Welcome to Module 2

This week we look at The CLINICAL EXAMINATION and a little bit of EQUIPMENT.
​THIS IS A BIG WEEK- KEEP SCROLLING DOWN.

The Clinical Examination

The Clinical Examination has changed a lot between the old examination and the new. It's important to understand these changes, as it allows us to better predict the exam. 

In the old examination, we would teach a total of 11 clinical exams including CVS, Respiratory, Gastrointestinal, Neck, Eyes etc. Real patients were used in the examination and it was difficult to find them. Usually these patients had to be well, to withstand a half or whole day of examinations, so they were usually outpatients. They came in, did the exam, had some lunch and left. Occasionally they used a real patient, but again they had to be relatively well. You therefore knew you weren't going to get Osler's Nodes and Janeway lesions, because they weren't going to bring a patient with infective endocarditis to the exam.
Today the exam has changed even further. It is rare to have a real patient in the OSCE. Usually an actor or another FACEM will play the patient. In terms of communication OSCE's that's fine, i.e., the range of topics haven't changed, however in terms of the clinical examination they certainly have. Why? Because there are only so many conditions that can be faked by a FACEM or actor and most of these are neurological.

Of course you can never say 'never' however, I want to concentrate, in this course on a few examinations that will help you significantly.

Cranial Nerves Examination

The following video, starts with a video from Youtube, showing the examination, then I go over the whole examination explaining what is happening and proposing the clumping technique. Please watch a become really good at this. In terms of the cranial nerves learn to clump them together. Also, take extra care to learn the 'Eye Examination' very well.

Higher Centres Examination

Cerebellar Examination

The Hand Exam

This is a really important examination to know.
Starting The Hand Exam
In performing the clinical examination we need a place to start. The hands are the answer. Start by shaking the patient’s hand in greeting and the rest will follow. We need to remember how invasive an examination is for the patient and also remember how necessary it is. The clinical examination should progress smoothly from one part to the next. Let’s start now, with the hands.
SHAKE HANDS
Feel the palms. Are they moist? Is this nervousness? Could it be secondary to thyrotoxicosis? Is there a tremor and are there eye signs of the latter? Does the patient have difficulty letting go of the handshake? Rare as this is, it is some kind of myotonica, think Dystrophia Myotonica.
LOOK AT THE HANDS
Are they enlarged, as in acromegaly?
Are they distorted as in arthritis?
Rheumatoid Arthritis
  • Ulnar deviation
  • Boutonnierre deformity
  • Swan neck deformity
  • Z deformity of the thumb
Osteoarthritis
  • Heberden’s nodes(DIP joint)
  • Bouchard’s nodes (PIP joint)
Are the fingers sausage shaped?
  • Think of Psoriatic arthropathy and Reiter’s disease
Is there finger shortening?
  • beware not to miss destructive arthritis (arthritis mutilans) of psoriatic disease
Is there wasting of the palm, or other part of the hand?
Are the fingers held abnormally?
The Muscles of the Hand
The MEDIAN nerve controls the 
  • Lumbricals 1 & 2 as well as the
  • Thenar muscles OAF 
    • Opponens pollicis, 
    • Abductor pollicis brevis and 
    • Flexor pollicis brevis
Together the LOAF muscles.
The ULNAR nerve supplies all other small muscles of the hand.
The Benediction Sign or Pope’s Hand results from the inability to flex the 2nd and 3rd digits at the metacarpophalangeal joints, due to the lumbricals not being innervated. This is as a result of median nerve injury at the level of the elbow. The same sign is sometimes incorrectly used, for the claw-like hand of ulnar nerve damage. In the ulnar claw hand, the 4th and 5th digits are extended at the metacarpophalangeal joints(MCPJ) and flexed at the interphalangeal joints.
To distinguish between a median and ulnar nerve lesion, ask the patient to clench the hand into a fist. The patient with a median nerve injury CANNOT CLENCH THE FIST as the index and middle finger cannot be flexed by the lumbricals. With median nerve lesions, the more proximal the lesion, the greater the deformity. With ulnar nerve lesions, there is the ‘ulnar nerve paradox’, where the more distal lesion causes the greatest deformity.
IN OCHSNER’S CLASPING TEST ASK THE PATIENT TO CLASP THEIR FINGERS TOGETHER, WITH A MEDIAN NERVE INJURY, THE INDEX FINGER DOES NOT FLEX AT THE MCPJ.


​IN FROMENT’S SIGN YOU ASK THE PATIENT TO GRASP A PIECE OF PAPER BETWEEN THE THUMB AND THE LATERAL ASPECT OF THE FOREFINGER. LOSS OF POWER TO ADDUCTOR POLLICIS (SUPPLIED BY A DEEP BRANCH OF THE ULNAR NERVE) OF THE THUMB WILL CAUSE FLEXION OF THE DISTAL THUMB AS FLEXOR POLICIES LONGS COMPENSATES.
NORMAL ULNAR NERVE
ABNORMAL ULNAR NERVE
Picture

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IN PATIENTS WITH A MEDIAN NERVE PALSY, THE INABILITY TO OPPOSE THE THUMB CAN RESULT IN A PINCHING MOTION WHEN ASKED TO MAKE THE ‘OK’


FINGER ABNORMALITIES

​​LOOK FOR DUPUYTREN’S CONTRACTURE, USUALLY CAUSING FLEXION OF THE RING FINGER(BUT MAY ALSO BE OF THE 5TH FINGER). IT RESULTS FROM THICKENING OF THE PALMAR FASCIA AND MAY BE FAMILIAL, OR OCCUR SECONDARY TO TRAUMA, OR BE RELATED TO ALCOHOLISM(NOT LIVER DISEASE)

​​ARE THERE OSLER’S NODES? PAINFUL, NODES ON THE FINGERS OR TOES AS A RESULT OF IMMUNE COMPLEXES IN ENDOCARDITIS.

​​ARE THERE JANEWAY LESIONS? NON-PAINFUL LESIONS IN THE PALMS OR THE SOLES AS A RESULT OF SEPTIC EMBOLI, MOST COMMONLY IN STAPH AUREUS INFECTIVE ENDOCARDITIS.



​​ARE THERE TENDON XANTHOMATA? THESE ARE YELLOW LIPID DEPOSITS IN THE TENDONS OCCURRING AS A RESULT OF TYPE II HYPERLIPIDAEMIA.
THE NAILS
 NEXT LOOK AT THE NAILS.
SO MUCH CAN BE DIAGNOSED BY LOOKING AT THE NAILS; CARDIAC DISEASE, LIVER DISEASE, RENAL DISEASE AND MORE.
LOOK FOR THE FOLLOWING THREE CHARACTERISTICS:
  1. COLOUR
  2. DEFECTS
  3. PATTERNS
COLOUR
​
WHITE NAILS ( LEUCONYCHIA), MAY INDICATE HYPOALBUMINAEMIA AND CHRONIC LIVER DISEASE. IT CAN APPEAR AS EITHER A WHITE NAIL OR WHITE SPOTS ON THE NAIL.
RED NAILS– THINK OF POLYCYTHAEMIA OR CARBON MONOXIDE POISONING
BLUE NAILS – THINK CYANOSIS AND WILSON’S DISEASE
YELLOW NAILS – THESE ARE THE RESULT OF HYPOPLASIA OF THE LYMPHATIC SYSTEM. THE DISTAL NAIL IS SEPARATED.
​

​TERRY’S NAILS – THE PROXIMAL NAIL IS PALE AND THE DISTAL NAIL IS DARKER, BUT IT IS NOT HALF AND HALF. IT RESULTS FROM LIVER DISEASE, CONGESTIVE CARDIAC FAILURE AND DIABETES.
​

​LINDSAY’S NAILS OR HALF AND HALF NAILS. THE PROXIMAL PORTION IS WHITE OR PINK AND THE DISTAL PORTION IS RED OR BROWN. THEY ARE IN A RATIO OF 50% EACH. IT INDICATES CHRONIC RENAL FAILURE.
DEFECTS
CLUBBING

​THERE IS A LOSS OF HYPONYCHIAL ANGLE IE., BETWEEN THE NAILED BED AND THE FINGER. THERE ARE MANY CAUSES OF CLUBBING, ALL EASILY FOUND IN THE EXAMINATION TEXTBOOKS. I REMEMBER 2 CAUSES IN EACH SYSTEM FOR CLUBBING.
CAUSES OF CLUBBING
CARDIOVASCULAR
  1. CYANOTIC CONGENITAL HEART DISEASE
  2. INFECTIVE ENDOCARDITIS
RESPIRATORY
  1. ABSCESS INCLUDING EMPYEMA AND BRONCHIECTASIS
  2. CARCINOMA
GIT
  1. CIRRHOSIS
  2. INFLAMMATORY BOWEL DISEASE
ALSO UNILATERAL CLUBBING, REMEMBER THE FOLLOWING:
  1. BRONCHIAL ARTERIOVENOUS ANEYRYSM
  2. AXILLARY ARTERY ANEURYSM

OTHER NAIL ABNORMALITIES
​SPLINTER HAEMORRHAGES
THESE ARE PAINLESS LESIONS THAT LOOK LIKE A SPLINTER UNDER THE NAIL. CAUSES INCLUDE: TRAUMA, INFECTIVE ENDOCARDITIS, RAYNAUDS’S DISEASE AND VASCULITIS. A SPLINTER HAEMORRHAGE UNDER ONE NAIL MAY BE DUE TO TRAUMA, HOWEVER, IF THEY APPEAR ON MORE THAN ONE DIGIT, THINK OF SYSTEMIC DISEASE.
​KOILONYCHIA
THIS IS A SPOON SHAPED NAIL THAT CAN OCCUR IN IRON DEFECIENCY ANAEMIA, FUNGAL INFECTIONS AND RAYNAUD’S DISEASE.
​ONYCHOLYSIS
THE NAIL LIFTS FROM THE NAIL BED. IT OCCURS IN PSORIASIS AND THYROTOXICOSIS AND MAY ALSO OCCUR IN INFECTION AND TRAUMA, ALTHOUGH TRAUMATIC CAUSES ARE LOCALISED TO THE AFFECTED NAIL(S).
​PATTERNS
THERE ARE THREE PATTERNS TO LOOK FOR IN THE NAIL:
​BEAU’S LINES  THESE ARE TRANSVERSE DEPRESSED RIDGES, THAT OCCUR IN INFECTION, HYPOCALCAEMIA, POST SURGERY, POST CHEMOTHERAPY, POST KAWASAKI’S DISEASE AND IN MYOCARDIAL INFARCTION. THEY ARE BELIEVED TO BE CAUSES BY A TEMPORARY CESSATION OF CELL DIVISION IN THE NAIL.
​MUEHRCKE’S LINES  THESE ARE HYPO PIGMENTED, OR OPAQUE TRANSVERSE BANDS, BUT ARE NOT DEPRESSED. THEY ARE WHITE BANDS THAT RUN PARALLEL TO THE LUNULA AND IN A TRANSVERSE MANNER. THEY ARE CAUSED BY DECREASED PROTEIN SYNTHESIS, OR IN TIMES OF SIGNIFICANT ILLNESS. CAUSES INCLUDE, HYPOALBUMINAEMIA, NEPHROTIC SYNDROME, DURING CHEMOTHERAPY OR OTHER ACUTE ILLNESS.
MEE’S LINE THEY ARE A SINGLE TRANSVERSE WHITE LINE THAT HAS NO DEPRESSION. THEY ARE PRODUCED DURING TIMES OF SIGNIFICANT METABOLIC STRESS. CAUSES INCLUDE ARSENIC POISONING, THALLIUM, RENAL DISEASE, CARDIAC FAILURE AND MALIGNANCY. (IMAGE REFERENCE: THE LANCET, VOLUME 372, ISSUE 9647, PAGE 1410, 18 OCTOBER 2008)
THE HAND EXAMINATION IS NOW COMPLETE.
I WOULD NEXT MOVE TO THE ARM. THE FIRST PART IS TO PALPATE THE RADIAL ARTERY AT THE WRIST, LOOK FOR RADIAL-RADIAL AND RADIO-FEMORAL DELAY,SLIDE THE HAND UP TO THE EPITROCHLEAR NODE, THE AXILLARY NODES, TAKE THE BLOOD PRESSURE AND MORE…..BUT THIS IS IN THE NEXT PART.
EXAMINATION OF THE HAND; IT TAKES LESS THAN A MINUTE AND GIVES A WEALTH OF INFORMATION ABOUT THE PATIENT.
​​

The Cardiovascular Exam

Here is a 1 + hour presentation on the cardiac exam. Please keep in mind that this was recorded for the previous SCE exams as CVS was examined as a short case, so some of the comments about getting 2 or 3 of these, is related to the old exam and not the new one.

However for those wondering if they can get a description of symptoms and be asked about the findings of the cardiac exam 'in theory', again I don't think it will happen. However if you watch this lecture it takes you though the exam with videos throughout, so you can learn by watching and listening to what is said.

EQUIPMENT

Equipment that you use every day will be tested in this examination. It is imperative that you have studied this. Here are two examples of equipment you must know.
Remember one key point. If you have a piece of equipment and you know very little about it, but should, don't freeze.
​JUST START WITH KNOBOLOGY. Name all the bits that are there. It's a start.
  • DEFIBRILLATOR
  • OXYLOG 3000
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WHAT DETERMINES SUCCESS?
  • Time to defibrillation- 30seconds to define = 95% success vs 25% success in 2 min
  • Transthoracic resistance
WAVEFORMS
  • Biphasic waveforms – charge is delivered in one direction for half shock and then for second half in opposite.
  • Lower energy required than monophasic


​KNOBOLOGY
The defibrillator has an ON/OFF button
Energy can be selected and the machine charged
It can then be discharged.
DC is more effective than AC and has less post reversion arrhythmias. It can also be battery driven
There is a SYNC button, indication synchronisation vs non-synchronised. The default is non-synchronised.
  • The defibrillator senses the QRS, so that it doesn’t receive a current in the relative/absolute refractive period- if this occurred it may precipitate VF
  • Use SYNCHRONISED for all except VF
The PACER area allows a rate increase as well as current increase.
APPROACH TO DEFIBRILLATION/CARDIOVERSION
  • Ensure informed consent
    • Make sure patient is aware of the procedure and outcomes
  • Connect patient to leads, to read trace
  • Ensure sensing R waves
  • Analgesia and sedation
    • Painful procedure. Consider Ketamine 0.5mg/kg i.e.., in adults ~40mg PLUS propofol say 50mg also
    • Rapid Procedure
    • Ensure all resuscitation equipment including airway is in place.
  • Select energy
    • Atrial Fibrillation is most resistant arrhythmia; use 200J
    • Others can use 100J
    • Approach may be to use 200J single shock for all
  • Remove hazards
    • Remove anything that could burn patient
    • Oxygen- safe
  • Charge
  • Ensure all clear
  • Shock- deliver charge
COMPLICATIONS OF DEFIBRILLATION
  • Burns
  • Electrocution
  • Asystole(poor sign if occurs to someone with VF)- in ~15%
  • VF in ~0,8% with VF
  • Can cause myocardial damage- if repetitive high shocks

​This is electronically controlled and gas driven, but must have electricity(4 hour battery) OR gas supply to work
It is a compact ventilator, that is time cycled pressure/volume controlled.
BiPAP is possible as well as IPPV, SIMV, CPAP
Small tidal volumes are possible, as low as 40 mL, so can be used for paediatrics.
KNOBOLOGY
Volume Controlled Ventilation
Volume Controlled Ventilation is by far the most common type of ventilation used in the emergency department.
We think about this in terms of the patients that have:
  1. Obstructive airways disease or COPD and
  2. All other patients (protective lung strategy)

OBSTRUCTIVE PICTURE- COPD
In these patients there is a need to allow for complete expiration.
  • VT is 6ml/kg, with a
  • Low frequency of 6-8 breaths per minute, allowing permissive hypercapnoea
  • The FiO2 starts at 100% but is titrated to achieve sats of 88-95%
  • ZERO PEEP
  • I:E ratio = 1:4 i.e. an Insp time of 0.4s
  • Slope on the screen will be a modest incline
  • If the insp pressures are high then press inspiratory hold button
    • this holds the patient in inspiration
    • If the pressures are still >30, lower the VT
These are the patients that may develop gas trapping, so pressing the curves button allows us to see what the insp/exp curves look like
PROTECTIVE LUNG STRATEGY
The aim here is low tidal volume and high PEEP.
  • Tidal Volume: 6ml/kg
  • Frequency- need rapid breathing 16-18 breaths per minute
  • Pressures > 40
  • FiO2 is set at 100% for the first few minutes(perhaps 5 minutes), then dial to 40% and use PEEP to achieve sats of 89-95%
When higher pressures occur, to work out if they are coming from the trachea, or the lungs, hold down the ‘inspiratory hold button’. The breath is held allowing the the pressure to equilibrate across the whole lung= plateau pressure. A plateau pressure of < 30 is safe.
If plateau pressure is > 30, it may lead to lung damage, so decrease the tidal volume to 4-5ml/kg
When you see this curve, decrease the ventilation rate, to allow time for expiration

OKAY- A big module, but make sure you know these as a bare minimum.
​Keep going- you're in the home stretch!

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