease] Language 1) Fluency No special testing is required to assess fluency. Assess whether the patient's phrases and sentences are of normal length during conversation, are spoken effortlessly and at a normal rate, and have normal grammatical structure. Fluency is independent of content; speech can be completely fluent and still be incomprehensible. 2) Comprehension Comprehension is often adequately assessed through the routine history and physical but can be tested explicitly. Give the patient progressively more complex commands, such as one step (eg, "Touch your nose."), two steps (e.g. "Touch your nose and then stick out your tongue"), and three steps (e.g. "Touch your nose, then stick out your tongue and then raise your right foot"). Commands that require a body part to cross the midline (e.g. "Touch your right ear with your left thumb") are more complex than those that do not. Increasingly complex grammatical structures can also be used (e.g. "Touch the coin with the pencil"; "With the comb, touch the coin"). Ask the patient progressively more complex questions (e.g. "Does a stone sink in water?" "Do you put on your shoes before your stockings?"). 3) Repetition Ask the patient to repeat phrases or sentences of progressively greater length and complexity (e.g. "It is cold outside"; "We all went over there together"; "The lawyer's closing argument convinced the jury"). 4) Naming Observe whether the patient frequently pauses and struggles to think of words during routine conversation. Test naming explicitly by asking the patient to name items as you point to them (e.g., shirt, shoe, phone, and collar). Less common objects are generally harder to name; parts of an object are harder to name than the entire object. 5) Reading Ask the patient to follow a written command. This can be one of the same commands used to test comprehension of spoken language. 6) Writing Ask the patient to write an original sentence and to write a sentence from dictation. Look for omitted or added words, or for word substitutions. Memory 1) Immediate Ask the patient to repeat a string of seven digits immediately after you complete it. Lengthen or shorten the string until you find the longest string the patient can repeat correctly. Despite its categorization as "immediate memory," this is really more appropriately considered "attention." 2) Short-term Ask the patient to memorize three unrelated words (e.g. baseball, horse, purple), distract him or her for five minutes (usually by performing other parts of the examination), then ask the patient to recall the list. Give clues if an item is missed (e.g. "One was an animal"); offer a multiple choice if this is not enough (e.g. "It was a cat, a bear, or a horse"). 160

3) Long-term Long-term memory includes both recent and remote memory. a) Assess recent memory by testing orientation to time (e.g., day, date, month, season, year), place (e.g. state, city, building), person, and by asking questions about events of the past few days or weeks, (e.g. "Who are the current candidates for president?" or, assuming an independent source is available for verification, "What did you have for breakfast this morning?"). b) Remote memory can be tested by asking about important historical events and dates. The patient can also be asked about details of personal life such as birth date, names and ages of children and grandchildren, and work history, assuming independent verification is available. Calculation

Ask some straightforward computation problems (e.g. 5 + 8; 6 x 7; 31 - 18). Construction

Ask the patient to draw a clock, including all the numbers, and to place the hands at 4:10. Ask the patient to draw a cube; for patients who have trouble doing so, draw a cube and ask them to copy it. Abstraction

Ask the patient to explain similarities, "What do an apple and an orange have in common?"; "a basketball and a grapefruit?"; "a tent and a cabin?"; "a bicycle and an airplane?" and differences "What is the difference between a radio and a television?" and "a river and a lake?"

Mini-Mental State Examination

The Mini-Mental State Exam (MMSE) is the most widely used cognitive test for dementia. The examination takes approximately seven minutes to complete. It tests a broad range of cognitive functions including orientation, recall, attention, calculation, language manipulation, and constructional praxis. A total maximal score on the MMSE is 30 points. Generally a score of less than 24 points is suggestive of dementia or delirium. The test is not sensitive for mild dementia, and scores may be influenced by age and education, as well as language, motor, and visual impairments.

161

Tutor should demonstrate to class how to complete this examination with a volunteer. Class should work in pairs to complete task. MMSE on hospital patients are usually completed by Interns

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Peripheral nervous system Lower limb

Gait Begin by testing gait if this is possible Make sure the patients legs are clearly visible. Now ask the patient to walk normally for a few metres and then to turn around quickly and walk back. Ask the patient to walk heel-to-toe [midline cerebellar lesion]. Ask the patient to walk on the toes [S1 lesion will make this impossible]. Ask the patient to walk on the heels [L4/L5 lesion causing footdrop will make this impossible]. Ask the patient to squat and then stand up [proximal myopathy]. Ask the patient to stand erect with the feet together and the eyes open. Once the patient is stable ask them to close the eyes. Compare steadiness shown with eyes open then closed. Marked unsteadiness with the eyes closed is seen with cerebellar or vestibular dysfunction. The Romberg test: a tendency to sway or fall while standing upright with the feet to-gether, the arms outstretched and the eyes closed. A positive Rombergs sign suggests loss of proprioceptive sensation.

Inspection
Inspect the legs with the patient lying in the bed and the legs and thighs entirely exposed. If a urinary catheter is present this may indicate a spinal cord lesion.

The Motor system

Tone/Power/Coordination/Reflexes

163

Inspect for muscle wasting and fasciculation

Tone
Resistance felt when a joint is moved passively. Patient must be relaxed lying on the bed. Place your hands on the right leg below the knee and rock the leg gently from side to side. The passive movements of the ankle are observed. Repeat on left side. Place your hand under the knee and flex and extend the knee joint. Feel for resistance to muscle stretch. When the patient is relaxed this should occur without resistance. Normal tone can be assessed by repeated examination of normal people. Tone may be increased [hypertonia] or decreased [hypotonia]. Now test for clonus. Ankle clonus This is sustained rhythmical contraction of the muscles when put under sudden stretch. It is due to hypertonia from an upper motor neuron lesion. Hold the leg with the knee bent and sharply dorsiflex the foot. When ankle clonus is present, recurrent ankle plantar flexion movement occurs. This may persist for as long as the examiner sustains dorsiflexion of the ankle. Patellar clonus To test for patellar clonus place your hands on the lower part of the quadriceps with the knee extended and move the patella down sharply. Sustained rhythmical contraction of the quadriceps occurs as long as the downward stretch is maintained.

Power
A measure of muscle strength Age, gender and build should be taken into account 0 Complete paralysis 1 Flicker of contraction possible 2 Movement is possible when gravity is excluded [sideways] 3 Movement is possible against gravity but not if any further resistance is added 4 Movement is possible against gravity and some resistance 6 Normal power If power is reduced decide if it is symmetrical or asymmetrical and whether it is proximal, distal or general. Hip Flexion Ask patient to lift up their straight leg. Place your hand on the leg above the knee and attempt to push the leg down saying to the patient do not let me push down your leg. 164

Extension Ask the patient to keep the leg down and not to let you pull it up. Abduction Ask the patient to abduct the leg and not to let you push it in. Adduction Ask the patient to keep the leg adducted and not to let you push it out. Knee Flexion Ask the patient to bend the knee and not to let you straighten it. Extension With the knee bent ask the patient to straighten the knee and not to let you bend it. Ankle Plantar flexion Ask the patient to push the foot down and not to let you push it up. Dorsiflexion Ask the patient to bring the foot up and not to let you push it down. Eversion With the foot in complete plantar flexion ask the patient to evert the foot against resistance. Inversion Ask the patient to invert the foot against resistance Toes Plantar flexion Ask the patient to plantar flex the big toe and not to let you push it up. Dorsiflexion Ask the patient to bring the big toe up and not to let you push it down.

Coordination
The cerebellum plays an integral role in coordinating voluntary movement. A number of tests are used to test coordination. Toe-finger test Ask the patient to raise the foot with the knee bent and touch the examiners finger with the big toe. Look for intention tremor. Heel-shin test 165

Ask the patient to place one heel on the opposite knee and to slide the heel accurately down the front of the shin to the ankle and back again at a moderate pace. Foot-tapping test Ask the patient to tap the sole of the foot quickly on the examiners hand; this movement is slow and clumsy in cerebellar disease.

Reflexes
Make sure the patient is resting comfortably Knee jerk Slide the left arm under the knees so they are slightly bent and supported. The tendon hammer is allowed to fall on to the infrapatellar tendon. Contraction of the quadriceps causes extension of the knee. If the knee jerk appears to be absent it should be tested again following a reinforcement manoeuvre. Ask the patient to interlock the fingers and then to apart hard at the moment before the hammer strikes the tendon [Jendrassik manoeuvre].

pull

Ankle jerk Have the foot in the mid-position at the ankle with the knee bent and thigh externally rotated. The hammer is allowed to fall on the Achilles tendon. The normal response is plantar flexion of the foot with contraction of the gastrocnemius muscle. Plantar reflex Use a blunt object such as a key. This is drawn slowly along the lateral border of the foot from the heel towards the little toe until a response is elicited. The normal response is flexion of the big toe at the metatarsophalangeal jointThe extensor response is abnormal [Babinski response] and indicates an upper motor neurone lesion. The reflexes can be recorded as follows: 0 Absent reflexes + Reduced reflexes ++ Normal reflexes +++ Exaggerated reflexes ++++ Exagerated reflexes and clonus

Sensation
Light touch Some fibres travel in the posterior columns [ipsilaterally] and the rest cross the midline to travel in the anterior spinothalamic tract [contralaterally] Use cotton wool to test for light touch. Initially touch the anterior chest wall [normal area]; this is to demonstrate to the patient how it feels. Ask the patient to close their eyes and begin proximally on the upper leg and test in each dermatome [memorise dermatomes] comparing right with left. Ask patient to tell you when they feel something. 166

Pain Spinothalamic pathway fibres enter the spinal cord and cross a few segments higher to the opposite spinothalmic tract. Using a sharp object touch the patients anterior chest wall [normal area], this is to demonstrate to the patient how it feels sharp. Ask the patient to close their eyes and begin proximally on the upper leg and test in each dermatome comparing right with left. Ask patient if they can feel object and if it feels sharp or dull. Map out any area of dullness. Always do this by moving from area of dullness to the area of normal sensation.

Vibration and proprioception

These fibres enter and ascend ipsilaterally in the posterior columns of the spinal cord to the nucleus gracilib and nucleus cuneatus in the medulla, where they decussate. Vibration The base of a vibrating tuning fork is placed on the anterior chest wall. It should be explained to the patient that it is the sensation of vibration and not cold or touch which is being detected. The base of the vibrating tuning fork is then placed on the dorsum of the terminal phalanx. The patient is asked can they feel it vibrate and to indicate when vibration stops. They are then asked to repeat this with their eyes closed. Stop the tuning fork vibrating by touching it and the patient should be able to say exactly when this occurs. Compare one side with the other. Should vibration sense be lost or impaired distally then the tuning fork should be moved proximallly in order to establish the level at which it is normally appreciated. [Lateral malleolus, upper part of tibia, iliac crest, costal margin] Proprioception Grasp the distal phalanx from the sides and move it up and down to demonstrate these positions. Then ask the patient to close the eyes while these manoeuvres are repeated. Normally movement through even a few degrees is detectable, and should be reported correctly. If there is an abnormality, proceed to test the ankles and knees similarly. Sensory level If there is peripheral sensory loss attempt to map out the upper level. This may involve testing over the abdominal or even the chest dermatomes. Establishing a sensory level on the trunk indicates the spinal cord level that is affected. The abdominal reflexes 167

Test these by lightly stroking the abdominal wall diagonally towards the umbilicus in each of the four quadrants of the abdomen. Reflex contractions of the abdominal wall are absent in upper motor neurone lesions above the segmental level. They are also absent in patients who have had surgical operations interrupting the nerves.

Ward tutorial
Peripheral nervous system Upper limb

Inspection
Arms and shoulder girdles should be completely exposed. Inspect the upper limbs and look for abnormal posture. Look for muscle wasting and compare one side with the other. Also look for abnormal movements such as a tremor in the wrist or arm.

General
Ask the patient to hold out both hands with the arms extended and the eyes closed. Watch the arms for evidence of drifting [movement of one or both arms from the initial neutral position]. Upper motor neurone lesion the drifting of the limb is due to muscle weakness. The drifting downwards starts distally with the fingers and spreads proximally. Cerebellar disease the drift is due to hypotonia and is usually upwards. Loss of proprioception the drift is due to loss of joint position sense and can be in any direction.

Ask the patient to relax arms and rest them on their lap. Inspect for fasciculations. These are irregular contractions of small areas of muscle which have no rhythmical pattern. If present with weakness and wasting, fasciculation indicates degeneration of the lower motor neurone e.g. motor neurone disease.

The Motor system

Tone/Power/Coordination/Reflexes

Tone
Resistance felt when a joint is moved passively. Tone is tested at the wrists and elbows. The patient should be told to relax and to allow the examiner to move the joints freely. Flexion and extension of the elbow and wrist joint is performed passively. Normal tone can be assessed by repeated examination of normal people. Tone increased - hypertonic, as in an upper motor neurone lesion. Tone decreased - hypotonic, as in a lower motor neurone lesion. 168

Power
A measure of muscle strength Age, gender and build should be taken into account 0 Complete paralysis 1 Flicker of contraction possible 2 Movement is possible when gravity is excluded [sideways] 3 Movement is possible against gravity but not if any further resistance is added 4 Movement is possible against gravity and some resistance 5 Normal power If power is reduced decide if it is symmetrical or asymmetrical and whether it is proximal, distal or general. Shoulder Abduction With the elbows flexed ask the patient to abduct the arms. The patient should resist the examiner pushing them down. Adduction The patient should adduct the arms with the elbows flexed. The patient should resist the examiner separating them. Elbow Flexion Ask the patient to bend the elbows and not to let you straighten it. Extension With the elbow bent ask the patient to straighten the elbow and not to let you bend it. Wrist Flexion Ask the patient to flex the wrist and not to let you straighten it. Extension Ask the patient to extend the wrist and not to let you bend it. Fingers Flexion The patient squeezes two of the examiners fingers. Extension The patient should straighten the fingers and not allow the examiner to push them down. Abduction 169

The patient should spread the fingers and not allow the examiner to push them together.

Coordination
The cerebellum plays an integral role in coordinating voluntary movement. A number of tests are used to test coordination. Finger-nose test Ask the patient to touch their nose with the index finger and then to touch the examiners outstretched finger at nearly full extension. The test should be done a number of times with the patients eyes open and then closed. Look for: 1] Intention tremor, which is tremor increasing as the target is approached [cerebellar disease]. 2] Past-pointing, where the patients finger overshoots the target [cerebellar disease]. Rapidly alternating movements Ask the patient to pronate and supinate their hand on the dorsum of the other hand as rapidly as possible. In cerebellar disease this movement is slow and clumsy and is called dysdiadochokinesis Rebound Ask the patient to lift rapidly the arms from the sides and then stop. Hypotonia from cerebellar disease causes delay in stopping the arms.

Reflexes
Make sure the patient is resting comfortably Biceps jerk Place one forefinger on the biceps tendon and tap this with the tendon hammer. The hammer should be held distally. There is brisk contraction of the biceps muscle with flexion of the forearm. If the biceps jerk appears to be absent it should be tested again following a reinforcement manoeuvre. Ask the patient to clench their teeth tightly just before you let the hammer fall. Sometimes normal reflexes can only be elicited after reinforcement, but they should be symmetrical. Triceps jerk Support the elbow with one hand and tap the triceps tendon. Triceps contraction results in forearm extension. Brachioradialis jerk Place your first two fingers over the lower end of the radius just above the wrist. Strike the fingers. Contraction of the brachioradialis causes flexion of the elbow. The reflexes can be recorded as follows: 0 Absent reflexes 170

+ Reduced reflexes ++ Normal reflexes +++ Exaggerated reflexes ++++ Exagerated reflexes and clonus

Sensation
Light touch Some fibres travel in the posterior columns [ipsilaterally] and the rest cross the midline to travel in the anterior spinothalamic tract [contralaterally] Use cotton wool to test for light touch. Initially touch the anterior chest wall [normal area]; this is to demonstrate to the patient how it feels. Ask the patient to close their eyes and begin proximally on the upper arm and test in each dermatome [memorise dermatomes] comparing right with left. Ask patient to tell you when they feel something. Pain Spinothalamic pathway fibres enter the spinal cord and cross a few segments higher to the opposite spinothalmic tract. Using a sharp object touch the patients anterior chest wall [normal area], this is to demonstrate to the patient that it feels sharp. Ask the patient to close their eyes and begin proximally on the upper arm and test in each dermatome comparing right with left. Ask patient if they can feel object and if it feels sharp or dull. Map out any area of dullness. Always do this by moving from area of dullness to the area of normal sensation.

Vibration and proprioception

These fibres enter and ascend ipsilaterally in the posterior columns of the spinal cord to the nucleus gracilis and nucleus cuneatus in the medulla, where they decussate. Vibration The base of a vibrating tuning fork is placed on the anterior chest wall. It should be explained to the patient that it is the sensation of vibration and not cold or touch which is being detected. The base of the vibrating tuning fork is then placed on one of the distal interphalangeal joints. The patient is asked can they feel it vibrate and to indicate when vibration stops. They are then asked to repeat this with their eyes closed. Stop the tuning fork vibrating by touching it and the patient should be able to say exactly when this occurs. Compare one side with the other.

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Should vibration sense be lost or impaired distally then the tuning fork should be moved proximally in order to establish the level at which it is normally appreciated. [Ulnar head at wrist, olecranon at elbow and then the shoulders] Proprioception Grasp the distal phalanx from the sides on the patients index finger and move it up and down to demonstrate these positions. Then ask the patient to close the eyes while these manoeuvres are repeated. Normally movement through even a few degrees is detectable, and should be reported correctly. If there is an abnormality, proceed to test the wrists and elbows similarly.
Tone Power Reflexes Other UMNL Increased(hypertonic)+/clonus Spasticity Weak abductors/extensors in upper limb Increased(hyperreflexia) Muscle wasting rare LMNL Decreased(hypotonic) Flaccidity Distal muscles weakened more than proximal Decreased Muscle wasting Fasciculation

WARD TUTORIAL Rheumatological history The rheumatologic system includes diseases of the joints, tendons and muscles. Some causes of Monoarthritis Septic arthritis Trauma Gout Haemarthrosis [haemophilia]

Some causes of polyarthritis Rheumatoid arthritis Connective tissue disease [systemic lupus erythematosus] Infection viral Spondylarthropathies : 1. Psoriatic arthropathy 2. Enteropathic arthropathy 3. Ankylosing spondylitis 4. Reiters Disease Primary osteoarthritis Gout Pseudogout Adult Stills disease 172

History Presenting complaint/history of presenting complaint Ask about joint pain and swelling. Arthralgia is the presence of joint pain.
1. Determine what joints are involved 2. Determine the pattern of joint involvement [bilateral, symmetrical, migrating] 3. Are symptoms acute or chronic in nature? 4. Is pain getting worse or better? [progression] 5. Any precipitating factors [trauma]? 6. Ask about the presence of early morning stiffness and the length of time that this stiffness lasts [morning stiffness can occur in rheumatoid arthritis and other inflammatory arthropathies]. 7. Enquire about the functional capacity of the patient - can they dress, make a cup of tea [with rheumatoid arthritis of the hands function can be severely limited]. 8. Enquire about the impact of the illness on work, social life, mood, 9. Ask about systemic symptoms 10. Fatigue [connective tissue diseases] 11. Rash [SLE, facial butterfly rash] 12. Fever [connective tissue diseases] 13. Weight loss [scleroderma] 14. Diarrhoea [scleroderma] 15. Mucosal ulcers [rheumatoid arthritis/SLE]

Associations
Ask about Raynauds phenomenon Disorder of the small arteries of the fingers and toes Exposure to cold causes these arteries to narrow and decreased blood flow causes digits to become cold and white The pallor is followed by blueness [cyanosis] Redness results as the arteries open and the blood flow returns

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Raynauds phenomenon

Primary RP Primary RP or idiopathic Raynauds disease describes those patients without a definable cause for their vascular events. Primary RP has an age of onset between 15 and 30 years of age, is more common in women, and may occur in multiple family members Secondary RP Secondary RP refers to those patients with RP in whom an associated disease or cause may underlie the attacks. More correctly termed Raynauds Syndrome. Causes include: 1. Scleroderma 2. Systemic Lupus Erythematosus 3. Other connective tissue diseases (mixed connective tissue disease, polymyositis, dermatomyositis, rheumatoid arthritis, Sjgren's syndrome and vasculitis) 4. Occlusive vascular disease (arteriosclerosis, atheroemboli, and thromboangiitis obliterans) 5. Drug-induced (amphetamines, beta-blockers, nicotine) 6. Haematological (Cold agglutinin disease, cryoglobulinemia, paraproteinemia, and polycythemia) 7. Vibration-induced (pneumatic drills and hammers)

Ask about dry eyes (xerophthalmia) and mouth (xerostomia) In Sjogrens syndrome, decreased exocrine gland function leads to the "sicca complex", a combination of dry eyes (xerophthalmia) and dry mouth (xerostomia). In addition, a wide variety of extraglandular disease features can occur in SS. Dry eyes can result in conjunctivitis/corneal ulcers. Dyspareunia may also occur, due to vaginal dryness. Dry cough and enlargement of the salivary glands may also be present.
Ask about red eyes This can occur with: 1. iritis which may complicate seronegative spondyloarthropathies [psoriatic arthritis, Reiters disease, ankylosing spondylitis]

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2. scleritis [ RA, SLE] 3. scleromalacia Scleral thinning due to chronic scleritis [RA]

Past Medical/Surgical History

Septic arthritis

Trauma Gout

Haemarthrosis [haemophilia]

o Inflammatory bowel disease can result in arthritis

o o Psoriasis can cause psoriatic arthropathy

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Arthritis mutilans in psoriatic arthropathy

o Tick bite may indicate Lyme disease

o o History of STI [gonorrhoea monoarthritis] o Enquire about physiotherapy/joint surgery o Previous endocarditis/pericarditis [SLE] o Heart failure [due to valvular disease in SLE, right-sided heart failure due to advanced pulmonary fibrosis] o Respiratory disease [pulmonary fibrosis in RA/SLE, pulmonary hypertension, pleurisy in SLE] o Renal disease [proteinuria, nephritic syndrome secondary to gold/penecillamine, glomerulonephritis in SLE, renal vascular disease in scleroderma] o HTN- can complicate RA, SLE, scleroderma if renal involvement

Medication/Allergies
Anti-arthritic medications: 1. Analgesics NSAIDs 2. Steroids oral, intra-articular 3. DMARDS azathioprine, gold, penecillamine, captopril 4. Anti-TNF alpha agents Anti-ischaemic agents [SLE accelerates coronary heart disease]

Social History
If the patient has a chronic disabling arthritis determine the patients domestic setup/support Bungalow/two-storey Bedroom/bathroom - upstairs/downstairs Stairs access rails, chairlift, etc. Walking aids

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Ramps/wheelchair access Modified bath/walk-in shower

Modified domestic tools, grooming instruments

Smoking history poor prognostic indicator in Rheumatoid Arthritis Alcohol history Home supports carers, specialist nurse, outpatient physiotherapy, occupational therapy. Recent foreign travel [tick-infested regions, Lyme disease] 177

Sexual history [gonococcal septic arthritis] Intravenous drug use [Increased risk of staphylococcal aureus septic arthritis]

Family History
Ask about family members with diseases associated with arthritis Rheumatoid arthritis Gout Osteoarthritis Spondylarthropathies Inflammatory bowel disease Other autoimmune disease

Review of Systems
Many rheumatological disorders can have varied and extensive systemic manifestations. A thorough review of systems is necessary to elicit the severity and extent of any extraarticular disease. CVS symptoms of heart failure/endocarditis Respiratory dry cough, dyspnoea [fibrosis], pleuritic chest pain [pleurisy] CNS Dysphasia, motor or sensory disturbance, unsteadiness indicative of TIAs/Strokes [thromboemboloic phenomenon increased in SLE, due to antiphospholipid syndrome and cerebral vasculitis in SLE/RA]. Seizures, cognitive impairment [SLE] GIT Dysphagia, constipation, diarrhoea, abdominal pain [scleroderma], Oral ulcers [palatal ulcers in SLE, aphthous ulcers in UC, secondary to drugs used in RA [gold, steroids], ulcers due to Reiters disease GUT dysuria, haematuria, circinate balanitis [Reiters disease], and calculi [associated with gout] Endocrine symptoms of DM, thyroid disease, Addisons disease [autoimmune in origin]
LEARNING OBJECTIVES: At the end of this tutorial you should be able to: 1. Define back pain 2. List the risk factors for back pain 3. Take a history from a patient with back pain, addressing the points which will help to narrow the differential 4. Perform physical examination focussing on the features which may be associated with each of the likely differentials. 5. Choose and justify appropriate investigations of the patient with back pain. DEFINITION: (also known as "dorsalgia") is pain felt in the back that usually originates from the muscles, nerves, bones, joints or other structures in thse spine. DIFFERENTIAL DIAGNOSIS: Trauma o Strain/sprain o Whiplash injury o Falls

BACK PAIN

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Mechanical/Degenerative o Hypermobility Ehlers Danlos syndrome, Marfans syndrome o Scoliosis/kyphosis o Sacroiliitis o Spinal stenosis o Rheumatoid arthritis o Osteoarthritis Malignancy o Primary bone tumours o Metastatic Infection/inflammation o Osteomyelitis S. aureus, tuberculosis, brucellosis o Spinal epidural abcess o Septic disk o Meningitis o Lumbar arachnoiditis Metabolic o Osteoporosis hyperparathyroidism, immobility o Osteosclerosis Pagets disease Vascular o Abdominal aortic aneurysm o Vertebral artery dissection Others o Referred pain from visceral disease o Postural o Sickle cell crisis o Psychogenic, malingering, chronic pain syndrome o Urinary tract infection/Pyelonephritis o Pelvic inflammatory disease o Herpes zoster
(2)

Red flags" for a potentially serious underlying cause for low back pain Preceding episode of trauma Unintentional weight loss History of malignancy IV drug abuser Immunosuppressives therapy, osteoporosis Age >70 years Progressive or disabling neurological deficit 5 Types of Back Pain:

Local pain due activation of pain nerve-endings from tears/stretching Referred pain usually abdominal or pelvic origin, pain unaffected by spine movement Radicular pain radiates from spine to the leg. Coughing, sneezing, lifting heavy objects or straining may elicit pain Pain of spine origin restricted to the back and referred to the lower limb. Diseases originating from the upper lumbar spine refer

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pain to upper lumbar region, groin or anterior thighs. Diseases of lower lumbar spine refer pain to buttocks or posterior thighs. Pain associated with muscle spasm accompanied by taut paraspinal muscles.

HISTORY: Onset of pain acute/progressive, post-trauma Location and exact point of the pain Character of the pain sharp, shooting, dull constant Radiation of pain/discomfort Timing of pain Severity of pain (scale out of 10), associated disability Relieving factors Associated symptoms extra-articular symptoms, constitutional/systemic symptoms The impact of the pain in patients daily activities, functional capacity Medications history steroids treatment Pathology -Herniated disk causing nerve root irritation -Sacroiliitis -Facet joint degenerative arthritis -Spinal stenosis -Sciatic nerve irritation -Malignancy (either a vertebral body metastasis or cauda equina tumour) -Compression fractures (multiple myeloma, osteoporosis) -degenerative bone diseases -Ankylosing spondylitis -Seronegative spondyloarthropathies

Symptoms Back pain radiating down the buttock and below the knee

Back pain at night, unrelieved by rest or change in position/posture

Back pain aggravated by activity and improves with rest Back pain that worsens with rest and improves with activity

EXAMINATION: Inspection look for abnormality of posture i.e. scoliosis or kyphosis, scars, skin lesions Passive range of motion - flexion and extension, adduction, abduction Palpation of the back - to elicit vertebral or soft tissue tenderness, bony deformities Straight leg raising - The test is considered positive when the sciatica is reproduced between 10 and 60 degrees of elevation. A positive straight leg test is sensitive, but not specific, for herniated disc.

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Neurologic testing if prolapsed disc is suspected, neurologic testing should be performed L5 motor nerve root testing evaluates strength of ankle and great toe dorsiflexion. L5 sensory nerve root damage would result in numbness in the medial foot and the web space between the first and second toe. The S1 nerve root is tested by evaluating ankle reflexes and sensation at the posterior calf and lateral foot. S1 radiculopathy may cause weakness of plantar flexion, but is difficult to detect until quite advanced. One strategy is to have the patient rise up on tip-toe three times in a row, on one foot alone and then the other. Observe the gait pattern antalgic gait wide-based gait (suggests unsteadiness) leaning forwards/stiff legged (spinal stenosis) shuffling (Parkinsonism) foot-drop (suggest L5 or S1 nerve root compression) flat-feet, hind feet valgus and genu recurvatum on stance phase might suggest hypermobility associated with various low back lesions

INVESTIGATIONS: Blood tests (CBC, ESR, CRP) raised WCC, ESR and CRP in spinal infection or malignancy Blood culture if infection is suspected as the cause of back pain Plain radiographs fractures, malignant infiltrations, osteomyelitis, narrowed disc spaces, degenerative changes and spondylolidthesis Tumour markers raised tumour markers with underlying malignancies Serum Ca raised calcium in myeloma, hyperparathyroidism MRI or CT urgent when the clinical examination suggests underlying cord compression. MRI is a better initial test for most patients with low back pain who require advanced imaging, though CT scan gives better definition of bony structures. Myelogram - useful in patients with multiple disc abnormalities, multilevel radiculopathies, extruded free disc fragments, a disc fragment in the lateral recess, or previous lumbar surgery DIAGNOSTIC ALGORITHM
FOR

LOW BACK PAIN

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Algorithm taken from http://www.uptodate.com/online/content/image.do? imageKey=PC%2F22468

WARD TUTORIAL Rheumatological examination 2

The rheumatological system includes diseases of the joints, tendons and muscles.

Temporomandibular joints
Look just in front of the ear for swelling. Palpate by placing a finger just infront of the ear and ask the patient to open and close their mouth. The head of the mandible is palpable as it slides forwards when the jaw is opened. Rheumatoid arthritis commonly affects the temporomandibular joint and may cause clicking, grating and tenderness of the joint.

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The Back
With the patient standing and wearing only underwear look for abnormal posture/deformity.Look from the back, front and the sides. 1. 2. 3. 4. 5. Cervical spinous process C1 Lumbar spinous process, L2 L3/L4 intervertebral space Iliac crests Sacro-iliac joints (dimple of Venus)

Note loss of the normal thoracic kyphosis and lumbar lordosis. Look for scoliosis [spinal deformity, a lateral curvature of the spine] Palpate each vertebral body for tenderness. Gentle percussion with the fist may elicit it.

Actively assess movement Flexion; ask the patient to touch their toes with the knees straight. Extension; ask the patient to lean backwards. Lateral flexion/bending; ask the patient to slide their right hand down the right leg as far as possible without bending forward and then to do the same on the left side. Rotation; with the patient sitting ask them to rotate the head and shoulders as far as possible to each side. Measure the lumbar flexion with Schobers test 183

A mark is made at the level of the sacro-iliac joints on the vertebral column [approx L5, no 2 in image]

One finger is placed 5cm below the mark and another 10cm above the mark.The distance between these two marks is then measured.The patient is then asked to touch their toes.

An increase of less than 5cm in the distance between the 2 fingers indicates limited

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Straight leg raising With the patient lying down lift the patients straight leg. The test should be performed slowly and the patient told to report as soon as it becomes painful. Normally 90 degrees of flexion at the hip should be possible. This will be limited by pain when the nerve root is stretched round or over a prolapsed disc.

Lasegues Test When the limit of straight leg raising has been achieved, further tension on the root is caused by dorsiflexing the ankle. If positive the pain is aggravated and is felt in the back of the leg, radiating into the lumbar region in some instances. This is usually dur to sciatic nerve compression.

Femoral Stretch Test With the patient lying prone, flex the knee to its limit of movement. In a positive test, the patient will feel pain in the ipsilateral anterior thigh, i.e. the distribution of the femoral nerve.

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Sacro-iliac joints These are involved in an early stage of ankylosing spondylitis. Ask the patient to lie on their stomach. Firm palpation with both palms overlying each other may elicit tenderness in sacroiliitis.

The Hips
Pain arising from the hip is most commonly situated in the groin, but may radiate down the thigh to the knee or be present in this joint alone. Move the hip joint passively with the patient lying on their back. The pelvis must be immobilised to ensure that movement being measured is coming from the hip alone and not also from the pelvis on the spine. Flexion The iliac crest is stabilised with one hand while the other grasps the leg. Flex the patients knee and move the thigh towards the chest. Rotation is tested with the knee and hip flexed. The foot is moved medially - external rotation of the hip. The foot is moved laterally internal rotation of the hip. Abduction The right hand holds the heel of the right foot while the left hand is placed over the opposite anterior iliac crest to steady the pelvis. The leg is then moved outward as far as possible. Adduction The leg is carried immediately in front of the other limb. Extension Ask the patient to roll over on to their stomach. Place one hand over the sacroiliac joints while the other hand raises each leg. Trendelenburgs Test Ask the patient to stand. Now ask them to stand first on one leg and then on the other. When the normal subject stands on one leg, the abducters contract so that the opposite side of the pelvis is tilted slightly up. If the patient stands on the affected leg when the 186

actions of the abducters are deficient, the opposite side of the pelvis will tilt downward and balance can be maintained only by leaning over towards the side of the lesion. The test is performed with the patients back to the examiner.

This test is useful in the late stages of congenital dislocation of the hip and in poliomyelitis affecting the lower leg. Measurement of leg length True leg length from the anterior superior iliac spine to the medial malleolus

The cause of the apparent leg length difference is the contracture ( permanent shrinkage) of the soft tissues and of the abductor musculature (the gluetus and tensor fasciae muscles When true shortening is present the normal limb must be measured in a comparable position to the abnormal one, in respect to abduction or adduction for accuracy. Apparent leg length from the umbilicus to the medial malleolus 187

Where a fixed deformity of the hip joint is present and the legs are brought parallel, the limbs will apparently be unequal in length. The amount of apparent shortening is measured from the umbilicus to the medial malleolus. Fracture of the neck of the femur the limb is externally rotated, adducted and shortened. This is common in the elderly, especially women.

The knee
With the patient lying down expose both legs. Look for wasting of the quadriceps and swelling and deformity of the knee joint. Swelling of the synovium is usually seen medial to the patella and in the joints suprapatellar extension. Palpate the quadriceps for wasting and the knee joint for warmth and tenderness. The patellar tap This is used to confirm the presence of a moderate/large effusion. One hand lies over the lower part of the quadriceps and compresses the suprapatellar bursa which is emptied.(milking the suprapatellar pouch). The other hand pushes the patella downwards. The sign is positive if there is sufficient fluid to allow the patella to tap off the femur.

The active range of movement is tested first in the normal and then in the abnormal knee. Passive movement is then tested in the same way. Place a hand on the knee to detect the presence of crepitus. 188

Tests of stability The lateral and medial collateral ligaments The patients ankle is held between the examiners elbow and side. This leaves both hands free to abduct and adduct the tibia on the femur while keeping the knee straight. Normally no movement should be present. The cruciate ligaments Anterior Drawer Test With the knee flexed to a right angle the examiner sits on the patients foot, or enure the foot is stabilised, and in the neutral position. To test the anterior cruciate the tibia is grasped just below the knee and is drawn forward (anteriorly). Excessive anterior movement is due to laxity of the anterior cruciate.

Lachmans test. This is the most sensitive test for anterior cruciate ligament injury. The examiner uses the right hand to place anterior force on the lower leg while simultaneously using the left hand to place posterior force on the distal thigh. A good end point should be felt. Hands are reversed to test the left knee. Excessive laxity indicates an anterior cruciate ligament tear.

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Posterior Drawer Test To test the posterior cruciate, this movement is reversed.
Excessive posterior movement is due to laxity of the posterior cruciate.

Stability of the patella With the knee extended the patella is grasped and moved from side to side.

The ankles and feet

Look for swelling, deformity and muscle wasting. Hallux valgus fixed lateral deviation of the main axis of the big toe.

Ankle dorsiflexion raise the foot up Plantar flexion push foot down

Hip examination
HISTORY

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It is important to bear in mind the following points when performing a hip examination:

Age of the patient o Younger patients - traumatic injuries, osteonecrosis and developmental dysplasia of the hip are more prevalent o Older patients - hip fractures and osteoarthritis are more common Mechanism of injury Duration of problem CLINICAL EXAMINATION

Follow the scheme below:

Inspection Palpation Measurment Movement

Before starting

Introduce yourself Explain what the examination entails Ask permission to perform examination Expose the patient appropriately - from waist down exposing both the lower limbs, but leaving the underwear on Preserve dignity by using a blanket appropriately Tell the patient to let you know if anything you do is uncomfortable Remember - always watch the patients face

Inspection

General observation o Does the patient look well? o Is there a walking stick? Frame? o Is there a shoe raise? o Hands (Rheuamtoid arthritis?)

Patient Standing

Remember to inspect from all sides (front, laterally and from behind): o Skin Scars (previous injuries or surgical scars) Sinuses (secondary to TB or infected hip replacements) Colour - discolouration? o Deformity Abduction / adduction contracture Fixed flexion deformity Limb shortening Limb rotation Scoliosis Lumbar lordosis o Swelling (the hip joint is deep and thus swelling is not generally seen) o Muscle wasting - look at the gluteal folds gluteals? quadraceps? o Pelvic obliquity (anterior superior iliac spines (ASIS) not horizantal) Is there a leg length discrepancy? Is there a fixed deformity?

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Patient Walking

Observe the patient walking. o Gait pattern. There are different types of gait: Stiff hip (pelvis swing) Antalgic (short stance phase) Short leg Trendelenburg (Lurching gait, watch the shoulders) Drop foot gait Broad based gait (ataxia) o Stride length o Use of a walking aid

Patient Lying down - supine with one pillow under the head

Observe the patient climb onto the examination couch Deformity o Rotational deformity is common in osteoarthritis (observe the position of the patella and foot on either side) o Fixed flexion deformity (look at the angle between the thigh and the bed). Perform Thomas's test at this stage (see below) o Abduction / Adduction deformity (adduction deformity - tilted pelvis and apparent shortening of that leg) Detailed check: o Skin - scars

Palpation Ask the patient.."Does it hurt anywhere?"

Skin temperature (use dorsal surface of your hand to compare temperatures over both hips) Is there tenderness over the bony landmarks? o Anterior and posterior superior iliac spines o Ischial Spine o Greater Trochanters (trochanteric bursitis) o Iliac crests o Ischial tuberosity (hamstring tear) o Pubic Tubercle Is there tenderness of the soft tissues? o Muscles o Femoral triangle Joint line tenderness (beneath the mid inguinal point)

Measurement Before measuring, if a fixed deformity of one leg has been observed, the unaffeted leg should be placed in the same position as the one affected to make them identical. The different types of measurements to be taken are:

Apparent length - the distance between the xiphi-sternum (a fixed point) and the medial mallelous. True length - the distance between the ASIS and the medial malleolus Circumference of the quadriceps at a fixed point (from the tibial tuberosity).

If a difference has been observed in true leg length measurements, it is important to determine whether the shortening is above (femoral) or below (tibial) the knee:

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Having asked the patient to bend their knees, keeping their ankles together, compare the position of both knees.

Movement These should be performed both actively and passively for both legs. When assessing hip movements, it is important to fix the pelvis and prevent any movement taking place at this anatomical structure. This is done either by dropping one leg over the edge of the couch and assessing movements of the other leg, or by placing one forearm between the ASIS's. Active movement

Flexion (0-130o)- "Can you bring your heel to your bottom?" Extension (0-10o) - Having asked the patient to lie prone, ask them to raise each leg off the bed with the knee straight. Abduction (0-45o) - "Can you move your leg away from the bed?" Adduction (0-30o) - "Can you move your leg across your other leg"

Passive movements Repeat the above movements but additionally testing for hip rotation.

Rotation - With each leg in turn, flex both hip and knee to 90o , and having stabilised it with one hand, move the heel first outwards (internal rotation - 0-45o) and inwards (external rotation - 045o) with the other hand.

Special Tests There are two special tests: Trendelenburg test - test of abductor function (gluteus medius weakness)

Stand behind the patient and identify the iliac crests Have another person in front of the patient for balance Ask the patient to stand on the normal and then the affected leg by flexing the knee rather than flexing the hip. This is for testing the abductors on the opposite side. Watch for the patients' response in terms of balance (truncal position) and pelvic tilt Negative test (normal) o If pelvis stays level or rises slightly, with the trunk staying over the pelvis (i.e. staying over the centre of gravity), AND can be maintained for 30 seconds. Positive test (abnormal) o The patient is unable to hold pelvis level and maintain this for 30 seconds. o The patient leans over to the affected side, in order to keep their centre of gravity over their foot

For further information about performing a Trendelenburg test, please Click Here. Thomas' test - test for fixed flexion deformity

Finally

With the palm up, place your hand beneath the lumbar spine Passively flex the unaffected hip until the hollow of the lumbar spine is eliminated The affected leg rises up from the bed, if there is a fixed flexion deformity present. Repeat for the other side

Check distal neurovascular supply.

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Examination of the patient with Rheumatoid Arthritis (RA)

The general principles of examining a joint:
1) Inspect from the front, back and sides: Skin Erythema: Suggests active inflammation or infection Scars: Previous joint replacement or tendon repair. Rash: Psoriasis is associated with Psoriatic arthritis, an important differential diagnosis for RA. A vasculitic rash is associated with multisystem inflammatory conditions including RA, SLE, and Sjogrens syndrome etc.

Psoriasis Joint

Vasculitis

Swelling: Can be due to hypertrophy of the synovial membrane, effusion or bony swelling caused by overgrowth of the bony joint margins. Deformity: See below for individual joints. Abnormal bony alignment: Dislocation or subluxation (partial dislocation) Muscle wasting

2) Palpate the joint You must at all times watch the patients face while palpating, looking for signs of discomfort Warmth: A sign of active synovitis, infection or crystal arthritis such as Gout. Tenderness: Remember to watch the face. Swelling Synovial swelling is boggy or spongy Joint effusion swelling is fluctuant. The fluid can be shifted within the joint 194

 Bony swelling is hard. 3) Move the joint Passive movement Check for limitation of movement in any direction (fixed flexion or fixed extension deformity). Measurement of movement range is also useful. Check for crepitus: A grating sensation from the joint as it is moved. It indicates irregularity in the articular surfaces. Check joint stability: This tests the integrity of the joint and surrounding ligaments. It is tested by gentle attempt to move the joint in abnormal directions. Active movement is used to assess integrated joint function.

Rheumatoid Arthritis (RA) patient

Rheumatoid arthritis eventually affects the peripheral joints in almost all patients. Involvement of axial and central joints, such as the atlantoaxial joint of the neck, acromioclavicular, sternoclavicular, temporomandibular, cricoarytenoid joints, and shoulders and hips is less common.

General inspection
Obvious deformity or asymmetry Posture Characteristic appearance such as Cushingoid facies Rashes (as above) Eye involvement may be evident ( Red eye due to iritis or scleritis) Walking aides

The hands
Inspection: With patients hands supported by a white pillow for comfort.

Start with the dorsal aspect from proximal to distal looking at skin and nails and check for swelling, erythema, skin atrophy, deformity, abnormal bony alignment, muscle wasting, rash, scars and nail changes. Vasculitic changes around the nail folds 1-2mm lesions due to skin infarction Splinter haemorrhages due to vasculitis

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Wasting of the small muscles of the hands wasting of intrinsic muscles with hollow ridges between the metacarpal bones

Joint swelling - Photo shows swelling and early damage from rheumatoid arthritis

Wrist Ulnar styloid prominence

Metacarpophalangeal joints Ulnar deviation deviation of the phalanges at the metacarpophalangeal joints towards the medial [ulnar] side of the hand. Volar subluxation [palmar subluxation of the fingers] Proximal and distal interphalangeal joints 196

Changes due to joint destruction and tendon dysfunction Swan neck deformity Boutonniere deformity Z thumb deformity

Palmar aspect of the hands Palmar erythema: Also occurs with liver disease, polycythemia, thyrotoxicosis, pregnancy.

Palmar crease pallor: Anaemia (Anaemia of chronic disease, associated pernicious anaemia, secondary to GI bleeding due to NSAIDS, due to disease modifying drugs used to treat RA, due to hypersplenism). Surgical incisions (tendon repair) Muscle wasting

Palpation (Palpate joints from proximal to distal with the palms down): Feel all joints in the hand individually. Tenderness, heat, and the character of the swelling observed. Note that synovial inflammation feels boggy, effusion is fluctuant. Move the joint Passive movement first

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Move all joints gently in their normal plane of movement. Start from the wrist and move distally. Check for tenderness on movement, limitation of movement, and crepitus. Test for trigger finger. The distal interphalangeal joint gets stuck in flexion. Test for volar subluxation (partial dislocation) of the metacarpophalangel joints (MCPs). This is done by flexing the joint with the proximal phalanx held between the thumb and forefinger. Test for carpal tunnel syndrome tap over flexor retinaculum [Tinels sign]

Active movement and functionality of the hand Test all joints active movement in normal planes starting with the wrist, MCP, PIP, DIP joints. Test thumb movements independently as it is a major cause of disability when impeded. Hand function tests include: Grip strength (Ask patient to squeeze your first two fingers) Opposition strength (Ask patient to hold piece of paper between thumb and forefinger and prevent you from pulling it free) Key grip Thumb opposition to other fingers Practical tasks like writing and buttoning up shirt.

Examination of the hands is not complete without feeling for subcutaneous nodules near the elbows.

The arms
Inspection Scars, erythema, rash. Rheumatoid nodules: The examination of the rheumatoid hands is incomplete without checking for rheumatoid nodules at the elbows. They occur in approximately 25% of patients with RA. They are hard to touch and can be differentiated from gouty tophi in that the latter appear yellow under the skin.

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Examination of the elbow and shoulder joints (These will be demonstrated in class, only point notes are included here). Elbow

Remember: Look, feel, move. It is very useful to watch the patient remove top here as it gives an idea of limitation of movement and functionality as well as discomfort.

Inspection: Subcutaneous nodules (RA, gout). Enlarged bursa (fluid). Colour of nodules (yellow: gout). Swelling (joint effusion). Psoriasis on elbows (psoriatic arthritis). Palpation: Warmth. Lateral epicondyle tenderness (tennis elbow). Medial epicondyle tenderness (golfer's elbow). Enlarged bursa (fluid). Nodules: hard (RA) or firm (gout). Motion: Flexion [normal: 150]

Shoulders Inspection: Swelling. Palpation: Warmth. Tenderness: localized or diffuse. Swelling. Axillary nodes (RA). Motion, asking if painful: Abduction [normal: 90]. Adduction [normal: 50]. Flexion [normal: 180]. Extension [normal: 60]. External rotation [normal: 60]. Internal rotation [normal: 90].

Pain during movement: All directions [intra-articular] One direction [inflamed tendon] No pain, only weakness [lesion to tendon or nerve]

The head
Eyes: 199

Anaemia Cataracts (Occur in this setting secondary to long-term steroid treatment) Dry eyes (Sjogrens syndrome occurs in about 10% of RA cases) Scleritis and episcleritis (Scleral redness secondary to rheumatoid lesions affecting the sclera ( Purple / red lesions which are pathologically rheumatoid nodules)

Scleromalacia (Due to scleral thinning in severe cases).

Fundus ( Hyperviscosity can lead to venous or arterial occlusion)

Mouth: Face: Parotid gland swelling (Sjogrens syndrome) Examination of the temporomandibular joint: Look for swelling in front of the ear Palpation with the examiner standing behind the patient: Feel for tenderness, crepitus when the patient opens and closes the mouth. Dry mouth (Sjogrens syndrome) Ulcers (Drug treatment with Gold)

The neck
Examination of the cervical spine Inspect and note any postural abnormalities. Palpate the individual spinous processes. Feel for tenderness and uneven spacing of the processes. 200

 Ask the patient to move the neck actively, note any limitation. Touch your chest with your chin (flexion), Look up at ceiling (extension), Touch each shoulder with ear (lateral bending) and finally rotation. Cervical spine involvement can produce upper limb neurological deficit. So neurological exam of the upper limb is part of the neck assessment.

The chest
Heart: Pulsus paradoxus (Constrictive pericarditis) Elevated JVP (Constricitve pericarditis) Impalpable apex beat (Constricive pericarditis) Auscultate for Pericardial friction rub (Acute pericarditis) Distant heart sounds (pericardial effusion) Regurgitant murmurs especially of aortic valve. Peripheral oedema ( Constricive pericarditis) Lungs: Palpation: Limitation of chest expansion (Fibrosis) Unequal expansion (Fibrosis or effusion) Tracheal deviation (towards fibrosis away from effusion) Percussion: Assess for stony dullness (effusion) Auscultation: Reduced or absent breath sounds in the base (effusion) Fine pan inspiratory or late inspiratory crackles (Fibrosis)

[Caplans syndrome is the presence of rheumatoid lung nodules in combination with pneumoconiosis] Pulmonary fibrosis on CXR

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The abdomen
Splenomegaly (Occurs in 10% of patients with RA and may Feltys syndrome) suggest

Feltys syndrome: Triad of RA, splenomegaly, and granulocytopenia. Although many patients are asymptomatic, some develop serious and life-threatening infections secondary to granulocytopenia. Hepatomegaly ( May occur secondary to treatment with Methotrexate)

The lower limbs

Inspect for rashes, erythema, scars, muscle wasting and joint swelling Examine the hips, knees and foot joints (hips and knee examination to be covered in ward tutorials) Look for foot drop [peroneal nerve entrapment or vasculitis] and examine the ankle joint for limitation of movement. Signs of cord compression due to anterior dislocation of the first cervical vertebra or subluxation of the odontoid process. Here upper motor neuron signs occur in the lower limbs mixed with lower motor neuron signs in the upper limbs. CLINICAL FEATURES
OF

LEARNING OBJECTIVES: At the end of this tutorial, you should be able to: 1. Define rheumatoid arthritis 2. List the diagnostic criteria for rheumatoid arthritis 3. Form a differential diagnosis for rheumatoid arthritis 4. Examine patients with RA, in order to: 1. Assess disease severity 2. Look for complications 5. Choose and justify appropriate investigations of the patient with deforming arthropathy.

RHEUMATOID ARTHRITIS

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DEFINITION: Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disease of unknown aetiology involving not only the joints but other organs. The pattern of joint involvement is typically symmetrical, may be remitting and can lead to destruction of joints due to erosion of cartilage and bone which leads to deformity (1). Diagnostic criteria The American College of Rheumatology has defined the following criteria for the classification of rheumatoid arthritis (2): Morning stiffness of >1 hour most mornings for at least 6 weeks. Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups present for at least 6 weeks Arthritis of hand joints, present for at least 6 weeks Symmetric arthritis, present for at least 6 weeks Subcutaneous nodules in specific places Positive rheumatoid factor titre Radiological changes suggestive of joint erosion At least four criteria have to be met for classification as RA DIFFERENTIAL DIAGNOSIS: Osteoarthritis typically affecting larger joints, asymmetrical distributions Gouty arthritis tender joints especially the metatarsophalangeal joints, crystal deposits over the small joints of the hands, pinna, Achilles tendon Psoriatic arthropathy scaly silvery plaques, asymmetrical distributions, telescoping of interphalangeal joints in severe disease Chronic juvenile arthiritis radial deviation, negative rheumatoid factors Infectious arthritis Infectious arthritis is usually monoarticular, but polyarthritis can occur. Paraneoplastic disease Joint pain or frank polyarthritis can occur in association with malignancy HISTORY: Age, occupation, sex (RA commoner in women) Presenting symptoms Joints o Degree of pain o Duration of morning stiffness and pattern of distribution, swelling, loss of function Extra-articular/systemic symptoms o signs such as fever, anorexia, malaise, weight loss, lethargy (due to anaemia) o skin palmar erythema, Raynauds phenomenon, rheumatoid nodules o painful eyes (scleritis) Disease modifying drugs, NSAIDS EXAMINATION: Inspection

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Face - Cushingoid from steroids treatment Eyes - Conjunctival pallor, episcleritis, uveitis, dry eyes (Sjogrens syndrome), scleromalacia, cataracts (steroid or chloroquine therapy) o Mouth xerostomia (Sjogrens syndrome) o Skin - rheumatoid nodule, vasculitis (microinfarcts around the nailfolds), livedo reticularis, pyoderma gangrenosum, erythema nodosum, scars, atrophy of digital skin, diffuse thinning (rice paper skin), and skin fragility (often worsened by corticosteroid use), Raynauds phenomenon, o Joints swelling, erythema, ulnar deviation, boutonniere deformity, swan neck deformity and "Z-deformity" (hyperextension of the interphalangeal joint, and fixed flexion and subluxation of the metacarpophalangeal joint), muscle wasting, ulcers, Palpation o Enquire patient whether any joint is tender o Assess degree of joint tenderness and tissue swelling o Palpate for tenderness and rheumatoid nodules (radius) Movement o Active and passive joint movement and the range of movement noted o Joint instability should be sought during passive joint movement o Function asses function by asking patient to unbutton shirt, hold a pen/tea cup, writing. Lungs o Crepitations from lung fibrosis (fibrosing alveolitis) and pleural effusions (stony dullness to percussion, reduced air entry over effusion, bronchial breathing above the level of effusions) Liver/spleen o Palpable spleen from Feltys syndrome Neurological o Peripheral neuropathy and mononeuritis multiplex o Carpal tunnel syndrome caused by compression of the median nerve by swelling around the wrist (Tinels sign) o o

INVESTIGATIONS CBC Anaemia of chronic disease, iron deficiency anaemia, megaloblastic anaemia Thrombocytosis - platelets are acute phase reactants, and their levels typically rise in a variety of inflammatory conditions Thrombocytopenia - hepersplenism Leukocytosis Leukocytosis can be a manifestation of active RA, but infection or treatment with glucocorticoids can also be responsible for this finding. Rheumatoid factors occur in 70 to 80 percent of patients with RA ESR /CRP not specific for RA however useful for distinguishing inflammatory conditions, of which RA is one, from noninflammatory disorders.

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Antinuclear antibody (ANA) A positive antinuclear antibody test is present in 30 to 40 percent of patients with RA, most commonly those with more severe, chronic disease Joint aspiration Synovial fluid examination typically reveals a leukocytosis with a predominance of polymorphonuclear cells, low glucose, low C3 and C4 complement levels Joint x-rays joint/bony erosions, deformity MRI detect bone erosions earlier in the course of the disease than is possible with plain films Ultrasound another alternative for estimating the degree of inflammation and the volume of inflamed tissue

CLINICAL FEATURES
LEARNING OBJECTIVES:

OF

OSTEOARTHRITIS

At the end of this tutorial you should be able to: 1. Define osteoarthritis 2. List the risk factors for osteoarthritis. 3. Take a history from a patient with deforming arthropathy, addressing the points which will help to narrow the differential 4. Perform physical examination focussing on the features which may be associated with each of the likely differentials. 5. Choose and justify appropriate investigations of the patient with deforming arthropathy. DEFINITION: Osteoarthritis is a form of degenerative bone disease characterized by progressive deterioration and loss of articular cartilage accompanied by proliferation of new bone and soft tissue in and around involved joint (1). There are recognized associations between OA, aging and trauma. Risk Factors (4) Age - Advanced age is one of the strongest risk factors associated with osteoarthritis Female sex there is a female preponderance in severe disease Obesity - the strongest modifiable risk factor Occupation Sports activities Previous injury/trauma Muscle weakness Proprioceptive deficits (peripheral neuropathy) Genetic elements Acromegaly Calcium crystal deposition disease PATHOGENESIS: Two principal mechanisms are thought to initiate osteoarthritis Damage to normal articular cartilage by injury and trauma. Chondrocytes react to this injury by releasing degradative enzymes and elaborating inadequate repair responses.

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Defective cartilage. Examples include a type II collagen gene defect or ochronotic cartilage that fails because of deleterious pigment deposition.

There are multiple factors that contribute to the development of OA. These include abnormalities in biochemical forces and the cartilage mixed with multiple risk factors (such as obesity, aging, mineral deposition, systemic hormones, and abnormalities in neurogenic control). Types of Osteoarthritis:

1. Idiopathic osteoarthritis Idiopathic OA can be categorized into

localized or generalized forms of the disease. a. Localized OA - commonly affects the hands, feet, knee, hip, and spine. Other joints are less commonly involved (shoulder, temporomandibular, sacroiliac, ankle, and wrist joints). b. Generalized OA consists of involvement of three or more joint sites.

2. Secondary osteoarthritis a. Trauma b. Congenital or developmental disorders c. Calcium pyrophosphate dihydrate deposition disease (CPPD) d. Other bone and joint disorders (osteonecrosis, rheumatoid arthritis, gouty arthritis, septic arthritis, and Paget disease of bone) e. Other diseases such as i. Diabetes mellitus ii. Acromegaly iii. Hypothyroidism iv. Neuropathic (Charcot) arthropathy v. Inflammatory diseases (such as Perthes disease), Lyme disease vi. Ligamentous instability vii. Marfans syndrome viii. Obesity ix. Alkaptonuria x. Haemochromatosis xi. Wilsons disease DIFFERENTIAL DIAGNOSIS: Rheumatoid arthritis Calcium pyrophosphate crystal deposition disease Infectious monoarticular disease HISTORY: Pain o

Deep boring pain typically exacerbated by activity and relieved by rest. o It is often worse at night (increased body temperature increased blood flow increased stimulation of pain receptors).

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Painful joints are not usually tender, except in the active Heberdens or Bouchards nodes. Stiffness is also a common complaint in patients with OA. Morning stiffness typically resolves less than thirty minutes after a patient awakens, but may recur following periods of inactivity, a phenomenon termed articular or inactivity gelling Crackling noise (joint "crepitus") when the affected joint is moved or touched, muscle spasm and contractions in the tendons Loss of function Osteoarthritis is typically not associated with any systemic / constitutional symptoms o

EXAMINATION: Inspection o Skin - scars, hair distribution, coarse doughy skin from Acromegaly o Joints swelling, erythema, deformity of distal interphalangeal joint, and fixed flexion and subluxation of the metacarpophalangeal joint and muscle wasting Palpation o Enquire patient whether any joint is tender o Commonly affected joints First carpometacarpal joint Proximal interphalangeal joint Distal interphalangeal joint Cervical and lumbar spine Knee Hip Subtalar joint First metarsophalangeal joint o Uncommonly affected joints shoulder, wrist, elbow, metacarpophalangeal joints o Assess degree of joint tenderness and tissue swelling Hands osteoarthritic enlargements of the distal and proximal interphalangeal joints - Heberden's and Bouchard's nodes. The first carpometacarpal joint is also a common area affected in OA. Enlargement of this joint result in a squared appearance to the hand Feet the first metatarsophalangeal joint - hallux valgus or hallux rigidus. Knees osteophytes, effusions, crepitus, and limitation of range of motion, malalignment (genu varus or genu valgus), varus angulation ("bow-legged") occurs more commonly than valgus ("knock-kneed"). Femerotibial malalignment may be a risk factor for more rapid progression of OA of the knee. A fluctuant swelling along the posterior aspect of the knee, or Baker's cyst, is a common complication Hips pain around the hip is common in patients with OA. It may be due to OA of the hip or to pain referred to the hip area from other structures, such as the lumbosacral spine

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Spine most common at spinal levels C5, T8, and L3, which represent the areas of greatest spinal flexibility. Spondylolisthesis, a slipping of one vertebral body on another, typically affecting the apophyseal joints at L4 to L5, may occur with severe OA. Shoulders glenohumeral joint (anterior shoulder pain), involvement of the acromioclavicular joint may cause vague shoulder pain. Osteophytes located along the undersurface of the acromioclavicular joint may result in rotator cuff tendonitis or tears due to the juxtaposition of tendons with the inferior portion of the acromioclavicular joint

Movement o Active and passive joint movement and the range of movement noted o Joint instability should be sought during passive joint movement

INVESTIGATIONS: Blood investigations CBC WCC level (raised in infection/inflammation), normal in OA Erythrocyte sedimentation rate (ESR) raised in inflammation, normal in OA Rheumatoid factor titre Joint aspiration -The presence of leukocytosis may help to distinguish an inflammatory from a noninflammatory process. In OA there is good viscosity of fluid with normal mucin clot. Synovial fluid analysis Clear fluid WBC <2000/mm3 Normal viscosity Bursal aspiration - Bursal aspiration is performed to distinguish bursitis due to trauma, crystal deposition disease (gout), or infection Joint x-rays - Joint space narrowing, subchondral sclerosis, marginal osteophyte (spur) formation, subchondral cysts, deformity MRI - is not necessary for most patients with suggestive symptoms of OA however MRI of the knee has a diagnostic role in patients with joint pain and symptoms such as locking, popping, or instability that suggest meniscal or ligamentous damage

CLINICAL FEATURES
LEARNING OBJECTIVES:

OF THE

VASCULITIDES

At the end of this tutorial you should be able to: 1. Define vasculitides 2. Outline the pathogenesis of vasculitides 3. Describe the clinical and laboratory features of the common vasculitides 4. Outline and justify investigations for diagnosis of vasculitides

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DEFINITION: Vasculitis is characterized by inflammation of and damage to blood vessels, compromise of vessel lumen and resulting ischaemia due to an underlying clinicopathological process. PATHOGENESIS: clinical manifestations depend on the size and location of the affected vessel. Most vasculitic syndromes appear to be immunemediated. This may be due to primary or sole manifestation of a disease or secondary to another disease process (1). CLASSIFICATION: Large vessels includes the aorta and its largest branches subclavian, carotid and femoral arteries. o Takayasu arteritis o Giant cell arteritis Medium vessels o Polyarteritis nodosa o Kawasaki disease Small vessels o Churg-Strauss syndrome o Kawasaki disease o Wegeners granulomatosis o Microscopic polyangiitis o Henoch-Schonlein purpura o Mixed essential cryoglobulinaemia o Vasculitis secondary to connective tissue disorders HISTORY: 1. Patients age - mean age at onset for Wegener granulomatosis and polyarteritis nodosa 45 and 50, HSP and Takayasu arteritis 17 and 25, Giant cell arteritis - >60 years. 2. Sex Takayasu and Giant cell arteritis occur primarily in women 3. Vasculitic disorders commonly present with constitutional symptoms: a. Henoch-Schnlein purpura - low-grade fever (38C), purpura, joint pains (usually in the ankles and knees), abdominal pain, bleeding in the digestive tract and boys with HSP often have inflammation of the testicles b. Kawasaki disease - high fever (40C), strawberry tongue and cracked lips, conjunctivitis, irritability, loss of appetite, the peeling of skin from the finger tips c. Polyarteritis nodosa - fever, loss of appetite, weight loss, and pain in the abdomen, joint pain or skin rashes d. Takayasu arteritis - fever, weight loss, pain caused by lack of blood supply such as aching in the legs while walking or cramping sensations in the abdomen after meals e. Wegener's granulomatosis symptoms from the upper respiratory tract, the eyes, ears, kidneys, and skin, recurrent ear infections that are slow to heal, inflammation of the tissues inside the eye, inflamed sinuses, nosebleeds, coughing up blood and saddle nose, which is a deformity caused by the collapse of cartilage inside the nose. The patient may also have joint pains, loss of appetite, skin lesions, and fever.

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4. Past medical history a. Connective tissue diseases are commonly associated with vasculitis (systemic lupus erythematosus, scleroderma, antiphospholipid syndrome, Raynauds disease, dermatomyositis). b. Hepatitic B and C are strongly associated with mixed cryoglobulinaemia. c. infective endocarditis may present with vasculitic lesions(splinter haemorrhages, Roths spots). 5. Medications certain drugs can cause hypersensitivity vasculitis or rash. EXAMINATION: A careful physical examination helps to determine the extent of vascular lesions, the distribution of affected organs, and the presence of additional disease processes. Presence of radial-radial delay with a collapsing pulse suggest Takayasu arteritis as one of the differential causes. Photophobia or reduced vision with tender scalp and jaw suggest Giant Cell Arteritis. Mononeuritis multiplex and palpable purpura are highly suggestive of an underlying vasculitic process. Look specifically for distribution of rash/vasculitis, lymphadenopathy, muscle weakness, diminished peripheral pulses, oral ulcers and any signs of bleeding. INVESTIGATIONS: Laboratory tests help ascertain the type of vasculitis, and the degree and types of organs affected. Basic investigations o CBC low Hb, increased WCC, eosinophilia (in Churg-Strauss syndrome) o Serum urea & creatinine (impaired function in renal involvement) o CPK levels (raised in myopathic disorders) o Liver function test (elevated liver transaminases in viral hepatitis) o ESR/CRP raised due to inflammation o ANA - A positive antinuclear antibody test suggests the presence of an underlying connective tissue disorder, particularly systemic lupus erythematosus o Serum complements level - low serum complement levels may be present in mixed cryoglobulinemia and SLE (low C3/C4) o Viral Hepatitis Serology positive Hepatitis B/C titres in mixed cryoglobulinaemia o ANCA - cANCA strongly suggests a diagnosis of Wegener granulomatosis, while pANCA favuors a diagnosis of microscopic polyangiitis o Urinalysis haematuria, casts, proteinuria o Chest x-ray (pulmonary haemorrhage in Wegeners granulomatosis)

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o Electromyography - useful if a systemic vasculitis is

suspected and neuromuscular symptoms are present, such as a mononeuritis multiplex o Tissue biopsy - biopsy examination of the most clinically involved tissue is essential for diagnosis. o Arteriography - helpful in identifying and characterizing a vasculitis of large and medium-sized arteries, such as polyarteritis nodosa, Takayasu arteritis, and giant cell arteritis with an aortic arch syndrome o Angiograms of mesenteric or renal arteries in polyarteritis nodosa may show aneurysms, occlusions, and vascular wall irregularities o Skin biopsy IgA deposition in HSP

JOINT SWELLING
LEARNING OBJECTIVES: At the end of this tutorial, you should be able to: 1. Define joint swelling 2. Form a differential diagnosis for the aetiology of joint swelling. 3. Outline the causes of joint swelling. 4. Take a history from patients with joint swelling, looking for features which may assist in narrowing the differential. 5. Examine patients with joint swelling to elicit features suggestive of underlying aetiology. 6. Choose and justify appropriate investigations of the patient with joint swelling. INTRODUCTION: Joint swelling is one of the four classical signs of inflammation (heat, pain, redness, and swelling). Joint swelling is commonly accompanied by pain. DIFFERENTIAL DIAGNOSIS: Common o Trauma meniscal tear, fracture, osteonecrosis o Rheumatoid arthritis o Osteoarthritis o Infection bacterial (gonnococcal, meningococcal, tuberculosis, Lyme disease), viral o Gout/pseudogout o Haemarthrosis/hematoma Hemophilia, Sickle cell, Anticoagulants o Neoplastic metastatic disease, osteosarcoma, chondrosarcoma Uncommon o Psoriatic arthropathy o Reiters syndrome o Enteropathic arthritis (inflammatory bowel disease) o Connective tissue disease SLE, MCTD, scleroderma o Sarcoidosis

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HISTORY Musculoskeletal emergencies Hot or swollen joints may suggest infection Constitutional symptoms (high-grade fever, weight loss, malaise) raise the suspicion of infection or sepsis. Weakness may be a symptom of a compartment syndrome or an acute myelopathy. Burning pain, numbness, or paraesthesia with joint swelling may suggest an acute myelopathy, radiculopathy, or neuropathy. Presence of a rash may suggest a vasculitic process including connective tissue diseases (SLE, Rheumatoid arthritis). Take a detailed history on o Symptom onset (sudden or gradual), progression (constant, intermittent, improving or worsening) and duration (acute or chronic). o distribution of swelling, number of joints involved, symmetry o progression of swelling over time o duration and time of onset o associated symptoms pain, redness, warmth, discharge/punctum, joint stiffness, extra-articular manifestations, weakness (suggest neurological or muscle problems) o pain character, quality, time of onset, exacerbating/remitting factors, duration o preceding history of trauma( fracture, meniscal tear, haemarthrosis) and travel history to endemic areas (infective causes-Lyme disease, tuberculosis, parasitic infection) o past medical history previous diagnosis of joints disorder, gout, blood disorder, medications lists, malignancy, GI or genitor-urinary complaints o a history of prior joint pain or swelling (single or multiple, symmetric or asymmetric, migratory or additive, small or large joints) should be ascertained

EXAMINATION General appearance a general inspection of the patient should determine whether the patient is ill or well appearing. Check for temperature and vital signs for any evidence of sepsis. Inspection Enquire patient whether any joint is tender. Assess degree of joint tenderness and tissue swelling. Each joint should be examined in comparison with its symmetrical partner. Look for rash (SLE, infection), at the nails (psoriatic nail changes, splinter haemorrhages in infective endocarditis, clubbing in inflammatory bowel disease), scars, bruises from trauma and discoloration (Raynauds phenomenon). Look for any joint deformity that may suggest RA, OA or psoriatic arthritis. Palpation the initial step in palpation is to detect any changes in the temperature of the skin overlying the affected joint. Increased warmth of the affected joint compared to the unaffected side could indicate inflammation due to infection or rheumatologic disorder. Palpate and locate carefully for any points of tenderness.

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Movement o Active and passive joint movement and the range of movement noted o Joint instability should be sought during passive joint movement Proceed with examination of other systems to determine the cause of the joint swelling.

INVESTIGATIONS: Joint x-ray Patients who presented with prior fall or trauma should have radiographs to rule out a fracture or tumor. Chondrocalcinosis, tophaceous erosions, joint space narrowing, subchondral sclerosis, marginal osteophytes, subchondral cysts can be appreciated on joint radiographs Joint aspiration should be attempted in all patients who have an effusion or signs suggesting inflammation with the joint swelling. The main purpose of synovial fluid analysis is to evaluate whether the effusion is inflammatory, infected, bloody, contains crystals, or is bland (1) Visual inspection for xanthochromia (suggestive of a recent haemorrhage due to a fracture or other trauma, or a coagulopathy), and clear (noninflammatory) versus cloudy fluid (inflammatory) Total leukocyte count and differential Gram stain and culture Crystal analysis utilizing polarizing microscopy Blood investigations The patient with bloody synovial fluid and no evidence of trauma, should have a prothrombin (PT), INR and platelet count. Blood cultures should be performed in patients with signs and symptoms of sepsis Others: ESR &CRP - elevated in infection, inflammatory states, and malignancy. ANA - high sensitivity but low specificity for systemic lupus erythematosus (SLE). Serum dsDNA more specific for SLE Serum rheumatoid factor (RF) positive in rheumatoid arthritis CBC & LFTs - should be considered if a multisystem disease is suspected based upon the history and physical examination. Raised WCC suggests infection and inflammatory causes. Other tests such as HLA-B27 and Lyme serologies should be ordered only when the clinical suspicion is high for a spondyloarthropathy or Lyme infection, respectively.

Examination of patients with Systemic Lupus Erythematosus (SLE) And Scleroderma

1) SLE
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 General inspection and vital signs

Blood pressure (hypertension may result from renal involvement) Temperature (pyrexia can occur due to infection due to leucopenia or due to the systemic inflammation itself) Mental state (neuropsychiatric manifestation is frequent either due to the disease itself or steroids) Weight loss Cushingoid appearance Obvious deformity, postural abnormality or Rashes (especially in sun exposed areas indicating photosensitivity) Scan the patients surroundings and note any walking aids, gloves (raynauds), urine sample

Hands
Look: Nails: Look for signs of vasculitis around the nail bed which may manifest as small punctuate lesions or telangiectasia.

Skin on dorsum: Look for photosensitive rash

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Look for Raynauds Phenomenon (An abnormal responser to cold which manifests as a tricolor change sequentially from white to blue to red. Also look for digital ulcers.)

Skin on palmar aspect: Rashes again Palmar crease pallor Joints for swelling and deformity: Small-joint arthritis of the hands and wrists is most frequent. Jaccouds arthropathy is the term for the nonerosive hand deformities due to chronic arthritis and tendonitis that develop in 10% of patients with SLE. This may mimic rheumatoid arthritis (RA) - ulnar deviation and phalangeal subluxations.

Muscle wasting Palpate the joints making note of tenderness and swelling characteristics Move the joins actively and passively making note of limitation of movement, tenderness and crepitus. Hand function should be tested with active movement.

Arms
Skin: Livedo reticularis (describes a lacy, mottled, erythematous skin pattern that develops in some patients with SLE)

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Purpura (Vasculitis or due to thrombocytopenia) Muscle: Check for proximal myopathy Nerves: Sensory loss due to peripheral sensory neuropathy

Head and neck

Skin and scalp: Look for alopecia which occurs in about 60% of patients. Often affects the temporal regions or creates a patchlike pattern of hair loss, note also the presence of thin, short and broken hairs just above the forehead. These are called lupus hairs. Butterfly rash (erythematous rash over the cheeks and bridge of nose.

Discoid lupus rash: plaquelike lesions with follicular plugging and scarring. They may be part of systemic lupus or may represent discoid lupus without organ involvement, which is a separate diagnostic entity.

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Eyes: Red eyes in SLE can occur due to dryness (Sjogrens), scleritis, episcleritis. Look for signs of anaemia (conjunctival pallor): Usually anaemia of chronic disease Look for signs of jaundice which may occur due to autoimmune haemolysis. Mouth: Oral ulcers may be noted, with palatal ulcers being most specific for SLE. Oral purpura may indicate thrombocytopenia or a sign of vasculitis Palpate for cervical lymphadenopathy Check for cranial nerve lesions (neuropathy)

Chest
Heart: Pericardial friction rub Also look for signs of heart failure due to pericardial constriction or myocarditis (SEE RA TUTORIAL NOTES) Lungs: Look for signs of pleuritis (pleural rub on auscultation), pleural effusion, pulmonary fibrosis, collapse. (SEE RA TUTORIAL NOTES) In a haemodynamically unstable patient with SLE think of pulmonary embolus which may indicate the presence of anti phospholipid syndrome 217

 Abdomen
Abdominal pain in SLE is significant because it may be directly related to active lupus, including peritonitis, pancreatitis, mesenteric vasculitis, and bowel infarction Hepatomegaly Splenomegaly Ascites (Due to nephrotic syndrome)

Lower limbs
Skin: Look again for vasculitic rash. Check also for ulceration over the malleoli or on the toes (Vasculitis) Muscle: Check for proximal myopathy Nerves: Check for sensory loss due to peripheral sensory neuropathy Cerebellar ataxia Hip joint: Avascular necrosis of the femoral head may occur (either due to SLE vasculitis or steroids) leading to tenderness with limitation of movement which spares extension.

2) Scleroderma
General inspection and vital signs
Blood pressure (Hypertension due to renal involvement) Pyrexia (Infection) Weight (Cachexia may result from oesophageal motility disturbance or from malapsorption) Comment on obvious features if present (such as bird like facies)

Hands
Look

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Nails: Look for dilated capillary loops in the nail folds due to Raynauds phenomenon. Skin: Calcinosis ( Palpable calcific nodules in the subcutaneous tissues of the fingers)

Telangiectasia on the fingers Raynau ds phenomenon which can also lead to a) atrophy of the subcutaneous tissues of the pulps of the fingers and b) digital infarcts

Sclerodactyly (Tapering of the fingers due to skin tightening): The skin of the hands may be oedematous or indurated early in the disease, and the patient may initially report this as puffy changes. This oedematous stage precedes the sclerotic stage; longer time to progression to the sclerotic phase indicates a better prognosis. A rapid progression of sclerosis is associated with a worse prognosis and, often, more extensive and aggressive visceral organ involvement with an increased risk of renal crisis development. In the sclerotic phase, the skin may appear tight and shiny, with a characteristic loss of hair, decreased sweating, and loss 219

of the ability to make a skin fold. This process of thickening generally begins distally on the fingers. Structures such as skin creases and dorsal veins begin to fade. The skin induration usually progresses proximally in a continuous symmetrical fashion.

Joints and deformity Joint swelling due to arthropathy of the small joints in the hands Fixed flexion deformity of the fingers due to both arthropathy and skin tightening Palpate the pulps of the fingers for calcific lesions, and palpate the joints for swelling and tenderness Movement is very important actively for the assessment of hand function given the sclerodactyly and flexion deformity. Ask the patient to perform the following test of function: Grip strength (Ask patient to squeeze your first two fingers) Thumb opposition to other fingers Opposition strength (Ask patient to hold piece of paper between thumb and forefinger and prevent you from pulling it free) Key grip Practical tasks like writing and buttoning up shirt

Arms
Skin Check for oedema (early) and skin thickening / tightening (extension of the thickened skin beyond the hands suggests limited scleroderma if it extends only to the elbows and diffuse scleroderma if it extends to the arms and trunk) Pigmentation: Salt and pepper pigmentation Vitiligo 220

 Muscle: Check for proximal myopathy

Head and neck

Scalp: Alopecia Face: General appearance can sometimes be described as bird like due to skin thickening with beaking of the nose, puckering of the mouth, and loss of normal skin folds

Ask the patient to close their eyes: This may be incomplete due to skin tightening Ask the patient to open mouth: Abnormal restriction is defined by inability to achieve 3cm between incisors (microstomia) Skin:

Scleroderma: facial changes Telangiectasia

Malar telangiectasia Eyes: Loss of eyebrows Red eyes: Dryness due to associated Sjogrens syndrome 221

 Look also for conjunctival pallor (anaemia due to chronic disease, haemolysis, GI bleeding from oesophagitis or drugs) and jaundice (Haemolytic anaemia).

Chest
Heart: Look for signs of pericarditis Right heart failure may occur due to cor pulmonale secondary to pulmonary fibrosis. Look for pedal oedema, elevated JVP, Loud pulmonary second heart sound, pericardial friction rub. Left heart failure suggests myocardial involvement by the disease itself. Check for bibasal crackles on auscultation of the lung fields. Lungs: Check for signs of pulmonary fibrosis

Lower limbs
As in upper limbs examine the skin for evidence of vasculitis including rash and ulcers Check for skin tightening. Check for proximal myopathy

Clinical cases
Case 1
A 40-year-old woman with a 2-year history of Raynaud's phenomenon presented because the skin on her hands was beginning to feel tight. Five weeks earlier, her hands had been swollen, erythematous, and pruritic, but these symptoms resolved without treatment. The patient also described flu like symptoms during this same period of time. The review of systems was significant for slight dyspnoea without chest pain, heartburn, difficulty swallowing pills, bloating, and abdominal distension.

Case 2
A 19-year-old female was admitted to hospital with dyspnoea, easy fatigability, palpitations, anorexia, weight loss, dry cough and episodic attacks of fever every three to four months with night sweats for the last two years. Five days prior to admission she developed pain in various large and small joints with swelling in interphalangeal and right wrist joints and described features of Raynaud's phenomenon.

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