The Pupils

Normal light reflex pathway



  • In steady illumination, normal pupil is continuously dilating and contracting. This is called hippus (pupil undulation).

Simple anicosoria

  • Definition of anicosoria: >0.5mm different in dize of the left and right pupil
  • Simple = cannot be atributed to secondary causes eg trauma, drugs etc, occurs in up to 40% of healthy persons

Normal light reflex

  • Direct and consensual reaction
    – Direct: ipsilateral pupillary constriction
    – Consensual: contralateral pupillary constriction
  • Clinical significance: Anicosoria is
    – absent in disorders of the optic nerve or retina (i.e afferent connections)
    – present in asymmetric disease of the iris, sympathetic nerve or oculomotor nerve
       (i.e efferent connections)

Near synkinesis reaction: when a person focuses on near object:

  • Constriction
  • Convergence
  • Accomodation

Abnormal pupils

  • RAPD (Marcus-Gunn pupil)
  • Argyll Robertson pupils
  • Oval (dilated pupils)
  • Anicosoria

Relative afferent pupil defect (Marcus-Gunn pupil)

  • Detected by swinging flashlight test
  • Finding: detection of absence of direct or consensual response of the pupil
  • Clinical significance:
    – Optic nerve disease (eg optic neuritis, ischemic optic neuropathy)
    ** Cataracts DO NOT cause RAPD as the retina behind it is intact.

Argyll-Robertson pupils

  • Mnemonic: ARP PRA
    – Accomodation reflex present, pupillary reflex absent
    – Bilateral SMALL PUPILS
    – Constriction & redilation of pupils are brisk
  • Historically due to 3rd stage of syphilis
  • Differential diagnosis of light-near dissociation
    – Adie’s tonic pupil
    – Parinaud syndrome (dorsal midbrain syndrome)
    – Aberrant regeneration of third nerve
  • Parinaud syndrome (dorsal midbrain syndrome)
    – Ddx: young: pinealoma; middle age lady: MS; old: basilar artery stroke
    CLUES: Convergence-retraction nystagmus, Light near dissociation, Upward deviation, Eyelid retraction, Setting sun sign

Oval pupil

  • Third nerve palsy from brain herniation
  • Adie’s tonic pupil
  • Previus surgery or trauma to iris (pupillary constrictor)

Pathological anicosoria

  • Which side is abnormal?
    – Swing a flashlight to the dilated eye. If the ipsilateral eye does not constrict, the pupillary constrictor at the side is abnormal. If it does constrict, the contralateral (smaller) eye is abnormal.
  • 2 questions
    i) Is there full 3rd nerve palsy?
    ii) Neurological findings?

Smaller eye is the problem:

  • Horner syndrome
  • Simple anicosoria

Bigger eye is the problem:

  • 3rd nerve palsy from brain herniation or Hutchinson pupil (if comatose) or PCA aneurysm (if not comatose)
    – Ptosis and pupil will appear “down and out” in 3rd nerve compression
  • Adie’s tonic pupil (respond to pilocarpine)
  • Anticholinergic mydriasis (does not respond to pilocarpine)

Adie’s tonic pupil

  • Unilateral LARGE PUPIL
  • Tonic = SLOW constriction and redilation in respponse to near vision
  • Light reflex is absent
  • Adie’s syndrome: tonic pupil + hyperhidrosis + areflexia
  • Due to injury to the ciliary ganglion and postganglionic fibers (eg viral infection)
    – The fibers destined to ciliary body instead aberrantly re-innervate pupillary constrictor. Hence, the loss of light reflex.

Horner syndrome

  • Ptosis, miosis, anhidrosis, enophthalmos
  • Presence or absence of anhidrosis may indicate level of lesion
    – 1st order (preganglionic eg stroke): anhidrosis present in face and trunk
    – 2nd order (ganglionic eg Pancoast syndrome, cervical rib): anhidrosis only in face
    – 3rd order (postganglionic eg ICA dissection): no facial anhidrosis 
    – This is because neurons to facial sweat glands are located in ECA
    – However, this was found to be limited in utility (not significant LR)





Steven McGee. Evidence based Physical Diagnosis. Pg 209-233





Pulse Oximetry

Advantages of pulse oximetry

  • More sensitive in hypoxemia
  • Readings do not depend on patient’s Hb level
    Unlike SaO2 which is directly measured in blood gas (OxyHb/Total Hb X 100)

Limitations of pulse oximetry

  • Dyshemoglobinemias
    – May underestimate the degree of oxygen saturation in carbon monoxide poisoning
    – In methemoglobinemia, the SpO2 decreases initially but then plateaus off
  • Poor peripheral perfusion
  • Other things
    – Dyes: eg nail polish can interfere with oximetry
    – Exaggerated venous pulsation maybe mistaken for arterial one, leading to spuriously low oxygen saturation techniques.

Reference: Steven McGee. Evidence Based Physical Diagnosis. Pg 203-206


Croup review


  • Viral infection, eg influenza, parainfluenza
  • The airway is swollen due to inflammation


  • Remember the S: seal bark cough, sound (hoarseness), stridor
  • Stridor defines severity
    – At agitation = moderate
    – Ar test = severe


  • Mainly clinical
  • If you do a neck X ray
    – AP: steeple sign
    – lateral: dilated hypopharynx


  • Remember the AA
    – Anaphylaxis
    – Aspiration of foreign bodies
    – Airway infections eg bacterial tracheitis, epiglottitis
    – Airway compression eg  double aortic arch


  • Anti-inflammatory – may take some time to work, so the cough and stridor may not stop immediately. It stops the inflammation from progressing
    – Dexamethasone, 0.15 mg/kg or 0.6 mg/kg PO once
    – Prednisolone, 1mg/k PO once for 2 days
    – Prednisolone has same efficacy as dexamethasone during the initial presentation
    as dexamethasone but re-attendance rate is higher for prednisolone, so need 2 doses
  • Epinephrine 1:1000, 5mL (= 5mg)
    – Only in severe resp.distress (i.e stridor at rest)
  • Other therapies
    – Heliox: alleviate the turbulent airflow
    – BiPAP
    – Intubation

What if it doesn’t respond to steroids?

  • Consider the ddx
  • bacterial tracheitis can present with croupy cough. But the kid is toxic looking, with painful swallowing.
  • Epiglottitis: toxic looking kid + painful swelling (normally with drooling) + muffled cough
    ** Can be difficult to be differentiated from tracheitis, cover with IV cefotaxime ! Cover for S.aureus and H.flu
  • Anaphylaxis and aspiration of foreign body





Systemic amyloidosis, purpura differential diagnosis

  • Dermatologic features
    – Purpura from capillary fragility – periorbital area is classical
    – Waxy papules or nodules, typically on eyelids (resembling xanthelasma), neck and anogenital areas
  • Macroglossia
  • Can affect heart, lung, liver, kidneys
  • A few types, more common ones are these two types:
    – AA type: from systemic inflammatory disorder
    – AL type: multiple myeloma (presence of immunoglobulin light chains or paraprotein)

Purpura differential diagnosis

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Ellen K Roh et al. Case 2-2016: An 84-Year-Old Woman with Chest Pain, Dyspnea, and a Rash. N Engl J Med 2016;374:264-74.

Respiratory Rate and Breathing patterns

Normal RR

  • 15-20 (average 20)/min
  • For unknown reason (and no data cited), most textbooks record the normal rate as 12-18/mins


Tachypnea = RR >25/min

Bradypnea = RR <10/minutes

Abnormal breathing patterns


** Pathogenesis:

  • Enhanced sens to CO2: causes hyperventilation excessively until the Co2 level drops so low that apnea happens, then Co2 builds up again to stimulate hyperventilation again
  • Circulatory delay between lungs and arteries: Co2 level in alveoli and in systemic arteries (that reach medulla) is out of sync. This delay causes waxing & waning of the tidal volume. This happens eg in CHF.

Grunting respirations

  • Expiration against closed glottis producing low-medium pitch voice
  • Indicates resp.muscle fatigue
  • Pathogenesis: grunting resp slows down expiration, so more time for gases exchange.

Chest and abdominal mvements during respiration

  • Normall in sync (chest moves out, abdomen moves out during inspiration and vice versa)
    – During inspiration, diaphragm flattens downwards, therefore pushing the abdomen outwards. In expiration, diaphragm domes upwards, pulling the abdomen inwards.
  • Out of sync

i) Asynchronous

  • During expiration, normal smooth inward abdominal movement is interrupted by sudden outward movement
  • Seen in COPD, when the strong action of accessory muscles push the diahragm temporarily downward during expiration and therefore abdomen moves outwards suddenly.

ii) Paradoxical

  • During inspiration, abdomen moves inwards (instead of outwards) and during expiration, abdomen moves outwards (instead of inwards)
  • Pathogenesis: during inspiration, the outward movement of chest wall drags the diaphragm upwards, therefore abdomen moves inwards
  • Seen in patients with diaphragmatic weakness.

Photo Jan 20, 10 08 52 PM


  • Breathlessness when lying down but relieved in upright position
  • Most important in CHF
  • Pathogenesis:
    – Due to decreased lung compliance and redistribution of venous outflow to RV on supine position, but not entirely due to this.
    – Other lung diseases eg IPF do not present with orthopnea
    – Orthopnea correlates poorly with pulmonary artery pressure
    – The fact that it can be relieved by elevation of head alone


  • Breathlessness when lying on one side
  • Seen in:
    – Unilateral lung disease: lying on good side improves oxygenation due to increase perfusion
    – CHF: lying on right side improves breathing, maybe due to left lung atelectasis from cardiomegaly
    – Endobronchial tumour: lying on affected side will cause obstruction and wheezing


  • Breathlessness when iin upright position but relieved in prone position
  • Seen in
    – Intracardiac shunt eg PE in a patient with ASD
    – Intrapulmonary shunt eg in hepatopulmonary syndrome


Steven Mcgee. Evidence Based Physical Diagnosis Pg 187-202



Associated findings


  • Not always due to hepatitis or cholangitis, jaundice can be due to non-specific complication of bacteremia (reactive hepatopathy termed by osler)

Relative bradycardia

  • Predicted HR = (Degree celcius X 10) – 320
  • Clinical utility is quite limited

Dry skin

  • Anhidrosis occurs late in heat stroke. The more sensitive finding is ABNORMAL mental status

Extreme hypothermia or hyperthermia

  • Worse prognosis
  • Extreme pyrexia often is due to GN bacteria infection/problems with temperature regulation eg heat stroke

Fever patterns

  • Due to use of antipyretics, limited clinical utility EXCEPT
    – Typhoid fever
    – Malaria
    – Dengue
  • Finding of unusually fever after antibiotics, consider
    – other diagnosis eg malignancy OR
    – resistant bacteria/wrong antibiotics/abscess


Steven McGee. Evidence Based Physical Diagnosis. Pg 174- 186

Blood pressure

Auscultatory Gap

  • As illustrated below, if the cuff is inflated  only to the initial disappearance of the sound, the actual SBP maybe underestimated.
  • Cause is a mystery.
  • Avoided by palpating the disappearance of the pulse by inflation of cuff before using stethoscope to estimate the SBP. Cuff should be inflated 20-30 mmHg higher than the estimated SBP.


Level of arm

  • Should be at the level of heart
  • Too high: the readings will be lower
  • Too lower: the readings will be higher
  • Due to hydrostatic effect

Blood pressure deficits between left and right arm

  • Normal is <10 mmHg, >20 mmHg is abnormal
  • Ddx:
    – Subclavian steal syndrome
    – Aortic dissection

BP deficits between arms and legs

  • Chronic ischemia of lower extremities
  • Coarctation of aorta (aorto-femoral delay in pulse)


Orthostatic hypotension

  • 500 mL of blood shifts to lower body on standing up.
  • Defined as drop in SBP >20 mmHg or drop in DBP >10 mmHg
  • Orthostatic hypotension happens when:
    – Excessive loss of fluid
    – Lack of compensatory mechanism (autonomic dysfunction)
  • Evidence showed that
    – Finding of postural drop in SBP has no proven value
    – The better findings are postural increment of pulse >30/min OR dizziness on standing up

Blood pressure and impaired consciousness

  • Cushing reflex – normally due to increased ICP (structural lesions)
  • Cushing triad: 3B: Blood pressure increases, Bradycardia, Breathing irregular

Pathogenesis of Cushing Reflex

Cushing’s Triad and Cushing’s Reflex


Steven McGee, Evidence Based Physical Diagnosis, pg 153-160