Sheet Abeer.pdf

Prepared by:

MBBS (U.OF.K) MRCP (Part1and 2) Medical Registrar (SMSB)

‫بـســم هللا الرحـمـــن الرحــيــم‬

‫قال تعالى‪:‬‬ ‫(وعلم آدم األسماء كلها ثم عرضهم على المالئكة فقال أنبئوني بأسماء هؤالء إن‬ ‫كنتم صادقين* قالوا سبحانك ال علم لنا اإل ما علمتنا إنك أنت العليم الحكيم )‬ ‫سورةالبقره‪32-31:‬‬

‫( ويسئلونك عن الروح قل الروح من أمر ربي وما أوتيتم من العلم إال قليالا )‬ ‫سورة اإلسراء‪58 :‬‬

‫( وقل رب زدني علما ا )‬ ‫سورة طه‪111 :‬‬

‫شكوت إلى وكيع سوء حـفـظي‬

‫فأرشدني الى ترك المعاصى‬

‫و أخــبـرني بأن العـــــلم نـــور‬

‫و نـور هللا ال يهـدى لـعـاص‬ ‫اإلمام الشافعى‬

‫‪Synopsis of Bedside Teaching: Dr.Abier Luai Atabani‬‬

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Dedication

To my dearest mother... Igbal Hassan Shafig Who helped and supported me by every means a person can be supported… Who sacrificed her career to look after my children … And without her love, care and advice, it would have been virtually impossible for me to continue my postgraduate studies.

To the soul of my beloved father… Dr. Luai Ahmed Atabani Who taught me medicine from its principles and ethics to its practice … Who helped me to defy the tough road of medicine and continued to do so till the day he left … Who gave me a reason to work hard, a reason to struggle, a reason to succeed, a reason to continue what he had begun and a reason to be distinguished as he was…

To my dear husband … Dr. Mustafa Alhakeem For his patience and enormous help and support.

To my lovely adorable sweet children… Luai & Lubna You are the reason I work hard …

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Acknowledgements

I would like to express great appreciation and gratitude for Professor. Mohamed Osman Mekki, an eminent Professor of Medicine, for encouraging me to write this book and suggesting its title, forrevising thoroughly and meticulously every chapter in this book and for his constructive suggestions, comments and advices. Without his encouragement, help and support it would have been virtually impossible for me to prepare such a book.

Dr. Abier Luai Atabani

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Sayings of the great

Medicine is not only a science; it is an art. It does not consist of compounding pills and plasters; it deals with the very processes of life, which must be understood before they may be guided. Paracelsus (1493 - 1541)

To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all. Sir William Osler (1849 - 1919)

For one mistake made for not knowing, ten mistakes are made for not looking. JA Lindsay

Medicine is learned by the bedside and not in the classroom. Sir William Osler

The best physician is the one who is able to differentiate the possible and the impossible. Herophilusof Alexandria

Experience is never limited, and it is never complete. Henry James

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Contents

Title History taking The cardiovascular system The respiratory system The gastrointestinal system The nervous system References

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Page 1 15 25 39 59 90

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

History Taking First of all you must introduce yourself to the patient, offer a greeting and take permission for history taking and clinical examination.

Demographic Data: Name: Marital Status:

Age:

Occupation:

Gender: Original home: Date of Admission:

Residence:

C/O: (same words of the patient and duration in a chronological order) History of presenting illness: 1. 2. 3. 4.

Full analysis of complaint The Story Similar Condition Complete the System

Review Of the systems: The Alimentary system: 1- Appetite: Increased: Decreased: Normal: If Decreased why? Lack of desire to eat (anorexia)?

Or eating causes pain?

2- Weight: Increased: Decreased: No change: If decreased, how much? (Clothes, people noticed, previous weight records): How quickly: (Significant weight loss: > 3kg in 6 months). 3- Painful mouth: (sore lips, tongue or buccal mucosa) 4- Xerostomia(dry mouth): 5- Halitosis (bad breath): 6- Globus (sensation of a lump in the throat): 7- Odynophagia (pain on swallowing): 1|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

8- Water brash (sudden appearance of excessive saliva in the mouth): 9- Dysphagia (difficulty in swallowing and sensation of something sticking in the throat or chest):  Is it Painful or painless?  Intermittent or progressive?  Duration:  Is it for solids, liquids or both?  Level at which food sticks:  Is there complete obstruction and regurgitation?  Previous history of dysphagia or heartburn: 10- Heartburn (hot, burning retrosternal discomfort which radiates upwards): What makes it happen?(Lying flat at night, bending or stooping) 11- Acid reflux (regurgitating gastric acid producing a sour taste in the mouth): 12- Dyspepsia (indigestion) : (epigastric pain, heartburn, distension, nausea or an acid feeling occurring after eating or drinking) 13- Hiccups(repeated sudden diaphragmatic contraction triggered by upper gastrointestinal irritation or brainstem disease): 14- Vomiting:  Frequency:  Volume:  Nature (recognizable food, digested food, clear acidic fluid, bile stained, blood stained or faeculent):  Is it preceded by nausea or does it occur without warning?  Associated symptoms (dyspepsia or abdominal pain):  Is it related to meal times, early morning or late evening?  Is it projectile? (Gastric outlet obstruction, high small bowel obstruction or raised intracranial pressure)  What medications has the patient been taking? 15- Haematemesis (vomiting of blood):  Frequency:  Volume:  Fresh blood or dark brown (coffee grounds):  Mixed with food or frank Blood:  Past history of dyspepsia or peptic ulceration: 2|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

      

Past history of liver disease: History of alcohol, NSAIDs or corticosteroid ingestion: Past history of gastrointestinal bleeding: Has the patient been admitted and received blood? Was the haematemesis preceded by intense retching? Was blood staining of the vomitus apparent in the first vomit? Recent nose bleed (swallowed blood):

16- Melaena: (passage of black tarry stool with a characteristic odour, due to partially digested blood) 17- Abdominal pain:  Site:  Time & mode of onset (sudden/gradual):  Severity: (effect of pain on Patient’s life; stop him/her from going to work? wake him/her at night? stop him/her going to sleep? force him/her to lie still or roll around? did he/she use analgesics?)  Nature or character:  Progression: (onset, course, end)  End of the Pain (ends spontaneously or as a result of action by patient or doctor): (Sudden/gradual):  Duration (from onset to end): *If it comes and goes; length of the period of pain and pain free:  Radiation:  Aggravating Factors:  Relieving Factors:  Associated Symptoms: 18- Flatulence (excessive wind): 19- Abdominal distension:  Progression:  Is it Constant or variable?  Is it Painful or painless?  Does it affect respiration?  Is it relieved by belching, vomiting or defecation? 20- Altered bowel habit: (normal bowel movement frequency ranges from 3 times/day to once every 3 days) a) Constipation:(Infrequent passage of hard stools; <3 times/week)  Frequency of defecation: 3|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

   

Consistency of stools: Onset: (recent change in bowel habit or chronic): Is it accompanied by abdominal pain, anal pain on defecation or prolonged straining? Associated symptoms: (Rectal bleeding, mucous discharge, tenesmus or weight loss)  Is there diarrhoea alternating with constipation?  Has the shape of the stool changed (pellet- like)?  What drugs has the patient been taking?

b) Diarrhoea:(Frequent passage of loose stools ;3 or more/ day)  Frequency:  Consistency (watery/semisolid):  Onset: (acute, chronic or intermittent):  Volume: (large/small)  Is there blood, mucus or pus?  Specific Gravity: (is it difficult to flush?)  Is there tenesmus, urgency or incontinence?  Does diarrhoea disturb sleep?  History of contact with diarrhoea patient:  History of travel:  Other people affected in household:  Does the sexual history provide a clue? (HIV)  History of alcohol abuse/drugs:  Past history of GI surgery, GI disease or IBD:  Family history of GI disorder (coeliac/Crohn’s disease):  Associated symptoms (abdominal pain, vomiting, fever or arthralgia): 21- Rectal Bleeding:  How much:  Is it mixed with stool, on the surface of stool or after passing stool?  Is there Mucous/Pus?  Is defecation painful?  If painful, when? (Before, during, after)  Is the patient passing more gas than usual? 22- Jaundice:  Is it progressive or intermittent?  Is there skin itching?  What is the colour of urine?  What is the colour of stool?  Accompanying symptoms (abdominal pain, loss of appetite, fever, vomiting):  Is it associated with weight loss? 4|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

  

    

Past history of blood transfusion, surgical operations, intravenous drug abuse or tattooing: Sexual and contact history: Drug history: (Paracetamol overdose, INH, Rifampicin, Pyrazinamide, Statins, Sodium valproate, Monoamine oxidase inhibitors, Halothane, fungal toxins and carbon tetrachloride). Alcohol intake: how many units/day? For how long? History of travel and immunizations (hepatitis A): Past history of jaundice: When? How long did it last? Past history of hepatitis: Family history of jaundice:

The Cardiovascular system: 1- Chest Pain:  Site:  Time & mode of onset:  Severity:  Nature:  Progression:  End of pain:  Duration:  Aggravating factors:  Relieving factors:  Radiation:  Associated Symptoms: 2- Dyspnoea:  Mode of onset: (sudden/gradual)  Progression: (rapid/slow)  Duration:  Severity:  Exertional: (what exercise precipitates it? how many stairs? how far can he/she walk):  Does it occur at rest?  Is there orthopnoea? If yes, how many pillows needed at night?  Is there Paroxysmal Nocturnal Dyspnoea? (Wake up at night short of breath): 3- Exertional fatigue: 4- Palpitation:  Onset (abrupt/gradual):  Termination (abrupt/gradual, spontaneous or by medication): 5|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

       

Frequency: Duration: Precipitating factors: (anxiety, stress, alcohol, caffeine or recreational drugs) Relieving factors: (breath-hold, exercise) Rhythm (Regular/Irregular): (ask patient to tap it out) Rate (rapid/slow): Sensation of missed or dropped beats: Associated symptoms: (dizziness, syncope, chest pain or S.O.B)

5- Dizziness &Syncope (light headedness/fainting/falling down): 6- Lower limb swelling:  Site:  When? (In the morning or at the end of the day):  What is the effect of bed rest or elevation of the leg on the swelling?  Progression: 7- Peripheral Vascular Symptoms: a. Pain in the limb on exercise(intermittent claudication):  Site (calf, thigh or buttocks):  How far can he/she walk before pain begins (claudication distance)?  Severity (force him/her to stop):  Duration (of the Pain to wear off):  Can he/she walk the same distance again? b. Pain in the limb at rest:  Site:  Severity (Interfere with sleep):  Relieving Factors (hanging the leg out of bed/ getting up and walking around):  Are the extremities cold?  Colour changes in the skin (In response to a cold environment):  Paraesthesia in the limb (tingling or numbness):  Paralysis:

The Respiratory System: 1. Breathlessness: Same as CVS, in addition to:  Is there variability in the symptom? (good days and bad days)  Is it worse during the day or at night?

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani



 2. Cough:

Triggering/ precipitating/aggravating factors:{exercise, allergens (house dust mites, cats, pigeons, dogs, horses, grass pollens),smoke, perfumes, fumes, cold air anddrugs (Aspirin, NSAIDs)} Associated symptoms (Wheeze, cough and chest pain):

   

For how long? (days or weeks)

 

Frequency (how often):

Is it dry or productive? Is it worse during the day or night?

Aggravating factors: (dust, fumes, pollen or cold air) 3. Sputum:  Amount: small (teaspoonful) or large (cupful)  Colour (white, yellow, green):  Consistency (serous, mucoid, purulent, mucopurulent, rusty, very thick):  Smell: 4. Haemoptysis:

 

Duration: Amount: Nature (frank blood, blood stained,blood streaked,rusty,pink-frothy):



Associated conditions (bleeding per gums, epistaxis or melaena): 5. Chest Pain: (Same as CVS) 6. Wheezing: 7. Other symptoms (ENT):  Recurrent sinusitis/rhinitis:  Hoarseness of voice:

The Genitourinary System: 1.

Pain:           

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Site (loin, groin or suprapubic): Time & mode of onset: Severity: Nature: Progression: End of pain: Duration: Radiation (iliac fossa, testicles, labia): Aggravating factors: Relieving factors: Associated symptoms: Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

2. Haematuria:  When (beginning of micturition, full stream or terminal):  How often (continuous or intermittent):  Is it associated with pain? 3. Frequency of micturition: (Day/night ratio): 4. Volume of Urine:  How much: (Polyuria, oliguria or anuria)  Colour: 5. Dysuria (burning micturition): When (before, during or after micturition): 6. Urgency (inability to postpone urine): 7. Incontinence (involuntary passage of urine): 8. Hesitancy (difficulty in initiating micturition): 9. Terminal dribbling: 10. Stream (weak/good): 11. Urethral discharge: 12. Others (symptoms of uraemia): (Headache, vomiting, visual disturbances, fits, drowsiness, oedema‘‘lower limbs or periorbital’’ )

The Nervous System: 1. Episodic loss of consciousness: a) Syncope:(transient loss of consciousness) (Patients may use terms such as: blackout, faint, dizzy spells or funny turns)  Where the attack has taken place?  What are the triggering factors? (pain, emotional upset, unpleasant sights, exercise or change in position from lying or sitting to standing)  Are there any warning symptoms? (light-headedness, tinnitus, nausea and blurring of vision)  Duration of the attack:  Frequency:  What happens during the attack? (ask a witness): Incontinence of urine: Body stiffening: Brief twitching of the limbs (abnormal movements):  Skin colour during the attack: (pale)  How quickly the patient recovers?  What induces recovery? (lying flat)  Are there any associated symptoms (palpitations, chest pain, dyspnoea)?

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

b) Seizures: 





  

What type of seizures? (ask the patient and a witness)  Primary generalized: (tonic- clonic, tonic, myoclonic, atonic, absence)  Secondary generalized:  Partial: (motor, sensory, complex) What are the triggering factors? (sleep deprivation, alcohol withdrawal, recreational drug misuse, physical and mental exhaustion, flickering lights: TV/computer screens and intercurrent infections) What happens before, during and after the seizures?  Pre-ictal: aura: {alterations of mood, memory and perception such as: undue familiarity (déjà vu) or unreality (jamais vu), hallucinations (auditory, olfactory, visual or gustatory), emotional changes (fear, sexual arousal) or visceral sensations (nausea, epigastric discomfort)}.  Ictal: (tongue biting, frothing, upward rolling of eyeballs, cyanosis and loss of sphincteric control)  Post-ictal: (confusion, headache, sleeping and amnesia) Duration of the seizures: Frequency: If multiple, did the patient regain consciousness between the attacks?

2. Persistent loss of consciousness: (coma)  Mode of onset:  Any precipitating events: {drug overuse, alcohol, history of (diabetes, hypothyroidism, renal/hepatic/respiratory disease), trauma, history of (hypertension, ischaemic heart disease, previous stroke, atrial fibrillation, epilepsy), any preceding febrile illness}. 3. Dizziness and vertigo : (feeling of spinning of the patient or surroundings due to abnormal perception of movement) 4. Disorders of movement: a) Negative symptoms: (motor weakness, lack of co-ordination, lack of stability and body stiffness).  Motor weakness: ask about:  Site: {a few muscles, a limb, both lower limbs (paraparesis), both limbs on one side (hemiparesis) or all limbs (quadriparesis)}.  Onset (gradual/sudden): What time of the day? What was he/she doing?  Progression (slow/rapid): How did it occur? (In one limb then involved the others)? After how long it reached the maximum? 9|Page

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

For how long it remained steady? When did it begin to improve?  Associated Symptoms: o In cases of paraplegia: {Numbness, lower limb pain, backache, history of recent trauma to the back, sphincteric disturbances, weakness of abdominal muscles (patient cannot roll from side to side), upper limb weakness, neck pain/stiffness/weakness and vaccination or infections ( diarrhoea, upper respiratory tract infection or any febrile illness) preceding the weakness}. o In cases of hemiplegia: {headache, vomiting, blurring of vision, seizures and loss of consciousness}  Past history of: Similar condition, transient ischaemic attack (transient loss of vision: amaurosisfugax), back trauma and chronic cough or contact. b) Positive symptoms: (abnormal movements such astremor, chorea, athetosis, hemiballismus, dystonia, myoclonus and tics).

5. Sensory Symptoms: a/ Abnormal sensations (tingling, paraethesia ‘‘pins and needles’’, pain): b/ Loss of normal sensations (touch, pain, temperature): 6. Headache:  Time and mode of onset:  Frequency & Periodicity:  Duration:  Time of the day(morning,night):  Precipitating Factors:  Aggravating & Relieving Factors:  Where does it start and how does it evolve:  Quality & severity:  what is the effect of posture, coughing and straining?  Symptoms preceding the headache (aura): {focal neurological symptoms e.g.: zigzag (fortification spectra), spreading scintillating scotoma or senosory symptoms (tingling sensation over part of the body)}.  Associated symptoms: (nausea, vomiting, photophobia, phonophopia, fever, rash, neck stiffness)  Family History of Headache:  Other medical or neurological problems:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

7. Symptoms suggestive of raised ICP: Early morning vomiting, blurring of vision, headache and seizures 8. Symptoms of cranial nerves affection: I: (Anosmia): II: (Decreased visual acuity, field defects): III, IV, VI: (Diplopia) V: Difficult mastication (motor): Abnormal face sensation (Sensory): VII: (Accumulation of food behind cheeks, mouth deviation): VIII: (Decreased hearing, tinnitus and vertigo): IX, X, XI, XII: (Dysphagia, dysarthria, dysphonia and nasal regurgitation): 9. Symptoms of autonomic disturbances:  Sphincteric Disturbances: (difficulty in initiating micturition, overflow incontinence, frequency, urgency, urge incontinence, incomplete bladder emptying,constipation or faecalincontinence ).  Fainting or falling down when standing (postural hypotension):  Erectile dysfunction: 10. Higher Functions: Memory:

Behaviour:

Orientation:

11. Speech disorders: Aphasia: Dysarthria: Dysphonia:

The Musculoskeletal System: 1. Joints:  Joint pain:  Swelling:  Stiffness: *Time: (early morning or comes at rest and disappear with activity) *Associated symptoms: (redness, warmth, tenderness, swelling, fever, and sweating)  Restriction of movement: 2. Soft tissues:(muscles, tendons, ligaments) Pain: Swelling: 3. Bone: Pain:

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History of injury or overuse:

History of injury:

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

4. Skin: Rash:

Itching:

Hypo/hyperpigmentation:

Endocrine system: 1) Thyroid:  Weight loss: Weight gain:  Heat intolerance: Cold intolerance:  Muscle weakness:  Excessive sweating: Tremor:  Visual disturbances (diplopia, decreased acuity):  Loose stools: Constipation:  Dysphagia: S.O.B:  Neck pain: Neck swelling:  Oligo/amenorrhoea: Menorrhagia:  Dry/yellow skin:  Vitiligo:  Family history:

Palpitation:

2) Pancreatic islets:  Polyuria: polydipsia:  Weight loss:  Impotence:  Family history:  Symptoms of hypoglycaemia (palpitation, sweating, tremor, decreased consciousness, tinnitus): 3) Adrenal glands:  Weight loss: Weight gain:  Muscle weakness:  Postural unsteadiness:  Nausea: Vomiting:  Amenorrhoea:  Skin hyperpigmentation: Vitiligo:  Excess hair growth: 4) Hypothalamus/pituitary:  Polyuria: Polydipsia:  Impotence:Gynaecomastia:  Galactorrhoea: Amenorrhoea:  Visual field defects (type):  Delayed puberty (absence of secondary sexual characters):

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

5) Parathyroid:  Paraethesia (pins and needles):  Polyuria:Polydipsia:  Family history of renal stones: 6) Gonads:  Impotence  Galactorrhoea: Amenorrhoea:  Delayed puberty:

Gynecological history:       

Menarche: Katamine: Regularity: Dysmenorrhoea: Contraceptives: Vaginal discharge: Menopause:

Past medical history: (If positive: ask about: duration, medications, regular follow up, any complications)         

Diabetes mellitus: Hypertension: Bronchial asthma: Cardiac/renal diseases: Others: Hospitalization: Surgical operations: Jaundice: Blood transfusion:

Family history:     

Diabetes mellitus: Hypertension: Similar condition: Cardiac/renal disease: Others:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Social history:     

Smoking:(type, frequency, quantity and duration) Alcohol consumption: (type, quantity and duration) Tobacco dipping: Socioeconomic status: Housing conditions: (when relevant)

Drug history:   

Long term medications: Current medications: Allergy to any known drug/food:

Summary:      

Age: Gender: Past medical problems: Presenting complaint: Important positives and negatives: Medications:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

The Cardiovascular System History & Examination First of all you must introduce yourself to the patient, offer a greeting and take permission for history taking and clinical examination.

History: Demographic Data: Name, Age, Gender, Original home, Residence, Marital Status, Occupation, Date of Admission.

C/O: (same words of the patient and duration in a chronological order: e.g.: lower limb swelling / 5 days , shortness of breath / 3days and chest pain / 1 day)

History of presenting illness: (1- Full analysis of the complaint 2- The story 3- Similar condition 4- Complete the system)

1. Chest pain: ( myocardial ischaemia/infarction, pericarditis, aortic dissection)           

Site: Time & mode of onset: Severity: Nature: Progression: End of pain: Duration: Aggravating factors: Relieving factors: Radiation: Associated Symptoms:

e.g.: 

Myocardial ischaemia (Angina): severe retrosternal chest pain, constricting/ gripping/ crushing in nature (or just tightness or heaviness), radiates to arms/ throat/ jaw, provoked by exercise or cold weather and relieved by rest or sublingual nitrates. Duration: 2 to 10 minutes.



Myocardial infarction: same as angina but the pain is more severe, more prolonged and not relieved by rest or nitrates. It is associated with restlessness, shortness of breath, sweating, nausea, vomiting and feeling of impending death (autonomic stimulation).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani



Pericarditis: central chest pain, sharp/ stabbing in nature, aggravated by deep inspiration/cough/ change in posture and relieved by leaning forward and NSAIDs.



Aortic dissection: very severe tearing chest pain, of abrupt onset, radiates to the back between the scapulae. May be associated with sweating and syncope.

2. Dyspnoea: (abnormal awareness of breathing at rest or minimal exertion) a. Exertional: (what exercise precipitates it? how many stairs? how far can he/she walk?): b. At rest: c. Orthopnoea (dyspnoea on lying flat): (how many pillows the patient uses to feel comfortable?) d. Paroxysmal Nocturnal Dyspnoea (PND): (patient wakes up at night with distressing dyspnoea (gasping for air) and fear of imminent death, usually associated with cough and frothy, blood stained sputum).

3. Exertional fatigue: 4. Palpitation: (unexpected awareness of heart beats) o Onset (abrupt/gradual): o Termination (abrupt/gradual, spontaneous or by medication): o Frequency: o Duration: o Precipitating factors: (anxiety, stress, alcohol, caffeine or recreational drugs) o Relieving factors: (breath-hold, exercise) o Rhythm (Regular/Irregular): (ask patient to tap it out) o Rate (rapid/slow): o Sensation of missed or dropped beats: o Associated symptoms: (dizziness, syncope, chest pain or S.O.B suggest ventricular arrhythmias) e.g.: Types of palpitation: a. Normal sinus rhythm: occurs in healthy people, precipitated by anxiety, physical stress, excessive caffeine intake (tea, coffee, and cola) or nicotine. (rapid and regular). b. Intermittent irregularities of heart beats (extrasystoles/ectopics): sensation of missed or dropped beats followed by a strong beat, occurs at rest and abolished by exercise. c. Sustained arrhythmias: starts suddenly, lasts for minutes or hours and not usually triggered by anxiety or stress. e.g.: Atrial fibrillation: (rapid, irregular, heart jumping or racing) Supraventricular/ventricular tachycardia :( rapid, regular, heart racing/fluttering)

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

5. Dizziness & Syncope: (Dizziness: light- headedness) (Syncope: fainting with loss of consciousness) Cardiac causes: i. Arrhythmias: sick sinus syndrome, AV block (Stokes-Adams attacks) and ventricular tachycardia. ii. Mechanical obstruction to cardiac output: severe AS, HOCM.

6. Lower limb swelling: o o o

Site: When? (In the morning or at the end of the day): What is the effect of bed rest or elevation of the leg on the swelling? o Progression:

7. Peripheral Vascular Symptoms: a. Pain in the limb on exercise (intermittent claudication):  Site (calf, thigh or buttocks):  How far can he/she walk before pain begins (claudication distance)?  Severity (force him/her to stop?):  Duration (of the pain to wear off):  Can he/she walk the same distance again? b. Pain in the limb at rest/night: o Site: o Severity (Interfere with sleep): o Relieving factors (hanging the leg out of bed/ getting up and walking around): o Are the extremities cold? o Colour changes in the skin (in response to a cold environment): o Paraesthesia in the limb (tingling or numbness): o Paralysis:

Past medical history: HTN, DM, dyslipidaemia (risk factors for coronary artery disease), rheumatic fever in childhood (valvular heart disease), renal disease and thyrotoxicosis (AF). *If infective endocarditis is suspected, ask about: recent dental work, skin infection, penetrating trauma or IV drug abuse.

Family history: HTN, DM, familial hypercholesterolaemia, IHD and HOCM (history of sudden unexpected death at a young age). 17 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Social history: o

Smoking: how many cigarettes per day? If ex-smoker: age at starting and stopping? o Alcohol abuse (cardiomyopathy, arrhythmias): type of alcohol: quantity:

Duration: How many cigarettes per day? duration:

Drug history:       

Beta- blockers: bradycardia and exacerbation of heart failure (dyspnoea) Verapamil and diltiazem: bradycardia Nifedipine and amlodipine: lower limb oedema Thyroxine, beta agonists (salbutamol) and tricyclic antidepressants (TCA) lead to tachycardia. Nitrates, alpha blockers and ACE inhibitors: dizziness and syncope. Cytotoxic drugs (doxorubicin) lead to cardiomyopathy. NSAIDs: exacerbate heart failure (dyspnoea), aggravate angina and may cause lower limb oedema.

Clinical examination: 1) Inspection of the patient: a. General appearance: (Unwell? Breathless? Distressed? Cyanosed?) Body built: Marfan's/ other syndromes: b. Hand :  Finger clubbing:  Splinter haemorrhages: (multiple linear reddish-brown marks along the axis of finger/toe nails due to circulating immune complexes)     

Osler’s nodes: (tender erythematous nodules on the finger pulps) Janeway lesions: (painless erythematous lesions on the palm) Tobacco staining: Tremor: Skin temperature:

2) Examination of the pulse: a. Rate: (normal rate is 60 – 100 beats/min)  Tachycardia is a pulse rate > 100 beats/min: i. Sinus: (anxiety, exercise, fever, pain, hyperthyroidism or drugs: symathomimetics/ vasodilators) ii. Arrhythmia: (atrial fibrillation, atrial flutter, supraventicular/ ventricular tachycardia) 18 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani



Bradycardia is a pulse rate < 60 beats/min: i. Sinus: (sleep, athletes, hypothyroidism or drugs: beta blokers, digoxin, verapamil and diltiazem) ii. Arrhythmia: (carotid sinus hypersensitivity, sick sinus syndrome, second degree and complete heart block)

b. Rhythm: (regular , irregular) e.g.:

 

 

Occasional irregularity: due to premature beats which occur earlier than expected, weak and followed by a long pause then a forceful beat. Regularly irregular: premature beats occurring at regular intervals for example every normal beat is followed by a premature beat (bigeminy) or 2 normal beats are followed by a premature beat (trigeminy). It is due to digoxin toxicity. Irregularly irregular: atrial fibrillation ( calculate the pulse deficit which is the difference between pulse rate and heart rate) Sinus arrhythmia: pulse rate is faster during inspiration and slower during expiration (occurs in children ,young adults and athletes)

c. Volume: (means the degree of pulsation and reflects the pulse pressure): *large: (exercise, pregnancy, fever, thyrotoxicosis, anaemia, aortic regurgitation, hypertension and Paget's disease of bone). *small: (left ventricular failure, hypovolaemia and peripheral vascular disease) d. Character: (means the waveform or shape of the arterial pulse)  Slow rising: (gradual upstroke with a reduced peak occurring late in systole): aortic stenosis  Collapsing (water- hammer): (early peak followed by a rapid descent): aortic regurgitation  Pulsus bisferiens (biphasic): 2 systolic peaks are palpaple in one pulse (mixed aortic valve disease)  Jerky pulse: hypertrophic cardiomyopathy  Pulsus alternans: a strong beat alternates with a weak beat (severe left ventricular failure)  Pulsus paradoxus: a fall in systolic blood pressure > 10 mmHg during inspiration. It is an exaggeration of the normal variability of pulse volume with the respiratory cycle. Occurs in cardiac tamponade and severe bronchial asthma. e. Synchronicity: f. Radiofemoral delay: (coarctation of aorta) g. Peripheral pulses:

3) Measurement of blood pressure:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

4) Examination of the face:  Xanthelasma: (yellow- orange plaques around the eyelids and periorbital area due to high cholesterol)  Corneal arcus: (a creamy yellow discolouration at the boundary of the iris and cornea caused by precipitation of cholesterol crystals)  Pallor:  Central cyanosis:  Malar flush: (cyanosis over malar area in mitral stenosis)  Fundoscopy: i. Roth spots (flame-shaped retinal haemorrhages with a cotton-wool centre) seen in infective endocarditis. ii. Hypertensive retinopathy: iii. Diabetic retinopathy:

5) Examination of the neck: 



Carotid pulsations: are not normally apparent on inspection of the neck but may be visible (Corrigan's sign) in conditions associated with a large-volume pulse: (thyrotoxicosis, anaemia, fever and aortic regurgitation). *listen for carotid bruit. Jugular venous pressure (JVP): *How to differentiate jugular from carotid pulsation?  Has an upper limit.  Wavy inward movement.  2 venous pulsations (peaks) for each heart beat.  Not palpable.  Disappears when the base of the neck is compressed.  Varies with respiration and position of the patient.  Rises with pressure over the right upper abdomen (hepatojugular reflux). *How to measure it?  JVP is the vertical distance in centimetres between the top of the venous pulsation and the sternal angle. Normally it is 3 - 4 cmH2 O. It reflects the right atrial pressure which is equivalent to: JVP + 5 (5 cm is the distance between sternal angle and right atrium), so normal right atrial pressure is 8 – 9 cmH2 O. *What is the waveform of the JVP?  {a} wave: is due to atrial systole  {c} wave: is due to tricuspid valve closure  {x} descent : due to descent of the tricuspid valve ring during ventricular systole

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 {v} wave: is due to right atrial filling during ventricular systole  {y} descent: is due to opening of tricuspid valve and ventricular filling *Abnormalities of JVP:  Raised: in congestive heart failure, constrictive pericarditis, cardiac tamponade, pulmonary embolism/COPD (cor pulmonale), superior vena caval obstruction and iatrogenic fluid overload in surgical and renal patients.  Prominent {a} wave: tricuspid stenosis (TS) and pulmonary HTN.  Cannon waves: (giant "a" wave) seen in complete heart block (irregular Cannon) and ventricular tachycardia (regular cannon). (due to atrial contraction against a closed tricuspid valve).  Absent {a} wave: atrial fibrillation.  Giant {v} wave: tricuspid regurgitation (TR)  Prominent {x} and {y} descent: constrictive pericarditis  Kussmaul’s sign: a paradoxical rise of JVP during inspiration (constrictive pericarditis, cardiac tamponade and restrictive cardiomyopathy).

6) Examination of precordium: a. Inspection:  Chest deformities: (pectus excavatum, pectus carinatum): may displace the heart.  Scars: (midline sternotomy indicates coronary artery bypass surgery or aortic valve replacement, left submammary indicates mitral valvotomy, infraclavicular indicates pacemaker implantation).

 

Visible pulsations: Prominent veins : (superior vena caval obstruction)

b. Palpation: i. Apex beat: (is the lowermost outermost part of the precordium at which the cardiac impulse can be distinctly felt). *comment on location and character:  Normal apical impulse: is in the 5th left intercostal space at, or medial to, the midclavicular line. It is localized.  Displaced apex (downwards and laterally): due to left ventricular dilatation (aortic stenosis, severe hypertension and dilated cardiomyopathy), chest deformities and mediastinal shift: (massive pleural effusion, tension pneumothorax).  Impalpable apex: (overweight/muscular people, patients with emphysema or asthma, pericardial/pleural effusion and dextrocardia).  Tapping apex: is a palpable first heart sound, occurs in mitral stenosis (MS).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani





Heaving apex: is a palpable impulse that lifts the finger noticeably: a) ill – sustained heave: lifts the finger for a short period, due to volume overload (mitral and aortic regurgitation). b) well- sustained heave (thrusting): lifts the finger for a longer period due to left ventricular hypertrophy (aortic stenosis and hypertension). Double apical impulse: in hypertrophic obstructive cardiomyopathy.

ii.

Left parasternal heave: due to right ventricular hypertrophy (secondary to pulmonary hypertension) or left atrial enlargement.

iii.

Second heart sound (S2): pulmonary component (P2 ) palpable in pulmonary HTN. Aortic component (A2 ) palpable in systemic HTN

iv.

Thrill (palpable murmur): comment on: *Timing with carotid pulsation: systolic (with carotid pulse), diastolic (alternates with carotid pulse). *Location: (apex, lower sternum, pulmonary area, aortic area and neck) e.g.: aortic stenosis: systolic thrill palpable at the aortic area and radiates to the neck. Ventricular septal defect: systolic thrill best felt at the left sternal border.

c. Auscultation: i. Heart sounds :  First heart sound (S1): is caused by closure of the mitral and tricuspid valves at the onset of systole, best heard at the apex. *comment on intensity : (normal, loud , soft)  Soft S1: (mitral regurgitation, low cardiac output and poor left ventricular function)  Loud S1: (mitral stenosis, increased cardiac output and atrial myxoma)  Variable intensity: (complete heart block and atrial fibrillation). 

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Second heart sound (S2): is caused by closure of the aortic and pulmonary valves at the end of systole, best heard at left sternal edge. *comment on intensity and splitting:  Soft S2: (calcific aortic stenosis, aortic regurgitation and low cardiac output)  Loud S2: systemic hypertension (aortic component) and pulmonary hypertension (pulmonary component).  Splitting: (physiological, fixed, reverse) o Physiological: occurs during inspiration and disappears during expiration because the aortic valve closes before the pulmonary valve. o Wide (enhanced physiological splitting): (wide in inspiration and disappears during expiration), occurs in: RBBB, pulmonary HTN and ventricular septal defect.

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

o

Fixed: occurs during inspiration and expiration (ASD) *reverse: occurs during expiration and disappears during inspiration (LBBB, severe AS, hypertrophic cardiomyopathy and right ventricular pacing).



Third heart sound (S3): low- pitched early diastolic sound due to rapid ventricular filling. It is either physiological (in children, young adults and during pregnancy) or pathological (left ventricular failure and mitral regurgitation).



Fourth heart sound (S4): low-pitched, late diastolic sound due to atrial contraction against a stiff ventricle (HOCM, HTN, AS). It is always pathological.

ii.

Added sounds:  Opening snap: in MS, due to sudden opening of a stenosed mitral valve, occurs early in diastole just after S2.  Ejection systolic click: in AS, occurs early in systole just after S1 (it does not occur if the valve is calcified).  Mid systolic click: in mitral valve prolapse  Prosthetic valve sound: high-pitched metallic sound occurs when the valve close and open.  Pericardial friction rub: is a coarse scratching sound audible during systole and diastole. It is best heard at left lower sternum with the breath held in expiration and the patient leaning forward. (occurs in pericarditis and following myocardial infarction).

iii.

Murmurs: (caused by turbulent blood flow across an abnormal valve, septal defect, outflow obstruction or by increased flow through a normal valve)  Timing: (with carotid pulsation). Systolic (with carotid pulse), diastolic (alternates with carotid pulse).  Character: (rough, rumbling, harsh, blowing)  Pitch: (low, high)  Intensity:  Grade I: audible with great difficulty in a quiet room  Grade II: easily audible but not loud  Grade III: loud without a thrill  Grade IV: loud with a thrill  Grade V: very loud, audible outside precordium  Grade VI: extremely loud, heard without stethoscope  Location: (position of maximum intensity)  Radiation: (towards left axilla: MR , towards neck: AS)  Effect of respiration: (murmurs in the right side of the heart increase in intensity during inspiration while murmurs in the left side increase in intensity during expiration).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani



Effect of posture: (murmur of MS is best heard when the patient lies on his/her left side while murmur of AR is best heard when the patient sits up and leans forward).

Types of murmurs:  Ejection systolic: caused by: a. Increased stroke volume (innocent flow murmur): severe anaemia, fever, pregnancy and athletes b. Aortic stenosis: (harsh, high-pitched, audible all over the precordium, radiates to upper right sternal edge and carotids, usually loud with a thrill). c. Pulmonary stenosis d. HOCM e. ASD (pulmonary flow murmur)  Pansystolic: a. Mitral regurgitation: (loud, blowing, best heard at the apex and radiates to axilla) b. Tricuspid regurgitation c. VSD: (loud, audible at left sternal border and radiates to right sternal border).  Late systolic: in mitral valve prolapse  Early diastolic: a. Aortic regurgitation: high-pitched, best heard at left sternal edge and most obvious in expiration with the patient leaning forward. b. Graham Steel murmur: due to pulmonary artery dilatation secondary to pulmonary hypertension. (heard at pulmonary area)  Mid diastolic: a) Mitral stenosis: low-pitched, rumbling, best heard at the apex with the patient rolled to the left side. It is accentuated by exercise. b) Austin Flint murmur: accompanies aortic regurgitation, it is caused by the regurgitant jet striking the anterior leaflet of the mitral valve, restricting inflow to the left ventricle.  Continuous: (machinery- like) occurs in patent ductus arteriosus (PDA), best heard at upper left sternal border and radiates towards left scapula.

7) Auscultation of lung bases: for basal crackles (pulmonary oedema) 8) Examination of the Abdomen: for hepatomegaly and ascites 9) Lower limb/ sacral oedema:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

The Respiratory System History & Examination First of all you must introduce yourself to the patient, offer a greeting and take permission for history taking and clinical examination.

History: Demographic Data: Name: Occupation:

Age:

Gender: Original home: Date of Admission:

Residence:

Marital Status:

C/O: (same words of the patient and duration in a chronological order) History of presenting illness: 1. Breathlessness:   

Mode of onset: (sudden/gradual) Progression: (rapid/slow) Duration:  Sudden onset and rapid progression over minutes: respiratory (pulmonary embolism, pneumothorax, asthma, inhaled foreign body) and cardiac (acute left ventricular failure).  Gradual onset and progression over hours to days: respiratory (pneumonia, asthma, exacerbation of COPD).  Gradual onset and progression over weeks to months: respiratory (pleural effusion, neuromuscular disorders) and anemia.  Gradual onset and progression over months to years: respiratory (COPD, pulmonary fibrosis, pulmonary tuberculosis).

 

  

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Severity: Is it related to exertion? What exercise precipitates it: heavy exertion, carrying loads, walking up stairs (how many stairs?) Walking on the flat (how far can he/she walk?) Does it occur at rest? Orthopnoea (dyspnoea on lying flat): (how many pillows the patient uses to feel comfortable?) Paroxysmal Nocturnal Dyspnoea (PND): (patient wakes up at night with distressing dyspnoea (gasping for air) and fear of imminent death, usually associated with cough and frothy, blood stained sputum).

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Grading of severity: Medical Research Council (MRC) classification:  Grade 1: breathlessness when hurrying on the flat or walking up a slight hill.  Grade 2: breathlessness when walking with people of own age or on flat ground.  Grade 3: has to stop because of breathlessness when walking on the flat. 

Is there variability in the symptom? (good days and bad days) *Breathlessness which improves at the weekends or on holidays suggests occupational asthma or extrinsic allergic alveolitis.



Is it worse during the day or at night? e.g.: Bronchial Asthma is worst late at night and in the early morning (patients typically wake between 3 and 5 am and have associated wheezing). (Breathlessness that wakes the patient from sleep is typical of asthma and left ventricular failure (PND). *COPD patients get breathlessness in the morning and on exertion (may improve after coughing up sputum).



Triggering/ precipitating/aggravating factors: *Exercise: (patients with exercise-induced asthma may continue to be breathless for 510 minutes after stopping exercise). *Allergens: (house dust mites, cats, pigeons, dogs, horses, grass pollens). *Smoke, perfumes, fumes, cold air. *Drugs: (Aspirin, NSAIDs).



Associated symptoms: *Wheeze and cough: Asthma, COPD. *Pleuritic chest pain: Pneumonia, pneumothorax, pulmonary embolism, rib fracture. *Central chest pain: Myocardial infarction with left ventricular failure, massive pulmonary embolism/infarction. *Without chest pain: Acute left ventricular failure/pulmonary edema, hypovolaemia/shock, metabolic acidosis, pulmonary embolism, pneumothorax.

Causes of breathlessness:  Cardiac: left ventricular failure, mitral valve disease, cardiomyopathy, constrictive pericarditis, pericardial effusion.  Respiratory:  Airways: Asthma, COPD, bronchiectasis, lung cancer, foreign body, laryngeal tumor, cystic fibrosis, bronchiolitis.  Parenchyma: Pneumonia, pulmonary fibrosis, tuberculosis, sarcoidosis, alveolitis.  Pulmonary circulation: Pulmonary embolism, pulmonary vasculitis, pulmonary hypertension. 26 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

  

Pleural: Effusion, pneumothorax, diffuse pleural fibrosis. Chest wall: Kyphoscoliosis, ankylosing spondylitis. Neuromuscular: Myashenia gravis, Guillian-Barre syndrome ,neuropathies, muscular dystrophies.

 Non-cardiorespiratory: anaemia, metabolic acidosis, obesity, psychogenic.

2. Cough: (is a forced expulsive maneuver against an initially closed glottis causing a characteristic sound)  For how long? (days or weeks)  Is it dry or productive?  Is it worse during the day or night?  Aggravating factors: (dust, fumes, pollen or cold air). Types of cough:  Bovine: feeble non-explosive cough, associated with hoarseness. (Suggests lung cancer; invading the left recurrent laryngeal nerve and causing vocal cords paralysis, or neuromuscular disorder causing respiratory muscle weakness).  Barking: harsh, painful, associated with hoarseness and inspiratory stridor (due to laryngeal inflammation, infection or tumor).  Whooping: severe, persistent, dry and irritating bouts of coughing followed by a high-pitched intake of breath that sounds like “whoop”. It is caused by Bordetella pertussis.  Moist: suggests secretions in the upper and larger airways (asthma, COPD and bronchiectasis). *Persistent moist smoker’s cough first thing in the morning is typical of chronic bronchitis (COPD).  Dry/non-productive: ACE inhibitors, idiopathic pulmonary fibrosis, tracheitis.

Timing/associated features:  Nocturnal cough: suggestive of asthma or left ventricular failure.  Daytime cough: GORD, chronic sinusitis with postnasal drip.  During/after eating or drinking: neuromuscular disease of the oropharynx, trachea-oesophageal fistula. Causes of cough:  Acute (<3 weeks):  With normal chest X-ray: acute viral upper respiratory tract infection, acute bronchitis (bacterial), inhaled foreign body, inhalation of irritants (dusts/fumes). 27 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 With abnormal chest X-ray: pneumonia, acute extrinsic allergic alveolitis.  Chronic (> 8 weeks):  With normal chest X-ray: GORD, asthma, rhinitis/sinusitis with postnasal drip, smoking (COPD), drugs (ACE inhibitors), irritant dust/fumes.  With abnormal chest X-ray: lung cancer, pulmonary tuberculosis, bronchiectasis, interstitial lung disease.

Red flag symptoms: (if associated with cough, should prompt a chest X-ray)     

Haemoptysis. Breathlessness. Fever. Chest pain. Weight loss.

3. Sputum:  Amount: how much is produced per day? Small amount (teaspoonful) or large (cupful)

 



*Large amount of purulent sputum (> a cupful) varying with posture: suggests bronchiectasis. *Large amount of purulent sputum on a single occasion: suggests rupture of lung abscess or empyema into the bronchial tree. *Large volumes of watery sputum with a pink tinge: of acute onset suggests pulmonary oedema, but occurring over weeks: suggests alveolar cell cancer. Colour: (white, yellow, green) Consistency:  Serous (clear, watery, frothy, pink): acute pulmonary oedema, alveolar cell cancer.  Mucoid (white-grey viscid mucus): bronchial asthma and chronic bronchitis/COPD.  Purulent: yellow; in acute broncho-pulmonary infection. Green: in bronchiectasis, lung abscess, pneumonia and cystic fibrosis.  Mucopurulent: ( mucoid + purulent in chronic bronchitis with secondary infection).  Rusty (golden-yellow sputum due to degradation of haemoglobin): lobar pneumonia.  Very thick (or jelly-like difficult to cough up/mucus plug): in bronchial asthma. Smell: offensive in bronchiectasis, lung abscess and empyema.

4. Haemoptysis: (coughing up blood) {Clarify whether the blood is coughed up (respiratory tract), vomited (upper GI tract) or   

suddenly appeared in the mouth without coughing (nasopharyngeal)}. Frequency (how often): Duration: Amount: o *Bronchiectasis causes intermittent haemoptysis over years. o *Lung cancer, tuberculosis and lung abscess cause daily haemoptysis for a week or more.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

o





*Pulmonary thromboembolism/infarction cause large single episode of haemoptysis asscociated with breathlessness and pleuritic chest pain. Nature:  Frank blood: lung cancer, bronchiectasis, pulmonary infarction, tuberculosis.  Blood stained sputum (blood mixed with sputum): tuberculosis or lung cancer.  Blood streaked sputum (blood on the side of sputum): chronic bronchitis.  Rusty sputum: (lobar pneumonia).  Pink-frothy: in pulmonary oedema. Associated conditions: (bleeding per gums, epistaxis, melaena)

Causes of haemoptysis:     

Tumour: Malignant (lung cancer, endobronchial metastasis), benign (bronchial carcinoid). Infection: Bronchiectasis, tuberculosis, lung abscess mycetoma, cystic fibrosis. Vascular: Pulmonary infarction, arteriovenous malformation. Vasculitis: Wegner’s granulomatosis, Goodpasture’s syndrome. Trauma: Inhaled foreign body, chest trauma, iatrogenic (bronchoscopic biopsy, transthoracic lung biopsy).  Cardiac: Mitral valve disease, acute left ventricular failure.  Haematological: Blood dyscrasias, anticoagulation.

5. Chest pain:           

Site: Time & mode of onset: Severity: Nature: Progression: End of pain: Duration: Aggravating factors: Relieving factors: Radiation: Associated Symptoms:

Causes of chest pain: A. Non-central:  Pleural: 1) 2) 3) 4) 29 | P a g e

Infection: pneumonia, tuberculosis, bronchiectasis. Malignancy: lung cancer, mesothelioma, metastatic. Pneumothorax, pulmonary infarction. Connective tissue disease: rheumatoid arthritis, SLE. Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Chest wall: 1) Malignancy: Lung cancer, mesothelioma, bony metastasis. 2) Musculoskeletal: Muscle sprains/tears, costochondritis, rib fracture. 3) Persistent cough/breathlessness. 4) Intercostal nerve root compression, thoracic shingles (herpes zoster): cause chest pain in a thoracic dermatomal distribution. B. Central:  Cardiac: acute myocardial infarction/ischaemia, pericarditis, massive pulmonary thromboembolism.  Great vessels: aortic dissection.  Tracheal: infection, irritant dusts.  Oesophageal: oesophagitis, rupture.  Mediastinal: lung cancer, thymoma, metastasis, mediastinitis. 



 

Pleuritic pain: sharp, stabbing pain in the sides of the chest, aggravated by deep breathing or coughing. It is caused by: pulmonary embolism, pneumonia, pneumothorax, fractured ribs. Malignant chest wall pain (due to local invasion by lung cancer, mesothelioma or rib metastasis): dull, aching unrelated to respiration, progressively worsens and disturbs sleep. Intercostal nerve root compression, thoracic shingles (herpes zoster): cause chest pain in a thoracic dermatomal distribution. Sudden localized pain after vigorous coughing or direct trauma: suggests rib fracture or intercostal muscle injury.

6. Wheezing: (high-pitched whistling sound produced by air passing through narrowed small airways). It is limited to expiration. *Bronchial asthma: night wakening with wheeze, and on exercise. *COPD: wheeze after wakening in the morning and on exercise. **Do not mistake wheezing for stridor which is a high-pitched/harsh inspiratory sound (aggravated by coughing) caused by partial occlusion of a large airway (larynx, trachea or main bronchus) by tumour or foreign body.

7. Other symptoms (ENT):  

Recurrent sinusitis/rhinitis: (may be linked with bronchial asthma or bronchiectasis) Hoarseness (change in quality of voice): due to damage of the left recurrent laryngeal nerve by lung carcinoma.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Past medical history:        

Pulmonary tuberculosis or contact with a patient with pulmonary tuberculosis or chronic cough. Bronchial asthma, eczema and hay fever. Whooping cough, measles: recognized causes of bronchiectasis. Connective tissue disorders e.g. rheumatoid arthritis: pulmonary fibrosis, effusion, bronchiectasis.

Previous malignancy: recurrence/metastasis. Chemo/radiotherapy: pulmonary fibrosis. Recent travel, immobility, cancer: pulmonary embolism. Recent surgery, loss of consciousness: aspiration of foreign body/gastric contents, pneumonia, lung abscess.

Family history:    

Bronchial asthma, eczema and hay fever (atopy). Cystic fibrosis, alpha 1- antitrypsin deficiency. Tuberculosis: significant past exposure to the patient.

Family member working in asbestos- related occupation: (patient may have significant exposure to asbestos- contaminated work clothes brought home for cleaning).

Social history: 



Full smoking history: *Age at starting and stopping (if ex-smoker): *How many cigarettes/day: (for current and ex-smokers) *Pack- year calculation: Pack- year = number of packs smoked/day X number of years E.g. smoking 20 cigarettes (1 pack) per day for 1 year, equals 1 pack- year. 2 packs/day for 10 years equals 20 pack-years. *Almost all cases of lung cancer and COPD occur in smokers. *COPD patients usually have a consumption > 20 pack-years. Exposure to pets (cats, dogs, horses, pigeons): bronchial asthma

Occupational history: (Record any exposure to recognized hazards and length of exposure) Occupational Asthma: 

Results from exposure to:  Isocyanates (Spray painting).  Animals (vets, laboratory workers).  Grains/flour (farmers, bakers).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Hardwood dust (carpenters).  Enzymes (detergent manufacturing).  Epoxy resins (adhesives).  Formaldehyde/glutaraldehyde/latex (hospital workers)  Platinum salts. *Ask about relationship between symptoms and work e.g.: cough, shortness of breath and wheezing during the week days which improve at the weekends. Byssinosis: 

Due to exposure to Cotton dust: (symptoms are worse at the beginning of the working week, unlike occupational asthma which is worse at the end of the working week)

Industrial dust diseases:   



Exposure to Coal dust particles (coal miners): leads to coal worker’s pneumoconiosis (pulmonary fibrosis). Exposure to Silica particles (metal mining, stone quarrying, ceramic manufacture): causes silicosis (progressive dyspnoea, increased incidence of tuberculosis, pulmonary fibrosis). Exposure to Asbestos (shipyard, construction workers, plumbers): may cause asbestosis (progressive dyspnoea, pulmonary fibrosis) and mesothelioma (carcinoma of the pleura) 20 to 30 years later. Exposure to Beryllium (nuclear, aerospace industries): leads to berylliosis (pulmonary fibrosis).

Extrinsic allergic alveolitis (EAA):    

Exposure to Fungal spores (Micropolyspora faeni) in mouldy hay: causes Farmer’s lung. Exposure to Fungal spores (Thermophilic actinomycetes): Mushroom worker’s lung. Exposure to Aspergillus clavatus: Malt worker’s lung. Exposure to Avian proteins (droppings/excreta): Bird fancier’s and Pigeon fancier’s lung.

Drug history:  Beta blockers, opioids, NSAIDs: bronchoconstriction.  ACE inhibitors: cough.  Bleomycin, methotrexate, amiodarone, sulphasalazine, penicillamine, gold salts, nitrofurantoin    

and radiotherapy: diffuse parenchymal lung disease (fibrosis). Oestrogens: pulmonary thromboembolism. Oestrogens, fenfluramine: pulmonary hypertension. Amiodarone, nitrofurantoin, phenytoin, methotrexate, pergolide: pleural effusion. Opioids, benzodiazepines: respiratory depression.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Clinical examination: 1. General observation: A. B. C. D. E.

Breathlessness/Distress: Physique (weight loss, cachexia, obesity): Mental state (confusion): Voice (hoarseness): Wheezing/stridor:

2. Hands: o Finger clubbing:  Grade 1: loss of the normal angle between the nail and the nail bed.  Grade 2: Increased nail bed fluctuation.  Grade 3: Increased nail curvature.  Grade 4: Increased bulk of the soft tissues over the terminal phalanges (drumstick appearance). Causes of clubbing: 1) Familial. 2) Respiratory disease: lung cancer, mesothelioma, suppurative lung disease (bronchiectrasis, empyema, lung abscess), cystic fibrosis, idiopathic pulmonary fibrosis, asbestosis. 3) Cardiovascular disease: bacterial endocarditis, cyanotic congenital heart disease, atrial myxoma. 4) Gastrointestinal/liver: liver cirrhosis, coeliac disease, Crohn’s disease, ulcerative colitis. o o o

Peripheral cyanosis: Tobacco staining: Tremor: *Fine: due to hypoxia or excessive use of beta- agonists or theophylline. *Flapping ‘‘asterixis’’: intermittent failure of parietal mechanisms required to maintain posture. Causes:     

Respiratory: failure/acidosis (CO2 retention). Liver: failure, Wilson’s disease (hepato-lenticular degeneration). Renal failure. Electrolyte disturbances: hypokalaemia, hypomagnesaemia, hypoglycaemia. Drugs: barbiturates, alcohol, sodium valproate, phenytoin, carbamazepine, metoclopramide, gabapentin, opioids.  Nervous system: haemorrhage (intracerebral, subdural, subarachnoid), cerebral ischaemia.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

o

Hypertrophic pulmonary osteoarthropathy (HPOA): pronounced clubbing of fingers and toes with pain and swelling of the wrists and ankles. *X-rays of forearm/leg show subperiopsteal new bone formation. *It is almost always associated with squamous lung cancer.

o

Discolouration of the nails: *Yellow nail syndrome: yellow nails, lymphoedema and exudative pleural effusion. *Brownish stain: tobacco (tar) staining.

o

Wasting of the small muscles of the hand: Pancoast’s tumour.

o

Rheumatoid changes: (pulmonary fibrosis, pleural effusion).

o

Pulse: tachycardia (pneumonia, COPD, respiratory failure), pulsus paradoxus (severe asthma).

3. Face:  Horner’s syndrome (due to apical lung tumour ‘‘Pancoast’s tumour’’ compressing the sympathetic nerves in the neck).  Central cyanosis (lips and tongue)  Pursed lips (severe COPD). 4. Neck: o JVP: raised in:  Cor pulmonale (right-sided heart failure secondary to lung disease e.g. COPD)  Raised intrathoracic pressure (tension pneumothorax, acute severe asthma).  Massive pulomonary embolism.  Superior vena caval obstruction secondary to lung cancer or upper mediastinal tumours: (lymphoma, thymoma). o

Use of accessory muscles of respiration (sternocleidomastoid, scalene, intercostals muscles): characteristic of patients with COPD and acute severe asthma.

o

Lymph nodes: cervical, supraclavicular and scalene (in the angle between sternocleidomastoid and clavicle).

5. Examination of the chest: a) Inspection: I.

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Respiratory rate: (normal range: 12-16 breaths/minute)  Tachypnoea: is a respiratory rate > 16/min. It is caused by: increased ventilatory drive (fever, acute asthma, exacerbation of COPD) or reduced ventilator capacity (pneumonia, pulmonary oedema, interstitial lung disease).

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Slow respiratory rate: opioid toxicity, hypercapnoea, hypothyroidism, raised intracranial pressure, hypothalamic lesions.  Apnoea: cessation of breathing/air flow for > 10 seconds.  Obstructive sleep apnoea/hypoapnoea syndrome (OSAHS): is the combination of excessive daytime sleepiness and recurrent upper airway obstruction during sleep that leads to sleep fragmentation. II.

Type of respiration:  Thoraco-abdominal: females  Abdomino-thoracic: males, babies  Exclusively thoracic: peritoneal irritation  Exclusively abdominal: ankylosing spondylitis , pleurisy  Acidotic (Kussmaul’s) breathing: deep, rapid, laboured breathing (air hunger).Seen in patients with metabolic acidosis (DKA, acute renal failure, lactic acidosis, salicylates/methanol poisoning).  Cheyne-stokes breathing: cyclical deepening and quickening of respiration followed by a short period of complete apnoea then the cycle is repeated. *It is due to altered sensitivity of the respiratory centre to chemical control and delay in circulation time between the lungs and chemoreceptors. *Seen in severe cardiac failure, narcotic drug poisoning and brainstem lesions.

III.

Shape of the chest: (Normal chest is bilaterally symmetrical and elliptical in cross-section, transverse diameter is > AP diameter).  Barrel-shaped chest: AP diameter is > the transverse diameter (lung hyperinflation: severe COPD).  Pectus excavatum (sunken or funnel chest): localized depression of the lower end of the sternum (developmental deformity). *In severe cases, it may impair cardiorespiratory function (heart is displaced left and the ventilatory capacity is reduced).  Pectus carinatum (pigeon chest): localized prominence of the sternum and adjacent costal cartilages. Seen in lung hyperinflation (severe poorly controlled childhood asthma) and rickets.  Harrison’s sulcus: is a linear depression of the lower ribs just above the costal margin at the site of attachment of the diaphragm. It results from repeated, vigorous contractions of the diaphragm while the bony thorax is still pliable, (severe childhood asthma, rickets).  Kyphosis (roundback): exaggerated anterior (forward) curvature of the spine (thoracic vertebrae).  Scoliosis: abnormal lateral curvature of the spine. *Kyphoscoliosis may be idiopathic or secondary to childhood poliomyelitis, spinal tuberculosis or associated with Marfan’s syndrome.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

It may reduce the ventilatory capacity and increases the work of breathing. (ventilatory failure, CO 2 retention, cor pulmonale). IV.

Prominent veins: (superior vena caval obstruction) Pulsations, scars: (previous heart/lung surgery) Swellings: (metastatic nodules, neurofibromas, lipomas)

V.

Movement of the chest:  Symmetrical/ diminished on one side:  Paradoxical inward movement of the abdomen during inspiration: severe COPD, diaphragmatic paralysis.  Intercostal recession (paradoxical movement): in-drawing of intercostal spaces with inspiration due to severe upper airway obstruction.  Mobile (flail) chest: double fracture of a series of ribs or of the sternum allows the chest wall between the fractures to become mobile.

b) Palpation: I. Position of the trachea:  Well centralized or deviated to one side (upper mediastinal shift) Causes of tracheal deviation:  Towards the side of the lung lesion: *Upper lope collapse. *Upper lobe fibrosis. *Pneumonectomy.  Away from the side of the lung lesion: *Massive pleural effusion. *Tension pneumothorax.  Upper mediastinal mass: *Retrosternal goitre, *Lung cancer. *Lymphoma.  Distance between the suprasternal notch and the thyroid cartilage: is normally 3-4 finger breadths, if decreased it suggests lung hyperinflation.  Tracheal tug: downward displacement of the thyroid cartilage during inspiration, seen in hyperinflation/ COPD. (Demonstrated when your finger, resting on the trachea, moves inferiorly with each inspiration). II.

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Position of the apex beat: (displacement indicates lower mediastinal shift). *Displaced cardiac impulse without deviation of the trachea: left ventricular enlargement, kyphoscoliosis, severe pectus excavatum. Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

III.

Chest expansion:  Reduced expansion on one side: pleural effusion, lobar/lung collapse, pneumothorax, unilateral fibrosis.  Bilateral reduction in chest expansion: COPD, diffuse pulmonary fibrosis.

IV.

Tactile vocal fremitus: Increased in consolidation and cavitation. Decreased in pleural effusion and pneumothorax.

V.

Crepitus: characteristic crackling sensation over gas containing tissues due to subcutaneous emphysema (severe acute asthma, spontaneous/traumatic pneumothorax, rupture of the oesophagus, complication of surgery and intercostal drainage).

c) Percussion: (compare the two sides)  Resonant: normal lung tissue  Hyper-resonant: pneumothorax, hyperinflation (emphysema).  Impaired percussion note: fibrosis  Dull: consolidation, collapse, severe pulmonary fibrosis.  Stony dullness: pleural effusion, haemothorax.  Liver dullness (by tidal percussion): the upper border of the liver is in the 5th intercostal space in the right mid-clavicular line. If the chest is resonant below this level, it is a sign of hyperinflation (COPD or severe asthma).  Cardiac dullness: over the left anterior chest. It may be decreased in COPD/severe asthma.

d) Auscultation: I. Breath sounds:  Intensity: normal, increased (very thin individuals) or diminished (obesity, pleural effusion, marked pleural thickening, pneumothorax, hyperinflation due to COPD, over an area of collapse with occlusion of major bronchus).  Quality: *Vesicular (normal): louder and longer on inspiration than on expiration (fades rapidly) and there is no gap between the two phases. *Bronchial breathing: high- pitched sound with a blowing quality similar to that heard over the trachea and larynx. (The breath sounds are of similar length and intensity in inspiration and expiration with a characteristic pause between the two phases). It is heard in: 1. **Lung consolidation (pneumonia). 2. **At the top of a pleural effusion. 3. **Collapsed lung with a patent major bronchus. 37 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

II.

Added sounds:  Wheezes: (musical sounds associated with airway narrowing) in bronchial asthma and COPD. o High- pitched wheeze: arises from smaller airways. o Low- pitched wheeze: arises from larger bronchi. o Monophonic wheeze: due to fixed bronchial obstruction by a lung cancer. (localized wheeze with a single musical note that does not clear with coughing). o Polyphonic wheeze: multiple musical notes due to wide spread narrowing of airways (asthma, COPD).  Crackles: short, interrupted explosive sounds, result from peripheral airways collapse on expiration, then air rapidly enters theses distal airways on inspiration and the alveoli and small bronchi abruptly open producing the crackling noise.  Early inspiratory crackles: small airways disease (bronchiolitis).  In mid-inspiration: pulmonary oedema.  Late inspiratory: fine (pulmonary fibrosis), coarse (bronchial secretions in: COPD, pneumonia, lung abscess, tubercular lung cavities).  Biphasic: loud coarse crackles throughout inspiration and expiration (bubbling of air through secretions). Heard in bronchiectasis.  Pleural rub: (scratchy rough sound, does not change with coughing and is produced by rubbing of inflamed pleural surfaces). Indicates pleurisy (pneumonia, pulmonary infarction).  Pneumothorax click: rhythmical sound synchronous with cardiac systole.

III.

Vocal resonance: (resonance of sounds in the chest made by the voice):  Decreased : in pleural effusion.  Increased: in consolidation.  Whispering pectoriloquy: (whispered speech is distinctly heard). Occurs in consolidation and at the top of a pleural effusion.  Aegophony (goat voice): is a bleating or nasal sound. It is due to enhanced transmission of high frequency noise across abnormal lung. (When the patient says ‘‘e’’ it sounds like ‘‘a’’ ). *It is heard over a consolidated lung or at the upper level of a pleural effusion.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

The Gastrointestinal System History & Examination First of all you must introduce yourself to the patient, offer a greeting and take permission for history taking and clinical examination.

History: Demographic Data: Name: Marital Status:

Occupation:

Age:

Gender: Original home: Date of Admission:

Residence:

C/O: (same words of the patient and duration in a chronological order) History of presenting illness: 23- Appetite: Increased: Decreased: Normal: If Decreased why? Lack of desire to eat (anorexia)?

Or eating causes Pain?

24- Weight: Increased: Decreased: No change: If decreased, how much? (Clothes, People Noticed, previous weight records): How quickly: (Significant weight loss: > 3kg in 6 months). Causes of weight loss: - Reduced energy intake: starvation/dieting, loss of appetite, malabsorption and anorexia nervosa. - Increased energy expenditure (catabolism): hyperthyroidism, uncontrolled diabetes mellitus, malignancy, infections ‘‘tuberculosis and HIV’’, liver diseases, adoption of a more energetic lifestyle. 25- Painful mouth: (sore lips, tongue or buccal mucosa)  Idiopathic: recurrent aphthous ulcers.  Infections: candidiasis, dental sepsis, herpes simplex virus (HSV1, 2), coxsackie A virus {herpangina, Vincent’s angina (ulcerative gingivitis), hand-foot-mouth syndrome}.  Systemic disorders: Iron, folate and vitamin B12 deficiency, inflammatory bowel disease, coeliac disease, reactive arthritis, Behcet’s disease, acute leukaemia, leucopenia and drug allergies (sulphonamides, gold, cytotoxics).  Associated with skin disorders: lichen planus, erythema multiforme, pemphigus vulgaris.  Others: leukoplakia, trauma from teeth/dentures.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

26- Xerostomia (dry mouth): occurs in connective tissue disease (Sjogren’s syndrome). 27- Halitosis (bad breath): due to gingivitis (Vincent’s angina), dental caries, pharyngeal infection, bronchiectasis and lung abscess. 28- Globus (sensation of a lump in the throat): 29- Odynophagia (pain on swallowing): due to local infection in the oesophagus (candida, herpes simplex). Common in AIDS patients. 30- Water brash: sudden appearance of excessive saliva in the mouth. 31- Dysphagia: (difficulty in swallowing and sensation of something sticking in the throat or chest)  Is it Painful or painless?  Intermittent or progressive  Duration  Is it for solids, liquids or both?  Level at which food sticks:  Is there complete obstruction and regurgitation?  Previous history of dysphagia or heartburn: Causes: 1. Oral: painful mouth ulcers, tonsillitis, glandular fever, pharyngitis, peritonsillar abscess. 2. Neurological: (cerebrovascular accident, bulbar or pseudobulbar palsies): worse for liquids than for solids, may be accompanied by chocking and regurgitating fluid from the nose. 3. Neuromuscular: (achalasia, myasthenia gravis and oesophageal dysmotility): worse for solids. 4. Mechanical: usually presents with initial difficulty in swallowing solids then progresses to difficulty in swallowing liquids. *Benign (peptic) stricture: longstanding dysphagia without weight loss but accompanied by heartburn. *Malignant oesophageal stricture: short history, weight loss, no reflux symptoms. *Extrinsic compression: by lung cancer or goiter. *Systemic sclerosis. 32- Heartburn: (hot, burning retrosternal discomfort which radiates upwards) - Most likely due to gastro-oesophageal reflux disease and associated with acid reflux. *What makes it happen? (Lying flat at night, bending or stooping): 33- Acid reflux: (regurgitating gastric acid producing a sour taste in the mouth)

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

34- Dyspepsia (indigestion): ill- defined symptoms from the upper gastrointestinal tract. It is classified into: * Reflux- like dyspepsia: heartburn or an acid feeling occurring after meals. * Ulcer- like dyspepsia: epigastric pain/discomfort relieved by food or antacids. * Dysmotility- like dyspepsia: nausea, belching, bloating and early satiety. 35- Hiccups: (repeated sudden diaphragmatic contraction triggered by upper gastrointestinal irritation or brainstem disease) 36- Vomiting:  Frequency:  Volume:  Nature (recognizable food, digested food, clear acidic fluid, bile stained, blood stained or faeculent):  Is it preceded by nausea or does it occur without warning?  Associated symptoms (dyspepsia or abdominal pain):  Is it related to meal times, early morning or late evening?  Is it projectile? (Gastric outlet obstruction, high small bowel obstruction or raised intracranial pressure)  What medications has the patient been taking? Causes: A. Gastrointestinal: gastroenteritis, cholecystitis, pancreatitis, hepatitis, gastric outlet obstruction (projectile, large volume of vomitus, not bile stained) and small bowel obstruction (bile stained vomitus, associated with abdominal distension and intestinal colic). Vomiting is precede by nausea and accompanied by abdominal pain/discomfort. B. Neurological: raised intracranial pressure (meningitis, brain tumour: vomiting not preceded by nausea), labrynthitis, Meniere’s disease, migraine, vasovagal syncope, shock, fear and severe pain (renal colic, biliary colic, myocardial infarction). C. Metabolic/endocrine: pregnancy, diabetic ketoacidosis, renal failure, hepatic failure, hypercalcaemia and Addison’s disease. D. Alcohol and drugs: opioids, digoxin, theophylline, cytotoxic agents, antidepressants and others. E. Psychological: anorexia nervosa and bulimia. 37- Haematemesis: (vomiting of blood) *Frequency: *Volume: *Fresh blood or dark brown (coffee grounds): *Mixed with food or frank Blood: *Past history of dyspepsia or peptic ulceration: *Past history of liver disease: *History of alcohol, NSAIDs or corticosteroid ingestion: *Past history of gastrointestinal bleeding: 41 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

*Has the patient been admitted and received blood? *Was the haematemesis preceded by intense retching? *Was blood staining of the vomitus apparent in the first vomit? *Recent nose bleed (swallowed blood): Causes of upper GI bleeding: (bleeding above the ligament of Treitz) 1) Peptic ulceration (gastric or duodenal). 2) Oesophageal/gastric varices. 3) Oesophageal/gastric cancer. 4) Gastritis/gastropathy/ duodenitis. 5) Erosive oesophagitis/ulcer. 6) Mallory- Weiss oesophageal tear: (lower oesophageal mucosal tear due to the trauma of retching; the patient vomits forcefully several times and fresh blood only apperars after the initial vomit). 7) Aspirin, NSAIDS, corticosteroids, thrombolytics or anticoagulants. 8) Excessive alcohol ingestion (cause haematemesis from erosive gastritis, Mallory- Weiss tear or oesophageal varices secondary to liver cirrhosis). 9) Vascular malformation. 10) Oropharyngeal bleeding/ epistaxis (swallowed blood). 38- Melaena: (passage of black tarry stool with a characteristic odour, due to partially digested blood). * It indicates upper GI bleeding but can result from bleeding anywhere proximal to the transverse colon. * Melaena must be distinguished from the matt black stools associated with oral iron or bismuth therapy. 39- Abdominal pain: 1. Site: 2. Time & mode of onset: (sudden or gradual) 3. Severity: (effect of pain on Patient’s life; stop him from going to work? wake him at night? stop him going to sleep? force him to lie still or roll around? did he use analgesics?) 4. Nature or character: (burning, throbbing, constricting, gripping, crushing, tightness, heaviness, stabbing, colicky or just dull aching pain or discomfort) 5. Progression: (onset, course, end)  Begins at its maximum intensity, remains steady then suddenly ends (sudden-steadysudden)  Begins at its peak, declines slowly till it gradually ends (sudden-gradual-gradual):  Increases steadily till it reaches a peak then suddenly ends (gradual-gradual-sudden):  Fluctuates: 6. End of the Pain (ends spontaneously or as a result of action by Pt or Dr): Sudden or Gradual End:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

7. Duration (from onset to end): *If it comes and goes; length of the period of pain and pain free: 8. Radiation: (Extension of the pain to another site while the initial pain persists) e.g.: posterior penetrating duodenal ulcer and pancreatitis present as persistent epigastric pain which radiates to the back. Angina/myocardial infarction: persistent retrosternal chest pain that radiates to arm, throat and jaw. *Do not confuse radiation with ‘’referred pain’’ which is a pain that is felt at a distance from its source. e.g.: irritation of the diaphragm with an inflamed gallbladder (acute cholecystitis) is felt at the tip of the right shoulder. 9. Aggravating Factors: 10. Relieving Factors: 11. Associated Symptoms: Causes of abdominal pain:  Right upper quadrant:  Gallbladder/biliary tree: cholecystitis, cholangitis, mechanical obstruction (biliary colic).  Liver: hepatitis, Budd- Chiari syndrome, subdiaphragmatic abscess, distension of the hepatic capsule by haemorrhage, congestive hepatomegaly.  Pancreatitis.  Duodenal ulcer.  Hepatic flexure of the colon: cancer.  Appendicitis.  Right kidney: renal colic, pyelonephritis, perinephric abscess.  Lung: pneumonia, empyema, pleurisy.  Epigastrium:      

Stomach: peptic ulcer disease (gastric/duodenal), gastritis, gastric cancer. Pancreatitis. Oesophageal disease: GORD, inflammation, spasm, rupture. Gall bladder disease. Vascular: ruptured aortic aneurysm. Cardiac: myocardial infarction, pericarditis.

 Left upper quadrant:  Spleen: infarct, rupture, abscess.  Stomach: ulcer, cancer.  Pancreatitis.  Splenic flexure: cancer.  Left kidney: renal colic, pyelonephritis, perinephric abscess.  Subdiaphragmatic abscess.  Lung: pneumonia, empyema, pleurisy. 43 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Right iliac fossa (RIF):  Appendicitis.  Female genital system: salpingitis, tubo-ovarian abscess, twisted ovarian cyst, ruptured ectopic pregnancy.  Urinary tract: renal/ureteric stone, UTI.  Incarcerated hernia.  Bowel: inflammatory bowel disease (IBD), ca caecum, Meckel’s diverticulitis.  Mesenteric lymphadenitis.  Male genital system: testicular torsion (pain radiates to lower abdomen).  Peri-umbilical:  Early appendicitis.  Intestinal obstruction.  Vascular: mesenteric ischaemia (superior mesenteric artery occlusion: thrombosis, embolism), ruptured aortic aneurysm.  Left iliac fossa (LIF):  Sigmoid diverticulitis.  Female genital system: salpingitis, tubo-ovarian abscess, twisted ovarian cyst, ruptured ectopic pregnancy.  Urinary tract: renal/ureteric stone, UTI.  Incarcerated hernia.  Bowel: IBD, ca colon, volvulus.  Male genital system: testicular torsion (pain radiates to lower abdomen).  Others: (may affect any quadrant, more than one quadrant or may cause generalized abdominal pain)  Gastroenteritis, enteric fever, malaria.  Peritonitis (generalized or localized).  Abdominal wall: mesenteric traction, rectus sheath haematoma (anticoagulants), trauma, myositis.  Metabolic: diabetic ketoacidosis, uraemia, hyperlipidaemia, hyperparathyroidism, porphyria, acute adrenal insufficiency, familial Mediterranean fever, C1 esterase deficiency (angioneurotic oedema).  Neurologic/psychiatric: herpes zoster, tabes dorsalis, acute vertebral collapse, nerve root compression, irritable bowel syndrome, psychiatric disorders.  Toxic: lead poisoning, snake bite. 40- Flatulence (excessive wind): {Air swallowing (aerophagy), lactose intolerance, malabsorption}.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

41- Abdominal distension:  Progression:  Is it Constant or variable?  Is it Painful or painless?  Does it affect respiration?  Is it relieved by belching, vomiting or defecation? Causes of abdominal distension: (6 Fs) 1. Fat: obesity, 2. Flatus: pseudo- obstruction, obstruction 3. Faeces: subacute obstruction, constipation. 4. Fluid: ascites, ovarian cyst, distended bladder. 5. Fetus. 6. Functional (bloating associated with irritable bowel syndrome).

Ascites: is accumulation of free fluid within the peritoneal cavity. Causes: 1. Portal hypertension related: (high serum-ascites albumin gradient: > 1.1 g/dL)  Sinusoidal: liver cirrhosis, spontaneous bacterial peritonitis, acute hepatitis, extensive malignancy (hepatocellular carcinoma or metastatic tumours).  Pre- sinusoidal: portal vein thrombosis, splenic vein thrombosis, Schistsomiasis.  Post- sinusoidal: Budd- Chiari syndrome, hepatic veno-occlusive disease, congestive or rightsided heart failure, tricuspid regurgitation, constrictive pericarditis. 2. Non- portal hypertension related: (low serum-ascites albumin gradient: < 1.1 g/dL)  Peritoneal carcinomatosis.  Peritonitis: tuberculosis, ruptured viscus.  Pancreatitis.  Hypo-albuminaemia: nephrotic syndrome, protein loosing enteropathy.  Meig’s syndrome.  Bowel obstruction/infarction.  Lymphatic leak (obstruction of main lymphatic duct): chylous ascites.  Vasculitis.

42- Altered bowel habit: (normal bowel movement frequency ranges from 3 times/day to once every 3 days) a) Constipation: (Infrequent passage of hard stools ; < 3 times/week)  Frequency of defecation:  Consistency of stools: 45 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

     

Onset: (recent change in bowel habit or chronic): Is it accompanied by abdominal pain, anal pain on defecation or prolonged straining? Associated symptoms: (Rectal bleeding, mucous discharge, tenesmus or weight loss) Is there diarrhoea alternating with constipation? Has the shape of the stool changed (pellet- like)? What drugs has the patient been taking?

{Tenesmus: is a sensation felt in the rectum of incomplete emptying following defecation; as if something else left behind which cannot be passed, suggests rectal inflammation, tumour or irritable bowel syndrome }. Causes of constipation:  Common causes: low fibre diet, immobility (stroke, Parkinson’s disease), irritable bowel syndrome, hospital environment, old age.  Anorectal disease: anal fissure, anal stricture, rectal prolapse.  Intestinal obstruction: colorectal carcinoma, Crohn’s disease (stricture).  Metabolic/endocrine: hypothyroidism, hypercalcaemia, hypokalaemia, porphyria.  Drugs: opiate analgesics (morphine, codeine), anticholinergics, iron.  Neuromuscular: spinal or pelvic nerve injury. b) Diarrhoea: (Frequent passage of loose stools ; 3 or more/ day)  Frequency:  Consistency (watery/semisolid):  Onset: (acute, chronic or intermittent):  Volume: (large/small)  Is there blood, mucus or pus?  Specific Gravity: (is it difficult to flush?)  Is there tenesmus, urgency or incontinence?  Does diarrhoea disturb sleep? (nocturnal diarrhoea suggests organic disease)  History of contact with diarrhoea patient:  History of travel:  Other people affected in household: (suggest food poisoning)  Does the sexual history provide a clue? (HIV)  History of alcohol abuse/drugs:  Past history of GI surgery, GI disease or IBD:  Family history of GI disorder (coeliac/Crohn’s disease):  Associated symptoms (abdominal pain, vomiting, fever or arthralgia): Causes: (anorexia, weight loss, anaemia or nocturnal diarrhoea suggest an organic cause)

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Acute: (< 2 weeks)  Infective gastroenteritis: *Preformed toxin (food poisoning): Staph aureus, Bacillus cereus, Clostridium perfringens. * Viral: Rotavirus, Norovirus, CMV (immunocompromised). *Bacterial: E.coli (toxigenic) “accounts for > 50% of traveler’s diarrhoea”, Vibrio cholerae, Campylobacter, Salmonella, shigella, E.coli (O157:H7) “invasive/haemorrhagic”, Clostridium difficile, Yersinia. *Parasitic: E. histolytica, Giardia, Cryptosporidia, Cyclospora.  Drugs: antibiotics.  Chronic: (> 2weeks)  Inflammatory: IBD, parasitic infestations (Giardia, Strongyloides), radiation enteritis, ischaemic colitis.  Malabsorption: coeliac disease, Whipple’s disease, bacterial overgrowth, chronic pancreatitis, Small bowel resection (short bowel syndrome). ** malabsorption causes steatorrhoea which is the passage of pale, bulky stools containing excessive fats that commonly float in water and are difficult to flush away.  Osmotic: lactose intolerance, laxative abuse.  Drugs: proton pump inhibitors, cimetidine, digoxin, propranolol, colchicine, cytotoxics.  Neoplasms: colorectal cancer, intestinal lymphoma, villous adenoma.  Secretory: (frequently presents with nocturnal diarrhoea) , hormonal: VIP (VIPoma), serotonin (carcinoid syndrome), gastrin (gastrinoma: Zollinger-Ellison), calcitonin (medullary carcinoma of the thyroid).  Motility disorder: Irritable bowel syndrome, diabetic autonomic neuropathy, hyperthyroidism.  Others: Addison’s disease. Bloody diarrhoea: is caused by: infections {campylobacter, shigella, salmonella, entero-invasive/enterohaemorrhagic E.coli (O157:H7), amoebiasis, Clostridium difficile (pseudomembranoeus colitis), Yersinia}, IBD, colorectal cancer, colonic polyps, ischaemic colitis. Mucus with diarrhoea: occurs in irritable bowel syndrome, colonic adenocarcinoma, colonic polyps. Pus with diarrhoea: suggests IBD or diverticulitis. Small bowel diarrhoea: large volume (>1 litre/day), watery or steatorrhoea, may be associated with periumbilical or RIF pain not relieved by defecation. (e.g.: malabsorption, osmotic, secretory, Crohn’s disease, infections “E.coli, cholera, Rota/Norovirus, Giardia, cryptosporidia, cyclospora” and food poisoning).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Large bowel diarrhoea: small volume, frequent, watery/bloody or mucoid, may be associated with tenesmus, urgency, pelvic pain relieved by defecation. (e.g.: irritable bowel syndrome and all causes of bloody diarrhoea). 43- Rectal Bleeding: *How much: *Is it mixed with stool, on the surface of stool or after passing stool? *Is there Mucous/Pus? *Is defecation painful? *If painful, when? (Before, during, after) *Is the patient passing more gas than usual? Causes: 1) Diverticular disease. 2) Colorectal cancer, colonic polyps. 3) Colitis: ischemic, radiation, IBD. 4) Angiodysplasia. 5) Anorectal disorders: haemorrhiods, anal fissure, rectal ulcer, trauma. 6) Rapid severe upper GI bleeding. 44- Jaundice:  Is it progressive (carcinoma of the head of pancreas)? or intermittent (peri-ampullary carcinoma or gallstones)?  Is there skin itching?  What is the colour of urine?  What is the colour of stool?  Accompanying symptoms (abdominal pain, loss of appetite, fever, vomiting): (indicate acute hepatitis or gallstones)  Is it associated with weight loss? (malignancy)  Past history of blood transfusion, surgical operations, intravenous drug abuse or tattooing (hepatitis B, C)  Sexual and contact history: (hepatitis B, C)  Drug history: (see below)  Alcohol intake: how many units/day? For how long?  History of travel and immunizations (hepatitis A)  Past history of jaundice: When? How long did it last?  Past history of hepatitis:  Family history of jaundice: (hereditary spherocytosis, haemochromatosis, Wilson’s disease, Gilbert’s syndrome)

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Causes:  Pre-hepatic: (unconjugated/acholuric hyperbilrubinaemia) 1. Increased bilirubin production: Haemolysis, ineffective erythropoiesis, haematoma reabsorption 2. Defective conjugation: Gilbert’s, Crigler-Najjar syndrome.  Hepatocellular: (hepatocellular damage +/- some cholestasis) 1. Hepatitis: viral (A, B, C, D, E, CMV, EBV), alcoholic, autoimmune. 2. Drugs/toxins: Paracetamol overdose, anti- TB (INH, Rifampicin, Pyrazinamide), statins, Sodium valproate, Monoamine oxidase inhibitors, Halothane, fungal toxins and carbon tetrachloride. 3. Metabolic diseases: haemochromatosis, Wilson’s disease, alpha1- antitrypsin deficiency. 4. Vascular diseases: Budd- chiari syndrome, right- sided heart failure, constrictive pericarditis. 5. Nonalcoholic fatty liver disease (NAFLD). 6. Hepatic metastasis, liver abscess, leptospirosis. 7. Defective excretion: Dubin-Johnson, Rotor syndrome.  Cholestatic (obstructive): (conjugated/ choluric hyperbilrubinaemia) 1. *Intrahepatic cholestasis: drugs (flucloxacillin, co-amoxiclav, anabolic steroids, oral contraceptives, chlorpromazine, sulfonylureas), primary biliary cirrhosis. 2. *Extrahepatic cholestasis: common bile duct stone, pancreatic cancer, cholangiocarcinoma, sclerosing cholangitis, enlarged lymph nodes at the porta hepatis. Gastrointestinal alarm features:       

Chronic GI bleeding. Progressive dysphagia. Progressive unintentional weight loss. Persistent vomiting. Iron deficiency anaemia. Epigastric mass. Suspicious barium meal.

Mnemonics: ALARM Symptoms:      

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A: Anaemia. L: Loss of weight. A: Anorexia. R: Recent onset of progressive symptoms. M: Melaena/haematemesis. S: Swallowing difficulty.

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Past medical history: - Similar condition, peptic ulcer disease, GORD, IBD, jaundice, schistosomiasis, chronic liver disease, previous abdominal surgery. - DM, hypertension and other chronic illnesses.

Family history: - IBD, colorectal cancer, haemochromatosis, Wilson’s disease, Gilbert’s syndrome. - DM, hypertension and other chronic illnesses.

Social history: *Dietary history: allergy or food intolerance (lactose, gluten). *Alcohol consumption: ( type: quantity: (in units) duration: *Smoking: (quantity: duration: ) (smoking increases the risk of oesophageal/gastric and colorectal cancer, crohn’s disease and peptic ulcer disease). *Travel history: (diarrhoeal illnesses). *Risk factors for viral hepatitis: (see above) *Stress/emotional ill health: (irritable bowel syndrome and dyspepsia)

)

Drug history: *Aspirin/ NSAIDs: dyspepsia, gastric erosions/ulcers (GI bleeding). *Opioid analgesics: nausea, vomiting, constipation. *Antibiotics, proton pump inhibitors: diarrhoea *Oral corticosteroids: weight gain. *Hepatotoxic drugs: (see above)

Clinical examination: 1. General assessment:  Degree of illness: does the patient look well, mildly ill or severely ill?  Physical attitude: Is the patient lying comfortably at bed? Lying still (peritonintis)? Restless or roll about (colic)? Is he/she in pain? Is he/she breathless? Lying propped up at bed or sitting up and bending forward?  

Physique: weight: Height: Body mass index (BMI): (BMI) = weight in kilograms / (height) 2 in meters Hand:  Clubbing: (chronic liver disease, malabsorption, inflammatory bowel disease)  Pallor:  Koilonychia (soft, thin, brittle and spoon shaped nails seen in iron deficiency anaemia):

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Signs of chronic liver disease:  Leuconychia (white nails):  Palmar erythema:  Dupuytren’s contracture (thickening of palmar fascia which leads to flexion contracture of the ring and other fingers, occurs mainly in alcoholic liver disease).  Flapping tremor (asterixis): sign of decompensated liver disease. 

Face: pallor, jaundice and parotid enlargement (alcoholic liver disease).



Mouth & Throat:  The lips:  Angular stomatitis, angular cheilitis or cheilosis (reddish-brown cracks or fissures at the corners of the mouth): seen in iron deficiency anaemia and vitamin B 2 (riboflavin) deficiency.  Herpes labialis: (grouped vesicles on the lips on a red base with crusted lesions)  Hyperpigmentation of the skin around the mouth (circumoral) , lips and buccal mucosa: (Peutz-Jeghers syndrome)  Apthous ulcers (small, superficial, painful ulcers with a white-yellow base on the mucous surface of the lips): seen in Crohn’s disease, coeliac disease and Behcet’s disease.  The teeth:  Dental caries  Grey staining (tetracycline).  The gums:  Gum hypertrophy: seen in vitamin C deficiency (scurvy), AML, drugs (phenytoin, calcium channel blockers and cyclosporine), gingivitis, pregnancy.  Stippled blue-black line on the gum : seen in people exposed to Lead  The tongue:  Large tongue: (acromegaly, myxoedema, amyloidosis)  colour: (pale in severe anaemia)  State of hydration: (dry in dehydration)  Hairy leucoplakia: (white patches on the dorsum of tongue) seen in AIDS patients.  Smooth red tongue (atrophic glossitis): iron and vitamin B12 deficiencies.  The buccal mucosa:  Dark brown pigmentation: seen in Addison’s disease  Oral thrush: white patches caused by candida albicans.  Koplik’s spots: small bluish-white spots opposite the molar teeth (measles)  Mouth ulcers: (aphthous ulcers, lichen planus or malignancy)  The palate, tonsils & pharynx: Look for vesicles, erythema, petechiae, ulcers or white exudates/membrane on the tonsils.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 The breath:     

Halitosis : (see above) Acetone smell: in ketosis Fishy or ammonia odour: in uraemia Fetor hepaticus: sweet smell (like pear drops) in advanced liver disease. Alcohol smell



The neck: For lymph node enlargement: (submental, submandibular, pre-auricular, post-auricular, anterior/ posterior cervical, occipital and supraclavicular). *Examine for other groups of lymph nodes: axillary, epitrochlear and inguinal.



Stigmata of chronic liver disease: jaundice, spider naevi, gynaecomastia/breast atrophy in females, loss of secondary sexual hair, testicular atrophy, parotid swelling, clubbing, leuconychia and palmar erythema. *Pruritis and scratch marks: chronic cholestasis.



Signs of decompensated liver disease: Flapping tremor (asterixis), jaundice, ascites and hepatic encephalopathy (drowsiness, hyperventilation).



Extra-intestinal manifestations of Inflammatory bowel disease:  Erythema nodosum: symmetrical erythematous tender nodules on the shin.  Pyoderma gangrenosum: deep red necrotic ulcer with a violaceous border on the shin.

2. The Abdomen: I. Inspection:  Shape: (normal contour, distended or sunken)  Generalized distension: fat, fluid, flatus, faeces, fetus or functional.  Localized distension: enlarged organ (liver, spleen or ovary) or superficial swelling.  Scaphoid abdomen: indicates rapid weight loss (starvation/malignancy).  Umbilicus: Inverted, flat or everted. (In obesity: umbilicus is sunken, in ascites: flat or everted).  Movements of the abdominal wall:  Normally the abdomen moves with respiration In peritonitis the movement is absent or diminished (still abdomen).  Visible peristalsis: (obstruction at the pylorus, congenital pyloric stenosis or distal small bowel obstruction).  Visible pulsation: of the abdominal aorta in epigastrium (thin individuals). 52 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Striae: (pregnancy, ascites, Cushing’s syndrome).  Scars: (upper/lower midline, subcostal, paramedian, appendicectomy, inguinal, suprapubic: pfannenstiel).  Stomas: ileostomy/colostomy.  Prominent veins: (in inferior vena caval obstruction or portal hypertension) Note direction of blood flow (from below upwards in IVC obstruction), or away from the umbilicus (caput medusa) in portal hypertension.  Hernial orifices: (umbilical, para-umbilical, epigastric, inguinal, femoral or incisional)  Groins and genitalia: for pupic hair and swellings.

II.

Palpation: a) Superficial: 1. Tenderness: *Generalized: due to generalized peritonitis. *Epigastric: suggests peptic ulcer. *Right hypochondrial: cholecystitis. *Right iliac fossa: appendicitis/Crohn’s ileitis. 2.

Guarding: is resistance to palpation due to contraction of the abdominal muscles. *Voluntary guarding: is the voluntary contraction of abdominal muscles when palpation provokes pain. (due to tenderness or anxiety). *Involuntary guarding: is the reflex contraction of the abdominal muscles when there is inflammation of the parietal peritoneum.

3.

Rigidity: constant involuntary contraction of the abdominal muscles always associated with tenderness and indicates peritoneal irritation.

4. Superficial masses: (Site, size, shape, consistency, surface, tenderness, mobility, movement with respiration, upper and lower limits/edge, bimanually palpable, pulsatile?) … *To determine whether the mass is originating from the anterior abdominal wall or the abdominal cavity, ask the patient to tense the abdominal muscles (by lifting the head): if the mass disappears, it is intra-abdominal, if it persists: it is an abdominall wall mass. 5. Temperature: b) Deep: 1. Tenderness: 2. Rebound tenderness: the abdominal wall is compressed slowly then released rapidly and a sudden stab of pain results. (strongly suggests peritonitis). 3. Masses: 53 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

c) Palpation for viscera: 1. Liver: (the normal liver edge may be just palpable below the right costal margin)  Size (normal liver span is 8-12cm):  Surface: smooth (congestive heart failure) or irregular (cirrhosis or malignancy)  Consistency: soft (congestive heart failure), firm or hard (cirrhosis or malignancy)  Edge: sharp or rounded  Tenderness: in hepatitis, amoebic liver abscess and congestive heart failure  Pulsations: in tricuspid regurgitation, hepatocellular carcinoma, vascular abnormalities.  Percussion: for upper and lower borders  Hepatic bruit: (due to increased blood flow): occurs with alcoholic hepatitis or hepatic carcinoma (primary or secondary).  Venous hum: (in portal hypertension) Causes of hepatomegaly: 1) Chronic parenchymal liver disease:  Alcoholic liver disease.  Non-alcoholic fatty liver disease (NAFLD).  Primary biliary cirrhosis.  Viral hepatitis.  Autoimmune hepatitis. 2) Malignancy:  Hepatocellular carcinoma.  Metastatic tumours. 3) Hepatic congestion:  Right heart failure.  Constrictive pericarditis. 4) Infections:  Viral hepatitis.  Toxoplasmosis.  CMV.  Hydatid disease.  Liver abscess: pyogenic/amoebic. 5) Haematological disorders:  Lymphoma.  Leukaemia.  Myeloproliferative disorders.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

6) Vascular liver disease:  Budd-chiari syndrome.  Sickle cell disease. 7) Infiltration:  Amyloidosis.  Sarcoidosis.  Glycogen storage disease. 8) Others: (polycystic liver disease, syphilitic gumma) Another approach to causes of hepatomegaly: A. With pallor (anaemia):  Haematological disease: (sickle cell anaemia, haemolytic anaemias with extramedullary haematopoiesis).  Malignancy (haematological, hepatic). B. With jaundice:  Parenchymal liver disease (see above). C. With lymphadenopathy:  Infections (infectious mononucleosis, CMV, toxoplasmosis)  Malignancy.  Sarcoidosis. D. With signs of portal hypertension:  Parenchymal liver disease.  Budd-Chiari syndrome. E. Tender hepatomegaly: (stretch of the liver capsule)  Viral/alcoholic hepatitis.  Hepatic congestion.  Hepatocellular carcinoma/metastasis.  Vascular liver disease (Budd-Chiari syndrome, sickle cell disease)  Liver abscess. F. Hard knobbly (irregular) liver:  Hepatocellular carcinoma, metastatic tumour.  Early stages of cirrhosis.  Hydatid disease.  Sarcoidosis.  Amyloidosis.  Polycystic liver disease. 2. Gall bladder: (just lateral to rectus abdominis near tip of 9th costal cartilage)  Firm, smooth, globular swelling, moves with respiration (carcinoma of the head of pancreas or mucocele of the gallbladder).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

{Courvoisier’s law: in a jaundiced patient, if the gallbladder is palpable it is unlikely to be due to gallstones}  Stony, hard, irregular swelling (carcinoma of gallbladder).  Murphy’s sign: +ve in acute cholecystitis

3. Spleen: Not normally palpable, has to be enlarged to 2-3 times its usual size before it becomes palpable. (to palpate a small spleen turn the patient to his/her right side) Its characteristics are: 1) Firm swelling appearing beneath the left subcostal margin. 2) Dull to percussion. 3) Moves downwards on inspiration. 4) Not bimanually palpable. 5) Its upper border cannot be felt (i.e. one cannot get above it) 6) Has a notch in the lower medial border *If palpable measure its size below the costal margin. *Auscultation for a splenic rub Causes of splenomegaly:

 

1. Portal hypertension. 2. Haematological disorders:  Lymphoma/leukaemia.  Myeloproliferative disorders.  Haemolytic anaemias. 3. Infections:  Glandular fever.  Malaria.  Visceral leishmaniasis.  Bacterial endocarditis.  Brucellosis, tuberculosis, salmonellosis. 4. Rheumatological conditions: Rheumatoid arthritis (Felty’s syndrome). SLE. 5. Others: (sarcoidosis, amyloidosis, glycogen storage disease)

Another approach to causes of splenomegaly: a. With hepatomegaly: o Early cirrhosis with portal hypertension. o Lymphomas/leukaemias. o Myeloproliferative disorders. 56 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

b.

c.

d.

e.

f.

g.

o Haemolytic anaemias. o Glandular fever. o Amyloidosis, sarcoidosis, glycogen storage disease. With lymphadenopathy: o Glandular fever. o Lymphomas/leukaemias. o Sjogren’s syndrome. With fever: o Infections: (malaria, bacterial endocarditis, EBV, TB, CMV). o Malignancies and sarcoidosis. With anaemia: o Haemolytic anaemias. o Leishmaniasis. o Malignancy. With purpura: o Septicaemia. o Memimgiococcaemia. o DIC. With arthritis: o Rheumatoid arthritis. o SLE. o Sjogren’s syndrome. o Vasculitis. Massive splenomegaly: o Malaria. o Myelofibrosis. o CML. o Visceral leishmaniasis. o Gaucher’s syndrome.

4. Right & left kidneys: (Are they bimanually palpable?) 5. Urinary bladder: If distended can be palpated as a rounded swelling in the hypogastrium. 6. Aorta and para-aortic lymph nodes: 7. Femoral pulse:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

III.

Percussion: A. B. C. D. E.

Liver: Spleen: Urinary bladder: Other masses: Ascites:  Dull in flanks.  Shifting dullness positive.  Fluid thrill positive (in massive ascites). F. Large ovarian cyst: Resonant in flanks

IV.

Auscultation: A. Bowel sounds:  Normal (intermittent low or medium pitched gurgles).  Increased (borborygmi: frequent loud gurgles): in mechanical intestinal obstruction.  Absent: in paralytic ileus B. Vascular bruits:  Aortic: (above and to the left of the umbilicus)  Renal: (on either side of the midline in the mid abdomen)  Femoral: C. Succussion splash:  Heard in pyloric stenosis, advanced intestinal obstruction and paralytic ileus.

V.

Examination of the groin and genitalia:  Herniae (inguinal or femoral):  Lymph nodes:  Scrotal swellings: hydrocele (do transillumination test), epididymal cyst or epididymo-orchitis.

VI.

Rectal examination: For masses, prostate (males) and cervix (females).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

The Nervous System History & Examination

First of all you must introduce yourself to the patient, offer a greeting and take permission for history taking and clinical examination.

History: Demographic Data: Name: Occupation:

Age:

Gender: Original home: Date of Admission:

Residence:

Marital Status:

C/O: (same words of the patient and duration in a chronological order) History of presenting illness: 1- Episodic loss of consciousness: a) Syncope: (transient loss of consciousness due to inadequate cerebral perfusion): (Patients may use terms such as: blackout, faint, dizzy spells or funny turns)  Where the attack has taken place?  What are the triggering factors? (pain, emotional upset, unpleasant sights, exercise or change in position from lying or sitting to standing)  Are there any warning symptoms? (light-headedness, tinnitus, nausea and blurring of vision)  Duration of the attack:  Frequency:  What happens during the attack? (ask a witness): Incontinence of urine: Body stiffening: Brief twitching of the limbs (abnormal movements):  Skin colour during the attack: (pale)  How quickly the patient recovers?  What induces recovery? (lying flat)  Are there any associated symptoms (palpitations, chest pain, dyspnoea)? e.g.: causes of syncope are: i.

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Reflex: due to autonomic over-activity (reflex bradycardia and peripheral vasodilatation)  Vasovagal: o Triggered by emotions, pain, fear or standing for a long time.

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

o

Preceded by a prodrome of nausea, sweating, light headedness and greying of vision. o During the attack the patient becomes very pale. o Recovery is rapid on lying flat but associated with nausea.  Situational: occurs after a paroxysm of coughing or during micturition.  Carotid sinus syncope: due to carotid sinus hypersensitivity to external stimuli (shaving the neck, wearing a tight collar). ii.

Orthostatic: (postural hypotension)  Unsteadiness or loss of consciousness on standing from lying position.  Occurs in elderly, autonomic neuropathy, drugs (vasodilators, diuretics) and volume depletion (haemorrhage, diarrhoea).  Recovery is rapid on lying flat.

iii.

Cardiac:  Occurs suddenly without prodromal symptoms.  Due to: complete heart block, supraventricular/ventricular tachycardia, HOCM and aortic stenosis (AS).  Syncope occurring during exercise suggests HOCM or AS.  Recovery is rapid.

b) Seizures:  Defined as: any abnormal clinical event caused by an electrical discharge in the brain.  Major seizures cause loss of consciousness due to sudden dysfunction of the electrical mechanisms of the brain.  Epilepsy is defined as tendency to have recurrent seizures. 

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What type of seizures? (ask the patient and a witness) I. Primary generalized: a. Tonic- clonic (grand mal): Preceded by an aura then the body becomes rigid (tonic phase) and the patient looses consciousness, falls down heavily (if standing) often sustaining injury. Respiration is arrested and the patient becomes cyanosed. After a few moments the rigidity is periodically relaxed producing clonic jerks (clonic phase). b. Tonic: (without a clonic phase) c. Myoclonic: sudden violent jerks involving a group of muscles in a limb. d. Atonic: (becomes flaccid) e. Absence (petit mal): Sudden brief pauses (<10 seconds) e.g.: patient suddenly stops talking in mid-sentence then carries on where left off. Presents in childhood. Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

II.

Secondary generalized: Seizures have focal origin (face or limb) then progress to involve the whole body.

III.

Partial: a. Partial motor:  Epileptic activity arising in the motor cortex causes partial motor seizures in the form of rhythmical jerking or sustained spasm of the contralateral face, arm, trunk or leg.  May remain localized to one part or may spread to involve the whole side (Jacksonian seizures).  Prolonged episodes may cause paralysis of the involved limb lasting for several hours after the seizures (Todd’s paralysis). b. Partial sensory:  Seizures arising in the sensory cortex causes unpleasant tingling or electric sensations in the contralateral face or limbs.  May spread over the body (Jacksonian). c. Complex: (e.g.:. temporal lobe epilepsy)  Consciousness is impaired (without the patient collapsing to the ground) + automatism (lip smacking, chewing, swallowing, repeatedly scratching the head).  After a few minutes the patient regains consciousness but feels drowsy.



What are the triggering factors? (sleep deprivation, alcohol withdrawal, recreational drug misuse, physical and mental exhaustion, flickering lights: TV/computer screens and intercurrent infections)



What happens before, during and after the seizures?  Pre-ictal: aura: {alterations of mood, memory and perception such as: undue familiarity (déjà vu) or unreality (jamais vu), hallucinations (auditory, olfactory, visual or gustatory), emotional changes (fear, sexual arousal) or visceral sensations (nausea, epigastric discomfort)}.  Ictal: (tongue biting, frothing, upward rolling of eyeballs, cyanosis and loss of sphincteric control)  Post-ictal: (confusion, headache, sleeping and amnesia)

  

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Duration of the seizures: Frequency: If multiple, did the patient regain consciousness between the attacks?

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 N.B: How to differentiate between psychogenic non-epileptic seizures and true seizures? Features of psychogenic seizures are: Asynchronous purposeful limb movements Rhythmic pelvic movements (pelvic thrusting) Side-to-side head shaking Elaborate arching of the back Ictal crying Vocalization during the tonic clonic phase Closed eyelids and resistance to eyelid opening Lack of cyanosis and severe tongue biting Rapid post-ictal re-orientation  N.B: How to differentiate between syncope and seizures? Regarding syncope: there is no aura, cyanosis, tongue biting or post-ictal (confusion, amnesia, and headache). 2- Persistent loss of consciousness: (coma) Due to bilateral hemisphere or brain stem disease. Ask about: mode of onset and any precipitating events  Causes of coma are: 1. Metabolic disturbances: (drug overuse, DKA, hyperosmolar coma, hypoglycaemia, hyponatraemia, hypothermia, hypothyroidism, uraemia, hepatic and respiratory failure). 2. Trauma: (cerebral contusion, extradural/subdural haematoma). 3. Cerebrovascular disease: subarachnoid haemorrhage, intracerebral haemorrhage, brainstem infarction/haemorrhage and cerebral venous sinus thrombosis). 4. Infections: (meningitis, encephalitis, cerebral abscess and general sepsis). 5. Others: (epilepsy, brain tumour and thiamin deficiency). 3- Dizziness and vertigo : (feeling of spinning of the patient or surroundings due to abnormal perception of movement)  Causes of vertigo are: A. Peripheral: {labrynthitis (vestibular neuronitis), benign paroxysmal positional vertigo and Meniere’s disease (vertigo, tinnitus, sensorineural deafness and sense of fullness in the ear)}. B. Central: (brainstem ischaemia/infarction, acoustic neuroma). 4- Disorders of movement: a) Negative symptoms: (motor weakness, lack of co-ordination, lack of stability and body stiffness). 62 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Motor weakness: ask about: o Site: {a few muscles, a limb, both lower limbs (paraparesis), both limbs on one side (hemiparesis) or all limbs (quadriparesis)}. o Onset (gradual/sudden): o What time of the day? What was he/she doing? o Progression (slow/rapid): How did it occur? (In one limb then involved the others)? After how long it reached the maximum? For how long it remained steady? When did it begin to improve? o Associated Symptoms: In cases of paraplegia: {Numbness, lower limb pain, backache, history of recent trauma to the back, sphincteric disturbances, weakness of abdominal muscles (patient cannot roll from side to side), upper limb weakness, neck pain/stiffness/weakness and vaccination or infections ( diarrhoea, upper respiratory tract infection or any febrile illness) preceding the weakness}. In cases of hemiplegia: {headache, vomiting, blurring of vision, seizures and loss of consciousness} o

Past history of: Similar condition, transient ischaemic attack (transient loss of vision: amaurosis fugax), back trauma and chronic cough or contact.

b) Positive symptoms: (abnormal movements such as tremor, chorea, athetosis, hemiballismus, dystonia, myoclonus and tics).

 Tremor: rhythmic oscillating movement of a limb, part of a limb or the head. It is divided into: 1/ Rest tremor: (in Parkinson’s disease) 2/ Action:  Exaggerated physiological tremor: (anxiety, fatigue, thyrotoxicosis, alcohol withdrawal and drugs: beta agonists).  Essential tremor: (familial)  Postural: tremor of the head in the upright position (titubation)  Intention tremor: (at the end of movement, occurs in cerebellar disease).  Asterixis (flapping tremor): in metabolic disturbances (renal/hepatic failure, hypercapnia), drug toxicity (phenytoin) and acute focal parietal or thalamic lesions.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Chorea: (Greek for dance): rapid, jerky, small amplitude, semi-purposeful involuntary movements of the limbs (resemble fidgety movements) or the face (resemble grimaces). It is due to disease in the caudate nucleus.  Athetosis: slower writhing movements of the limbs. (Often combined with chorea: choreo-athetosis).  Hemiballismus: unilateral, sudden, jerky, wild flinging movements of the proximal limb muscles. It is due to vascular lesions of the subthalamic nucleus.  Dystonia: movement disorder in which a limb or the head involuntarily takes up an abnormal posture. It may be generalized (basal ganglia disease) or focal/segmental (spasmodic torticollis: head involuntarily turns to one side).  Myoclonus: brief,isolated, random, non purposeful jerks of muscle groups in a limb. May occur normally at the onset of sleep (hypnic jerks) or in some forms of epilepsy (disorders of cerebral cortex).  Tics: repetitive semi-purposeful movements such as blinking, winking, grinning or screwing up of the eyes. The patient can suppress them for a short time.

5- Sensory Symptoms: a/ Abnormal sensations: {tingling, paraethesia (pins and needles) and pain} b/ Loss of normal sensations: (touch, pin-prick, temperature, vibration and joint position)

6- Headache: a) b) c) d) e) f) g) h)

Time and mode of onset: (very sudden onset: subarachnoid haemorrhage or migraine) Frequency & Periodicity: Duration: Time of the day(morning, night): Precipitating Factors: Aggravating & Relieving Factors: where does it start and how does it evolve (progression): Quality & severity: What is the effect of posture, coughing and straining? i) Symptoms preceding the headache (aura): {focal neurological symptoms e.g.: zigzag (fortification spectra), spreading scintillating scotoma or senosory symptoms (tingling sensation over part of the body)}. j) Associated symptoms: (nausea, vomiting, photophobia, phonophopia, fever, rash, neck stiffness) k) Family History of Headache: l) Other medical or neurological problems:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Classification of headache:  Acute: due to subarachnoid haemorrhage, acute meningitis, migraine, cluster headache, neuralgias (trigeminal, post-herpetic), angle closure glaucoma, sinusitis and vasodilator drugs.  Subacute: due to infections (tuberculous meningitis, cerebral abscess), raised intracranial pressure (tumour, hydrocephalus), temporal arteritis and idiopathic intracranial hypertension. N.B: headache due to raised ICP is: *worse in the morning and improves through the day *associated with morning vomiting *worse with coughing, straining and bending forward * dull ache * relieved by analgesia  Chronic: tension headache (bilateral, constant, described as pressure over the head), analgesic overuse headache, cervical spondylosis and depression. 7-

Symptoms suggestive of raised ICP: Early morning vomiting, blurring of vision, headache and seizures

8- Symptoms of cranial nerves affection: I: (Anosmia): II: (Decreased visual acuity, field defects): III, IV, VI: (Diplopia) V: Difficult mastication (motor): Abnormal face sensation (Sensory): VII: (Accumulation of food behind the cheeck, mouth deviation): VIII: (Decreased hearing, tinnitus and vertigo): IX, X, XI, XII: (Dysphagia, dysarthria, dysphonia and nasal regurgitation): 9- Symptoms of autonomic disturbances: A. Sphincteric disturbances: 1. Bladder:  Atonic bladder (LMNL): difficulty in initiating micturition and overflow incontinence  Hypertonic bladder (UMNL): frequency, urgency, urge incontinence and incomplete bladder emptying  Cortical lesion: loss of awareness of bladder fullness, inappropriate micturition and loss of social control. 2. Bowel: constipation (damage to autonomic components) or faecal incontinence (Lesions in conus medullaris, somatic roots S 2, 3, 4 or pudendal nerves). B. Fainting or falling down when standing (postural hypotension): C. Erectile dysfunction:

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

10- Disturbances of higher cerebral functions: (Memory, behaviour, speech and language, orientation, attention and concentration, judgment and reasoning). * Global disturbance of higher cerebral function is divided into: a. Acute confusional state (delirium): Drowsiness with disorientation, confusion being worse at night and associated emotional disturbance (anxiety, irritability or depression) or psychomotor changes (agitation, restlessness or retardation). Causes of delirium are: 1. Infective: (Chest infection, UTI, septicaemia, meningitis, encephalitis) 2. Metabolic/endocrine: {Hypoxia (respiratory failure), renal failure, liver failure, hyper/hypoglycaemia, hyper/hypocalcaemia, hyponatraemia, hypo/hyperthyroidism}. 3. Vascular: (Acute cerebral haemorrhage/infarction, SAH) 4. Toxic: (Alcohol intoxication/withdrawal, drugs) 5. Neoplastic: (Primary or secondary brain tumours, paraneoplastic syndrome) 6. Trauma: (Subdural haematoma, cerebral contusion) 7. Others: (post-ictal state) b. General cognitive decline (dementia): Is a clinical syndrome characterized by loss of previously acquired intellectual function (memory, cognition and personality) in the absence of drowsiness.

11- Speech disorders: A. Aphasia: disturbance of understanding and/or expression of words due to damage in the language areas in the dominant hemisphere. It is classified into: 1. Receptive, sensory (Wernicke’s aphasia): Fluent, poor comprehension and poor repetition. (Wrong words are produced). Lesion in Wernicke’s area (superior posterior temporal lobe). 2. Expressive, motor (Broca’s aphasia): Non-fluent, good comprehension and poor repetition. (verbal output is low). Lesion in Broca’s area (inferior frontal lobe).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

3. Conduction aphasia: fluent, good comprehension and poor repetition. Damage to the arcuate fasiculus which connect between Broca's and Wernicke's areas. 4. Transcortical sensory aphasia: fluent, poor comprehension and good repetition. 5. Transcortical motor aphasia: non-fluent, good comprehension and good repetition. 6. Global aphasia: non-fluent, poor comprehension and poor repetition. Damage to both Broca's and Wernicke's areas. B. Dysarthria: difficulty in speech articulation due to local lesions of the tongue, lips, ill-fitting dentures or any disruption of the neuromuscular pathway such as: 1) Pseudobulbar (spastic) dysarthria: Due to bilateral upper motor neuron lesion of the corticobulbar tract. It is characterized by spastic contracted tongue, jerky speech, emotional lability and brisk jaw jerk. 2) Bulbar palsy: Due to lower motor neuron lesion of 9,10,11,12 cranial nerves (weakness of tongue and palatal muscles leading to nasal quality of speech). 3) Extrapyramidal dysarthria: Monotonous speech as in Parkinson's disease. 4) Cerebellar dysarthria: Slow slurred speech (similar to the speech of a drunken person). 5) Myasthenia gravis: Fatiguing speech. C. Dysphonia: failure of the vocal cords to generate sounds properly (hoarse voice or whispered speech) due to vocal cords pathology (laryngitis) or paralysis (recurrent laryngeal nerve damage).

Clinical examination: 1. Higher mental function: a) Assessment of the level of consciousness: Eye opening: Spontaneous: To speech: To pain: No response:

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by the Glasgow Coma Scale (GCS):

4 3 2 1

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Verbal response: Orientated: Confused (talks in sentences but disorientated): Inappropriate words (not sentences): Incomprehensive sounds (groans or grunts): No vocalization:

5 4 3 2 1

Motor response: Obeys commands: 6 Localizes to pain: 5 Withdrawal: 4 Abnormal flexion: 3 Abnormal extension: 2 No response: 1 *maximum GCS is 15, minimum is 3, 8 or less indicates coma. b) c) d) e) f)

Orientation: to time, place and person. Attention and concentration: Memory: short and long term Mood: Speech: (tested by listening to spontaneous speech, naming objects, obeying commands, repetition, reading, writing, counting steadily to 30 to assess muscle fatigue, coughing and saying "Aaah"). g) Handedness: 2. Examination of the cranial nerves: 1) The Olfactory nerve: pure sensory nerve conveys sense of smell.  Anatomy: Olfactory filaments pass from the smell receptors (high in the nasal cavity) through the cribriform plate to the olfactory bulb, synapse with 2nd order neurons which project via the olfactory tract to the olfactory centre in the temporal lobe.  Abnormal findings:  Anosmia: loss of the sense of smell (due to: head injury, skull base tumours, Parkinson's disease and Huntington's disease).  Parosmia: pleasant odours are perceived as unpleasant (due to: head injury, sinus infection and side effect of drugs).  Olfactory hallucinations: occurs in Alzheimer's disease and temporal lobe epilepsy). 2) The Optic nerve: Purely sensory, unable to regenerate.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Anatomy: The visual pathway consists of: The retina (Rod photoreceptors are responsible for night and peripheral vision, Cone receptors are responsible for colour and central vision), the optic nerve, optic chiasm (nasal fibres responsible for temporal visual field decussate), optic tract, lateral geniculate bodies of the thalamus, optic radiation (pass in posterior part of internal capsule and parietal and temporal lobes) and the occipital cortex.  Abnormal findings:  Unilateral lesion of the optic nerve: leads to total loss of vision.  Compression of the optic chiasm: leads to bitemporal hemianopia.  Lesion of the optic tract: leads to homonymous hemianopia.  Lesion of the lower fibres of optic radiation (in temporal lobe): leads to superior quadrantanopia.  Lesion of the upper fibres of optic radiation (in parietal lobe): leads to inferior quadrantanopia.  Lesion of the occipital lobe (primary visual area): leads to homonymous hemianopia with sparing of the macula.  Lesion of secondary visual areas: leads to visual agnosia (inability to recognize visual stimuli) and visual hallucinations.  Bilateral occipital lobe lesion: leads to cortical blindness.  Examination sequence: 1. Inspection: for A. Eyelids: *Ptosis (drooping of the upper eyelid) is due to : i. Neurogenic causes: 3rd nerve palsy and Horner's syndrome ii. Neuromuscular junction: myasthenia gravis iii. Myogenic: myotonic dystrophy iv. Local causes: chronic orbital inflammation, tumours, degenerative disease or trauma. v. Congenital (bilateral ptosis is due to: myotonic dystrophy, myasthenia gravis, syphilis or congenital) *Lid retraction: sclera is visible above the iris due to thyroid eye disease (do lid lag test) B. proptosis: forward bulging of the eyeball due to: thyroid eye disease, caroticocavernous fistula, local causes (orbital cellulitis, haematoma, tumour) or Wegner's granulomatosis. 2. Visual acuity: by Snellen chart 6 meters from the patient or by finger counting, hand movement or just light. 69 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

3. Visual fields: by confrontation method at the bedside or by perimetry (proper method). 4. Examination of the pupil: for shape, symmetry, light and accommodation reflexes. Light reflex (direct and consensual): when light is shown on one eye both pupils constrict due to the dual innervation of the pupils. Afferent limb of the reflex: optic nerve, chiasm, optic tract terminating in EdingerWestphal nucleus. Efferent limb: occulomotor nerve passing through the ciliary ganglion to constrictor pupillae muscle. Accommodation reflex: ask the patient to look at a far object then suddenly bring the object near to the eyes, the pupils constrict. Afferent and efferent limbs are the same as light reflex. Abnormal findings: 

Miosis (small pupil): seen in: *Horner's syndrome: (congenital or acquired damage to the cervical sympathetic chain leading to ptosis, miosis, enophthalmos and anhydrosis). *Argyl-Robertson pupil: (bilateral, small and irregular pupils do not react to light but react to accommodation associated with bilateral ptosis, due to syphilis). *Senile miosis *Pontine haemorrhage *Congenital *Drugs: opiates, pilocarpine (parasympathomimetic) and organophosphate toxicity.



Mydriasis (dilated pupil): seen in: *Oculomotor nerve palsy *Holmes-Adie pupil: (one pupil is larger than the other, react to accommodation but not to light, due to degeneration of parasympathetic nerves in ciliary ganglion). *Drugs: atropine, cocaine, cobalt and ethylene glycol.



Marcus Gunn pupil: due to optic nerve damage leading to relative afferent pupillary defect (RAPD): (loss of direct and consensual light reflex when light is shown on the affected eye with normal direct and consensual reflex when light is shown on the normal eye).



Essential anisocoria: (common normal variant, one pupil is larger than the other but they both behave normally).

5. Colour vision: by Ishihara test. 6. Ophthalmoscopy

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

3) The Oculomotor nerve: - Motor and parasympathetic, arises from the midbrain. - Supplies the external ocular muscles: superior, inferior and medial recti (which move the eye upwards, downwards and medially respectively), inferior oblique (moves the eye upwards and laterally) and Levator palpeprae superioris (elevates the upper eyelid). - Via its parasympathetic fibres (originating from the Edinger-Westphal nucleus), it supplies constrictor pupillae muscle and ciliary muscles (focuses the lens for near vision: accommodation).

     

  

Abnormal findings: Oculomotor nerve palsy: ptosis, dilated pupil and the eye is deviated downwards and laterally. It is caused by: Diabetes mellitus Vasculitis: temporal arteritis, SLE Posterior communicating artery aneurysm (headache or periorbital pain + 3rd nerve palsy). Cavernous sinus thrombosis (3rd,4th and 6th nerves palsies, hyperesthesia of the upper face and eye pain due to trigeminal nerve involvement (ophthalmic division), grossly oedematous eyelids and chemosis). Weber's syndrome: ipsilateral 3rd nerve palsy + contralateral hemiplegia (due to midbrain stroke). False localizing sign: due to uncal herniation throught tentorium if raised ICP. Others: amyloidosis, MS.

4) The Trochlear nerve: Purely motor, arises from the midbrain. Decussates posteriorly before leaving the midbrain (so, right nucleus supplies left eye and left nucleus supplies right eye). - Supplies superior oblique (moves the eye downwards and medially). Abnormal findings: 4th nerve palsy: patient complains of diplopia when reading or walking downstairs (superior oblique is maximally effective on looking medially).

5) The Trigeminal nerve: (see below)

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

6) The Abducens nerve: - Purely motor, arises from the pons. - Has a long course around the brainstem before it pierces the dura to enter the cavernous sinus (which also contains the 3rd, 4th, 5th cranial nerves and the internal carotid artery). - Supplies lateral rectus (abducts the eye). Abnormal findings: 6th nerve palsy: convergent squint (eye is deviated medially) and diplopia on lateral gaze.

Examination sequence: (3rd, 4th and 6th ) a) Ocular alignment: look for squint which is either congenital (non-paralytic, not associated with diplopia) or acquired (due to paresis of one of the ocular muscles and it is associated with diplopia). b) Ocular movement: ask the patient to follow your finger and note the following: * If the patient develops diplopia determine whether it is horizontal or vertical. * Nystagmus: involuntary oscillations of the eye, classified according to direction into: (horizontal, vertical and multidirectional) and according to type into: jerk (which has fast and slow phases) and pendular (equal oscillations about a central point). Jerk: is the most common type of nystagmus, it is due to: - Peripheral vestibular disease: (vestibular neuronitis and Meniere's disease), the direction of the jerk is either horizontal or vertical, usually associated with vertigo. - Central vestibular disease: (multiple sclerosis and cerebrovascular disease involving the central vestibular connections), not associated with vertigo.  Pendular: results from cerebellar or brainstem disease (multiple sclerosis, spinocerebellar degeneration and brainstem ischaemia).  Vertical: further subdivided into:  Upbeat: due to upper brainstem lesions (MS, infarction, Wernicke's encephalopathy) and cerebellar vermis lesions.  Downbeat: due to lesions around foramen magnum (Arnold- Chiari malformation or demyelination) or drugs (phenytoin and lithium intoxication). *Internuclear ophthalmoplegia: is due to demyelination of the medial longitudinal bundle within the brainstem (which co-ordinates the lateral rectus of one eye with the medial rectus of the other). It is manifested as ataxic nystagmus in the abducted eye with failure to adduct the other eye.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

The Trigeminal nerve: - Is a mixed cranial nerve (sensory and motor). - The cell bodies of the sensory fibres are located in the trigeminal ganglion then pass to the pons. - The sensory division has 3 branches: *Ophthalmic (V1): provides sensation to the skin of upper eyelid, forehead, scalp and eye (cornea and conjunctiva). *Maxillary (V2): supplies mucous membranes of the upper mouth, roof of pharynx, (gums, teeth and palate) of the upper jaw and sinuses. *Mandibular (V3): supplies the floor of the mouth, common sensation to the anterior two thirds of the tongue, gums and teeth of the lower jaw, mucosa of the check, skin of lower lips and jaw except the angle of the jaw (supplied by C2). The motor division: runs in the mandibular branch and supplies muscles of mastication (temporalis, masseter, lateral and medial pterygoids). Examination sequence:  Sensory: test sensation in V1, V2, V3  Motor: test muscles of mastication  Corneal reflex: afferent limb is V1; efferent limb is the facial nerve (touching the lateral edge of the cornea leads to direct and consensual blinking of the eyes).  Jaw jerk: is normally absent or just present. Brisk jaw jerk occurs in pseudobulbar palsy (bilateral upper motor neuron lesion above the level of the pons). Abnormal findings:  Unilateral loss of facial sensation: due to injury to V1, V2 or V3 in association with facial fractures or local invasion by tumour.  Lesions within the cavernous sinus: loss of corneal reflex, loss of sensation in the distribution of V1 and 3rd, 4th and 6th cranial nerve palsies.  Herpes Zoster (reactivation of the latent varicella zoster in the trigeminal ganglion): painful vesicular eruptions in the distribution of V1. (Less commonly affect V2 and V3).

7) The Facial nerve: is a mixed cranial nerve. – Motor: to muscles of facial expression. – Sensory: receives taste sensation from the anterior two thirds of the tongue (via chorda tympani branch). – Parasympathetic: to lacrimal, sublingual and submandibular salivary glands (via nervus intermedius). 73 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Anatomy: Arises from the lower pons, enters the internal auditory meatus together with the vestibulocochlear nerve, continues in the facial canal of the temporal bone where it forms the geniculate ganglion and gives off (nerve to stapedius, nervus intermedius and joined by the chorda tympani fibres), and then exists the skull via the stylomastoid foramen to pass through the parotid gland where it gives off its terminal branches to muscles of facial expression.

a) 





Abnormal findings: Unilateral lower motor neuron facial palsy (weakness of both upper and lower facial muscles) is due to: Lesions in the pons: (infarcts, tumours, demyelinating diseases (MS)  Ipsilateral 6th and 7th nerve palsies with contralteral hemiplegia (crossed hemiplegia).  Paralysis of facial muscles (salivation, lacrimation and taste are NOT affected). Lesions at the cerebello-pontine angle: (Acoustic neuroma) *Ipsilateral 5th, 6th, 7th and 8th nerves palsies. *Ipsilateral cerebellar signs. *Paralysis of facial muscles and diminished salivation, lacrimation and taste in the anterior two thirds of the tongue. Lesions in the facial canal (geniculate ganglion): (Bell's palsy, Ramsay hunt syndrome) * Paralysis of facial muscles, diminished (salivation, lacrimation and taste in the anterior two thirds of the tongue) and hyperacusis.  Bell's palsy: idiopathic condition presenting with acute lower motor neuron facial palsy, often preceded by post-auricular pain, may be associated with loss of taste in the anterior tongue (hypogeusia /ageusia), hyperacusis (high-pithched sounds are heard unpleasantly louder than normal) and dry eyes.  Ramsay- Hunt syndrome: reactivation of herpes zoster in the geniculate ganglion, presenting with severe lower motor neuron facial palsy, ipsilateral loss of taste, dry mouth (buccal ulceration) , dry eyes and painful vesicular eruptions within the external auditory meatus. Often the vestibulocochlear nerve is affected as well.



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Lesions distal to the stylomastoid foramen: * Paralysis of facial muscles only. * Due to: diabetes mellitus, leprosy, HIV and parotid tumours.

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

b) Bilateral lower motor neuron facial palsy: caused by:  Guillian- Barre syndrome  Sarcoidosis  Lyme disease  Poliomyelitis c) Upper motor neuron facial palsy: weakness is marked in the lower facial muscles with relative sparing of the upper face (because of the bilateral cortical innervation of the upper face), is due to supranuclear lesions (stroke above the level of the pons). 8) The Vestibulochoclear nerve: sensory nerve Arises from the pons, has 2 components: *Vestibular: concerned with balance and equilibrium (connected with the cerebellum) *Cochlear: concerned with hearing. Examination sequence: a) Testing hearing: properly by audiometry, at the bedside by: 1. Whispered voice test 2. Rinne's test: normally air conduction is better than bone conduction (AC > BC), this is a positive Rinne's test. If BC > AC, negative Rinne's test, indicates conductive deafness. 3. Weber's test: normally the sound is heard equally in both ears. - Weber's lateralizes to the affected ear in conductive deafness (the sound is better heard in the affected ear). - Weber's lateralizes to the unaffected ear in sensorineural deafness (the sound is better heard in the unaffected ear). b) Vestibular function: *Inspect for nystagmus *Dix- Hallpike positional test: if the patient has peripheral vestibular disease he/she develops vertigo and nystagmus which fatigues on repetition of the test (adaptation). If the patient has central pathology he/she develops nystagmus which persists on repetition (no adaptation). 9) The Glossopharyngeal nerve: mixed cranial nerve Arises from the medulla, leaves the skull through the jugular foramen. Sensory: to tonsils, pharynx and carries taste sensation from the posterior one third of the tongue. Motor: to pharyngeal muscles Parasympathetic: to the parotid gland.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

10) The Vagus nerve: mixed cranial nerve - Arises from the medulla, leaves the skull through the jugular foramen. - Motor: to soft palate, pharyngeal and laryngeal muscles (via the recurrent laryngeal nerve). - Sensory: to several viscera. - Parasympathetic: to several viscera. Abnormal findings: (9th and 10th)  Unilateral 9th and 10th nerves lesions: deviation of the uvula towards the normal side. Occurs in: skull base tumours, fractures and lateral medullary syndrome.  Bilateral 9th and 10th lesions: dysphagia, dysarthria, dysphonia and nasal regurgitation. Occurs in: bulbar palsy (motor neuron disease) and pseudobulbar palsy (MS, CVA).  Recurrent laryngeal nerve lesion: dysphonia and bovine cough. Occurs in: lung cancer, mediastinal tumours, aortic arch aneurysms and post thyroid surgery. 11) The Accessory nerve: has 2 components: Cranial part: arises from the medulla, closely related to the vagus. Spinal part: arises from the anterior horn cells of C1- C5, ascends through the foramen magnum then exits the skull through the jugular foramen together with the 9th, 10th and the cranial part. Abnormal findings:  Unilateral 11th nerve lesion: wasting and weakness of trapezius (with displacement of the scapula) and sternocleidomastoid. Occurs in: penetrating injuries, local invasion by tumours or surgery in the posterior triangle of the neck. 12) The Hypoglossal nerve: purely motor Arises from the medulla, exits the skull through the hypoglossal canal. Motor: to the muscles of the tongue. Abnormal findings:  Unilateral lower motor neuron lesion: unilateral wasting of the tongue and deviation towards the affected side.  Bilateral lower motor neuron lesion: global wasting (shrunken tongue) and fasciculations. Occur in bulbar palsy.  Bilateral upper motor neuron lesion: spastic tongue (bunched up or conical). Occurs in pseudobulbar palsy.

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

3. Examination of the neck: for:   

Stiffness: (see below for other signs of meningeal irritation) Weakness: (test the power: flexion, extension and rotation) Carotid bruit:

4. Examination of the motor system:  Inspection and palpation of muscles: for:  Muscle bulk: wasting/atrophy occurs in lower motor neuron lesions and longstanding upper motor neuron lesions (disuse atrophy). Hypertrophy occurs in certain occupations and sports Pseudo-hypertrophy occurs in muscular dystrophies (doughy feeling on palpation).  Deformities: (claw hand, pes cavus, flexion deformities or contractures)  Fasciculations: involuntary muscle twitches, occurs in lower motor neuron lesions.  Involuntary movements: tremor, chorea, athetosis, hemiballismus, myoclonic jerks, dystonia and tics. 

Tone: is the resistance felt by the examiner when moving a joint passively through its range of movement. Abnormal findings: 1. Hypotonia (flaccidity): occurs in lower motor neuron lesions, cerebellar disease and in the early phases of cerebral or spinal schock. 2. Hypertonia: has 2 principal types: *Spasticity: velocity- dependent resistance to passive movement (i.e. it is detected with quick movements). Occurs in upper motor neuron lesions. - In mild forms it is detected as a 'catch' at the beginning of passive movement (clasp- knife spasticity). - In more severe cases it limits the range of movement and may be associated with contracture. *Rigidity: sustained resistance throughout the range of passive movement easily detected when the limb is moved slowly (lead-pipe rigidity). Occurs in Parkinson's disease and other extrapyramidal conditions. - The presence of a Parkinsonian tremor leads to regular interruption of the movement giving it a jerky feel (cog-wheel rigidity).



Power: Grades of muscle power: Grade 0: no muscle contraction visible Grade 1: flicker of contraction but no movement Grade 2: joint movement when effect of gravity is eliminated

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

Grade 3: movement against gravity but not against resistance Grade 4: movement against resistance but weaker than normal Grade 5: normal power Examination sequence: a) Upper limb muscles: 1) Small muscles of the hand: {are supplied by the ulnar nerve (C8, T1) except 5 muscles supplied by the median nerve (C8, T1), which are: 1st and 2nd Lumbricals, Opponens pollicis, Abducter pollicis brevis and Flexor pollicis brevis (LOAF)}. They are tested in the following sequence:  Abductor pollicis brevis: abducts the thumb in a plane at right angle to the palmar surface of the index finger.  Opponens pollicis: brings the thumb into opposition to the fingers.  Adductor pollicis brevis: adducts the thumb towards the palmar surface of the index finger.  Dorsal interossei: abduct the fingers (DAB)  Palmar interossei: adduct the fingers (PAD)  Lumbricals: flex the metacarpophalangeal joints and extend the interphalangeal joints. 2) Flexors of the fingers: (hand grip) supplied by the median nerve (C7, 8). 3) Extensors of the wrist: extensor carpi radialis and ulnaris, supplied by the radial nerve (C6, 7). 4) Flexors of the wrist: flexor carpi radialis, supplied by the median nerve (C6, 7) and flexor carpi ulnaris, supplied by the ulnar neve (C7, 8). 5) Brachioradialis: flexes the elbow when the forearm is midway between pronation and supination, supplied by the radial nerve (C5, 6). 6) Biceps: flexes the elbow when the forearm is in full supination, supplied by the musculocutaneous nerve (C5, 6). 7) Triceps: extends the elbow, supplied by the radial nerve (C7, 8). 8) Supraspinatus & deltoid: abduct the shoulder (the first 30 degrees of abduction is carried out by supraspinatus, the remaining 60 degrees is by deltoid). Deltoid also flexes and extends the shoulder, supplied by the axillary nerve (C5, 6).

b) Lower limb muscles: 1. Extensors of the hip: gluteus maximus, supplied by (L5, S1, 2). 2. Flexors of the hip: Psoas and iliacus muscles, supplied by (L2, 3). 3. Adductors of the thigh: (Gracilis, adductor longus, brevis and magnus) supplied by the obturator nerve (L2, 3).

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Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

4. Abductors of the thigh: gluteus medius, minimus and tensor fasciae latae, supplied by (L4, 5, S1). 5. Extensors of the knee: quadriceps femoris, supplied by the femoral nerve (L3, 4). 6. Flexors of the knee: hamstring muscles, supplied by the sciatic nerve (L5, S1). 7. Dorsiflexion of the ankle: by tibialis anterior, supplied by the deep peroneal nerve (L4). 8. Plantarflexion of the ankle: by the calf muscles (gastrocnemius and soleus), supplied by the tibial nerve (S1, 2). c)

Muscles of the trunk: (the patient is asked to lift his/her head up from the pillow against resistence). If the muscles of the lower abdomen are paralyzed the umbilicus moves upwards, if muscles of the upper abdomen are paralyzed the umbilicus moves downwards (Beevor's sign).

Definitions of muscle weakness:      

Paresis: partial paralysis (weakness) Plegia: complete paralysis Monoplegia: paralysis of one limb (arm or leg) due to root or plexus disease. Hemiplegia: (see below) Paraplegia: paralysis of both legs, usually due to a spinal cord lesion. Quadriplegia: paralysis of all four limbs due to cervical cord disease.

Causes of muscle weakness:  Upper motor neuron lesion: muscle weakness, no wasting, hypertonia (spasticity), hyperreflexia, extensor plantar response and depressed abdominal reflexes. Common causes: cerebrovascular disease (hemiplegia), spinal injury/disease (paraplegia) and multiple sclerosis. - Hemiplegia: is paralysis of one side of the body involving the arm, leg and usually the face, due to a lesion in the corticospinal pathway. - Uncrossed hemiplegia: cranial nerve involvement and hemiplegia are on the same side, (cortical lesion). - Crossed hemiplegial/paresis: is weakness in an ipsilateral cranial muscle group with a contralateral paralysis, (brainstem lesion). *Features of hemiparesis: (see above), in addition to slow, dragging, rolling gait on the affected side (circumduction).

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*How to detect hemiplegia in a comatose patient?  Hypotonia in the paralysed limbs.  Facial asymmetry (angle of the mouth is more open on the paralysed side and the affected cheek moves loosely outwards and inwards with respiration).  Extensor plantar response on the paralysed side. (Abdominal and deep tendon reflexes may be absent on both sides).

 Lower motor neuron lesion: muscle weakness, hypotonia (flaccidity), hypo/areflexia, muscle wasting and fasciculations. Common causes: anterior horn cell damage (motor neuron disease or poliomyelitis), root lesion (radiculopathies) or peripheral nerve lesion (peripheral neuropathies).  Lesion in the neuromuscular junction: Myasthenia gravis: weakness of external ocular and bulbar muscles, worsened by repeated contraction of the affected muscles (myasthenic fatigue). Lambert-Eaton myasthenic syndrome (LEMS): muscle weakness initially but during continued contraction or exertion, strength improves at first followed by weakness if exertion is continued further. (associated with small cell lung cancer).  Lesion in the muscles (myopathies): muscle weakness and wasting (usually proximal), hypotonaia, muscle tenderness (myositis), pseudohypertrophy (muscular dystrophies). Common causes: hereditary conditions (Duchenne, Becker's, myotonic and fascioscapulohumeral muscular dystrophies), polymyositis, alcohol and other toxins. *Myotonia: relaxation is impaired/delayed following muscle contraction. (occurs in myotonic dystrophy).

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Reflexes: a) Deep tendon reflexes: involuntary contraction of a muscle in response to stretch (monosynaptic reflex), e.g.: Knee jerk: L3, 4 Ankle jerk: S1, 2 Triceps jerk: C6, 7 Biceps jerk: C5, 6 Brachioradialis jerk: C5, 6 Abnormal findings:  Hyper-reflexia: occurs in UMNL, thyrotoxicosis and tetanus.

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Hypo/areflexia: occurs in LMNL {lesions affecting the afferent pathway of the reflex arc (peripheral neuropathy and tabes dorsalis), anterior horn cell damage (motor neuron disease, poliomyelitis) and lesions affecting the efferent pathway (peripheral neuropathy)}.  Isolated loss of a reflex: occurs in mononeuropathy/ radiculopathy e.g.: loss of ankle jerk with lumbosacral (S1) disc prolapse.  A normal reflex contraction with delayed relaxation: occurs in hypothyroidism and hypothermia.  Pendular reflex: occurs in cerebellar lesions.  Inverted reflexes: occurs in combined spinal cord and root pathology (cervical spondylosis) e.g.: inverted biceps jerk (absent biceps jerk with brisk flexion of the fingers) due to lesion at C5/6 level.  Hoffman's sign: is a sign of hyper-reflexia, occurs in UMNL (when the distal interphalangeal joint of the patient's middle finger is flicked down into flexion, there is reflex flexion of the thumb).  Finger flexion jerk: is a sign of hyper-reflexia.  Clonus: is a rhythmic series of contractions evoked by sudden stretch of the muscles (tested in the patella and ankle). *Unsustained clonus may occur in healthy individuals. *Sustained clonus occurs in upper motor neuron lesions and is always asscocioated with hyper-reflexia and extensor plantar response. Grading the reflexes: 0: Absent 1: Present (as a normal ankle jerk) 2: Brisk (as a normal knee jerk) 3: Very brisk 4: Clonus b) Superficial reflexes: polysynaptic reflexes elicited by cutaneous stimulation. 1. Plantar reflex: (S1, 2):  Flexor plantar response: flexion of all toes with the ankle dorsiflexed and inverted. This is the normal response.  Extensor plantar response (Babinski's sign): extension (dorsiflexion) of the big toe and fanning (abduction and extension) of the other toes (sometimes it is accompanied by dorsiflexion of the ankle and flexion of the hip and knee). It is a sign of UMNL.  Causes of bilateral extensor (upgoing) plantar: bilateral UMNL (bilateral stroke), hypoglycaemia, deep coma, post epileptic fit and children below the age of one year.

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 Oppenheim's sign: extensor plantar response obtained by pressing heavily along the inner border of the tibia.  Gordon's reflex: extensor plantar response obtained by pinching the Achilles tendon. (Both indicate widespread and severe corticospinal lesion).  withdrawal response: exaggerated extensor plantar response accompanied by dorsiflexion of the ankle and flexion of the hip and knee. (sign of UMNL).  Absent plantar response: spinal shock, paralysis of extensor hallucis longus and sensory loss over S1 dermatome. 2. Abdominal reflexes: (T8-T12)  Absent in: UMNL above T8, LMNL affecting T8-T12, obese people, elderly and multiparous women. 3. Cremasteric reflex: (L1, 2) c) Primitive reflexes: Snout, grasp, palmomental reflexes and glabellar tap: indicate diffuse frontal lobe damage (trauma, anoxia, vascular disease, malignancy, encephalopathy, dementia) and Parkinson's disease.

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Co-ordination: smooth and efficient performance of purposeful movements. - It requires intact sensory, motor and cerebellar function (so test of coordination is influenced by muscle weakness, loss of proprioception and extrapyramidal dysfunction).

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Ataxia: impairment of coordination.

Examination sequence:  Upper limb: a) Finger- nose test: (past pointing, intension tremor and slow clumsy movement). b) Rapid alternating movements: (dysdiadochokinesis: slowness, disorganization and irregularity of movements).  Lower limb: Heel- shin test: (irregular movement)

Other signs of cerebellar dysfunction: 1. 2. 3. 4. 5. 6.

Rebound phenomenon Nystagmus Dysarthria (scanning speech) Hypotonia Pendular knee jerk Gait: ataxic (drunken, wide base) on tandem walking: unsteadiness and patient deviates towards the side of the lesion.

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Causes of cerebellar dysfunction: a) Vascular lesions, trauma, tumour, MS and toxins: alcohol and phenytoin. b) Lesions affecting the cerebellar vermis (concerned with equilibrium): leads to truncal ataxia (difficulty in sitting up and standing, patient tends to fall backwards) and nystagmus. c) Lesions affecting the cerebellar hemispheres (concerned with coordination): leads to incoordination (dysmetria, dysdiadochokinesis). Sensory ataxia: is due to sensory neuropathies or posterior column lesion (tabes dorsalis). The position sense is impaired in the legs and this sensory defect is compensated for by vision, so the unsteadiness becomes apparent only when eyes are closed or in the dark. Romberg's sign: is a test for sensory ataxia (ask the patient to stand with feet close together, then to continue in this posture with the eyes closed: patient becomes unsteady and sway about or may even fall). *In cerebellar disease the ataxia is equally severe whether the eyes are open or closed.

5. Examination of the sensory system: a) Proprioception, vibration and light touch:  1st order neuron: (large, fast-conducting, myelinated) conveys sensation from the peripheral tissues to the dorsal root then to the dorsal (posterior) column of the spinal cord then ascends to the nucleus gracilis and cuneatus in the medulla where it synapses with:  2nd order neuron: crosses the midline (in the medulla) then ascends in the medial lemniscus to the thalamus where it synapses with:  3rd order neuron: ascends from the thalamus to the sensory cortex (parietal lobe). b) Pain, temperature and crude touch:  1st order neuron: (small, slow-conducting, unmyelinated) conveys sensation from peripheral tissues to the spinal cord where it synapses with:  2nd order neuron: crosses the midline (in the spinal cord) and ascends in the contralateral spinothalamic tract to the thalamus where it synapses with:  3rd order neuron: ascends from the thalamus to the sensory cortex. c) Cortical sensations: (parietal lobe) Localization, two point discrimination, stereognosis (ability to identify objects by feeling them: tactile recognition) and graphaethesia (ability to identify letters or numbers written on the palm with the eyes closed). Examination sequence: *Light touch and pin prick (superficial pain): dermatomes tested: Upper limb: C5: lateral aspect of the shoulder, C6: thumb, C7: middle finger, C8: little finger, T1: medial aspect of the forearm, T2: medial aspect of the arm. 83 | P a g e

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Lower limb: L1: area of the inguinal ligament, L2: upper thigh (trouser's pocket) L3: medial aspect of the thigh, L4: medial aspect of the leg, L5: big toe, S1: little toe and sole, S2: back of the thigh (S3, 4: peri-anal region). *Temperature: by tubes of hot and cold water. *Vibration (over bony prominences) and joint position. *cortical sensations: tested only if the other modalities of sensations are intact. Abnormal findings: the lesion may be in:  Peripheral nerves: *Peripheral neuropathies: touch and pin prick sensations are lost in a glove & stocking distribution. *Large fibre peripheral neuropathies: vibration and joint position sense are lost (patient develops staggering/unsteadiness when eyes are closed: sensory ataxia/Rombergism). Occasionally when the patient is asked to close his/her eyes and hold the hands outstretched the fingers will make slow wandering movements. *Injury/damage to individual nerves: loss of all modalities in the nerve territory (e.g.: median/ulnar/radial nerves palsies).  Dorsal root: leads to dermatomal sensory loss.  Spinal cord: traumatic and compressive lesions lead to loss of sensation below the level of the lesion. *Anterior spinal artery occlusion and syringomyelia: lead to loss of pain and temperature sensation (below the lesion) with sparing of vibration and position (dissociated loss). *Hemisection of the cord: leads to ipsilateral UMN weakness, ipsilateral loss of vibration and position with contralateral loss of pain and temperature (Brown- Sequard syndrome).  Intracranial: *Lower brain stem lesion: leads to alternating analgesia (loss of pain and temperature on one side of the face and the opposite side of the body). *Thalamic lesion: leads to patchy sensory impairment on the opposite side of the body with a very unpleasant poorly localized pain (burning quality). *Cortical lesion: loss of localization and two point discrimination, astereognosis (loss of shape appreciation) and sensory inattention/ neglect (stimuli on the affected side are not perceived, the patient is neglecting the affected side). 84 | P a g e

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6. Examination of the autonomic nervous system: The autonomic nervous system is concerned with modulation of function in the cardiovascular and gastrointestinal systems, temperature regulation, sexual reflexes, bladder/bowel detrusor and sphincter activity, pupillary and respiratory reflexes. Features of autonomic dysfunction: (diabetic neuropathy, progressive autonomic failure):  Postural hypotension  Retention/incontinence of urine.  Constipation/faecal incontinence.  Impotence/erectile dysfunction.  Pupillary areflexia.  Disturbances of sweating (dry skin).  Snoring/ sleep apnoea.  Loss of cardiovascular reflexes. Examination sequence:   

Check pupillary reflexes (light and accommodation). Check skin for sweating. Cardiovascular reflexes: features of autonomic dysfunction: resting tachycardia, absence of the normal slowing of pulse rate with deep inspiration and valsalva manoeuvre, and postural hypotension (check the supine blood pressure then ask the patient to stand and check blood pressure again after 1-3 minutes: normally systolic blood pressure does not fall > 10 mmHg, in autonomic dysfunction it falls > 30 mmHg).

7. Signs of meningeal irritation: Stretching the nerve roots causes pain and reflex muscular spasm in the paraspinal and sacral muscles. The most frequent causes are meningitis and subarachnoid haemorrhage.  Neck stiffness: neck flexion causes pain in the posterior part of the neck and the movement is resisted by spasm in the extensor muscles. (occurs in: meningeal irritation, diseases of the cervical spine and increased intracranial pressure due to posterior fossa tumour).  Kernig's sign: extension of the knee with the hip fully flexed causes pain and spasm of the hamstring muscles.  Brudzinski's sign: flexion of the neck leads to flexion of both knees and hips.

8. Signs of root irritation: When nerve roots are damaged by entrapment at intervertebral foramina or by compression with disc prolapse, root pain occurs spontaneously and in response to movement. Straight leg raising test (SLR): for diagnosis of sciatica (sciatic nerve root compression with lumbosacral intervertebral disc prolapse): when the extended leg is passively elevated patient feels pain starting from the back and radiating along the back of the leg and movement is restricted. 85 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

9. Examination of the back: in cases of paraplegia/paresis: for deformities (Gibbus), swelling and tenderness.

10. Gait:     

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Spastic (hemiplegic): patient has difficulty in bending the knees and drags the feet (circumduction). Scissoring/stiff: in para/quadriparesis. High- stepping: in common peroneal nerve palsy (L5/S1); weakness of the extensor muscles of the feet (foot drop). Ataxic/drunken/wide- base: ataxia is equally severe whether the eyes are open or closed. Stamping/sensory ataxia: patient raises the foot very suddenly and abnormally high then jerks it forward and brings it again to the ground with a stamp (heel first). *Patient walks steadily when eyes are open but develops severe ataxia when eyes are closed or when walking in the dark. Festinant: is characteristic of Parkinson's disease. The patient is bent forwards and advances with rapid, short, shuffling steps without swinging of the arms. Waddling: sways from side to side as each step is taken. It is a feature of proximal pelvic girdle muscular weakness (myopathies, dystrophies) and diseases of the hip joint. *Trendelenburg's sign: weakness of gluteus medius muscle causes hip to drop when the affected leg is held off the ground in erect posture.

Localization of the lesion: Frontal lobe lesions:          

Monoplegia (lower limb is more affected than the upper limb). Expressive (Broca's) aphasia: lesion of the dominant lobe. Changes in personality and behaviour (apathy, disinhibition). Emotional lability. Cognitive impairment: difficulties with task sequencing, inability to generate a list and difficulties with executive skills. Preservation: repeatedly asking same question or doing same task. Primitive reflexes. Impaired memory. Anosmia. Urinary incontinence (loss of social control).

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Parietal lobe lesions:  Loss of cortical sensations on the opposite side of the body: (localization, two point discrimination, stereognosis and graphaethesia).  Contralateral inferior quadrantanopia.  Gerstmann's syndrome (lesion of the dominant lobe):  Dyscalculia: inability to perform mental arithmetic.  Dyslexia: inability to read.  Dysgraphia: impairment of writing.  Figner agnosia.  Right-left disorientation.  Lesion of the non dominant lobe:  Constructional apraxia.  Dressing apraxia.  Sensory inattention/neglect.  Spatial disorientation.

Temporal lobe lesions:      

Memory impairment. Contalateral superior quadrantanopia. Receptive (Wernicke's) aphasia: lesion of the dominant lobe. Complex partial seizures. Complex hallucinations (olfactory, auditory). Auditory agnosia: inability to recognize auditory stimuli.

Occipital lobe lesions:     

Homonymous hemianopia with sparing of the macula. Visual agnosia: inability to recognize visual stimuli. Distorted perception of visual stimuli: seeing things larger (macropsia) or smaller (micropsia). Visual hallucinations. Anton syndrome (cortical blindness): due to bilateral occipital lobe lesions ( the patient is blind but he/she is unaware or denies his/her blindness).

Lesions in internal capsule:  Contralateral dense hemiplegia with contralateral upper motor neuron facial palsy (uncrossed hemiplegia).  Contralteral hemisensory loss.

Lacunar lesions:  Isolated hemiparesis (pure motor). 87 | P a g e

Synopsis of Bedside Teaching: Dr.Abier Luai Atabani

 Isolated hemisensory loss (pure sensory).  Ataxic hemiparesis.  Dysarthria/clumsy- hand syndrome. Brainstem lesions: (lead to crossed hemiplegia):  Midbrain: (Weber's syndrome)  Ipsilateral 3rd nerve palsy.  Contralateral hemiplegia and hemisensory loss.  Pons:  Ipsilateral 6th and 7th nerves palsies (Conjugate/horizontal gaze palsy).  Contalateral hemiplegia and hemisensory loss.  Medulla oblongata:  Ipsilateral 9th, 10th, 11th and 12th nerves palsies.  Contralateral hemiplegia.  Alternating analgesia: loss of pain and temperature on one side of the face and the opposite side of the body.

 Lateral medullary syndrome: (Wallenberg's syndrome)  Ipsilateral 9th and 10th nerves palsies.  Ipsilateral Horner's syndrome (descending autonomic nerves).  Ipsilateral ataxia and nystagmus (cerebellar signs).  Ipsilateral loss of pain and temperature on the face.  Contralateral loss of pain and temperature on one half of the body. Sagittal sinus thrombosis:  Features of raised intracranial pressure: (headache, vomiting, seizures, visual disturbances and papilloedema).  Hemiplegia.

Lateral sinus thrombosis:  Features of raised ICP.  6th and 7th nerves palsies.  Hemiplegia.

Cavernous sinus thrombosis:  Features of raised ICP.  Peri-orbital swelling, proptosis and conjunctival injection.  3rd, 4th and 6th nerves palsies.

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 Hyperaesthesia of upper face and eye pain (due to involvement of the ophthalmic division of the trigeminal nerve).  Ophthalmoscopy: central retinal vein occlusion (CRVO).

Peripheral nerves lesions: Radial nerve: {arises from the posterior cord of the brachial plexus (C5-8)}  Weakness of extensors of the wrist (wrist drop).  Sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals.  Lesion at the axilla: as above + paralysis of triceps.

Ulnar nerve: {arises from the medial cord of the brachial plexus (C8-T1)}     

Claw hand (extension of the proximal phalanges and flexion of the distal phalanges) Wasting and paralysis of small muscles of the hand (except lateral two lumbricals). Wasting and paralysis of hypothenar muscles. Sensory loss to the medial one and a half fingers (palmar and dorsal surface). Lesion at the elbow: as above+ radial deviation of the wrist.

Median nerve: {arises from the medial and lateral cords of the brachial plexus (C5-T1)} Carpal tunnel syndrome:    

Weakness of thumb abduction and opposition. Wasting of thenar eminence. Sensory loss to the lateral three and a half fingers. Pain (pins/needles) and numbness over the lateral three and a half fingers.

Common peroneal nerve: {branch of the sciatic nerve (L5-S1)}       

Foot drop. Weakness of foot dorsiflexion. Weakness of foot eversion. Weakness of extensor hallucis longus. Sensory loss over the dorsum of the foot and the lower lateral part of the leg. Wasting of the anterior tibial and peroneal muscles. High- stepping gait.

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References 1. Macleod’s clinical examination. 2. Hutchison’s clinical methods. 3. Harrison’s principles of internal medicine. 4. Clinical examination, Talley and O’Connor. 5. Davidson’s principles and practice of medicine. 6. Kumar and Clark’s clinical medicine.

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