Clinical

Question 1

3 ways of assessing Volume Status in patients?

Answer 1

1) Clinical Assessment/Examination 2) Normal Saline Infusion Test 3) Central Venous Pressure

Question 2

5 ways of assessing volume status on examination?

Answer 2

Peripheral Oedema, Mucous membranes, Skin turgur, orthostatic hypotension and JVP

Question 3

In terms of volume status - how would you differentiate between Cerebral Salt Wasting and SIADH?

Answer 3

Cerebral Salt Wasting - Hypovolaemic SIADH - Euvolaemic/Hypervolaemic

Question 4

What is the prevalence of SIADH in head trauma (as a percentage)?

Answer 4

4.6%

Question 5

Name 3 potential side effects of fludrocortisone use.

Answer 5

Pulmonary Oedema, Hypokalaenia, Hypertension

Question 6

Out of SIADH and CSW - which could furosemide be used as an option for treatment, and in which should it be avoided?

Answer 6

Can be used for treatment of SIADH. Should be avoided in CSW

Question 7

Can you name 3 causes of Hyponatreamia as a result of Renal Solute Loss (Low Sodium, Raised urine Osmolarity, Raised urinary sodium)?

Answer 7

CSW Diuretic Use Addison’s Disease (Mineralo-corticoid deficiency)

Question 8

Classification of causes of SIADH?

Answer 8

Malignant tumours

CNS disorders

Pulmonary disorders

Drugs

Endocrine disturbances

Misc

Question 9

What is the effective serum osmolality?

Answer 9

Tonicity of solute

Question 10

Def: SIADH

Answer 10

Water retention in the face of hyponatraemia

Either due to inappropriate ADH secretion or heightened response to ADH due to certain drugs

Question 11

What are the two caveats to treatment of hyponatraemia 2o to SIADH

Answer 11

Ensure cause is not CSW

Avoid too rapid correction or overcorrection due to risk of osmotic demyelination syndrome

Question 12

Indications for aggressive treatment of SIADH

Answer 12

Na <125

And duration <24h or symptomatic

Question 13

Features of CSW

Answer 13

Renal loss of Na as a result of intracranial disease producing hyponatraemia and reduced ECF

Question 14

MOA fludrocortisone

Answer 14

Acts directly on renal tubule to promote Na reabsorption

Question 15

Which cranial nerve is most likely to be affected by herniation and why?

Answer 15

CN 6, Abducens nerve; comes off the pontomedullary junction to ascend the clival area - as it has an upward course it is more vulnerable to stretching/traction with downwards pressure compared to nerves with more direct trajectories.

Question 16

Complication of subfalcine / cingulate gyrus herniation

Answer 16

Anterior cerebral artery infarction

Question 17

Mechanism of Diabetes Insipidus secondary to herniation syndromes

Answer 17

Transtentorial/Central herniation may cause the pituitary stalk to be sheared (downward pressure against diaphragma sella)

Question 18

What are Duret haemorrhages?

Answer 18

Haemorrhages within the brainstem produced by shearing of perforating arteries from the basilar in transtentorial herniation

Question 19

Features of Parinaud’s Syndrome?

Answer 19

1. Supranuclear upward gaze palsy
2. Lid retraction (Collier’s sign)
3. Convergence-retraction nystagmus
4. Accommodation palsy

Question 20

Vessel(s) at risk by upwards cerebellar herniation

Answer 20

Superior cerebellar arteries

Question 21

What is Kernohan’s phenomenon?

Answer 21

Ipsilateral hemiplegia secondary to compression of the contralateral cerebral peduncle against the tentorial edge; a false localising sign

Question 22

What are the five most common herniation syndromes?

Answer 22

Supratentorial:

Central (transtentorial herniation)

Uncal herniation

Cingulate herniation

Infratentorial:

Upward cerebellar

Tonsillar herniation

Transcalvarial herniation

Question 23

Vascular consequence of cingulate herniation?

Answer 23

ACA occlusion which may cause bifrontal infarction.

Cingulate herniation usually warns of impending transtentorial herniation

Question 24

What are the stages of central herniation?

Answer 24

Diencephalic stage

Midbrain-upper pons stage

Lower pons- upper medullary stage

Medullary stage (terminal)

Question 25

What is the Px for patients who develop signs of the midbrain stage of central herniation?

Answer 25

\<5% will have a good recovery if successfully treated at this stage

Question 26

Why do pinpoint pupils occur in pontine haemorrhage in contrast to dilated pupils in central herniation?

Answer 26

Pontine haemorrhage causes loss of sympathetics, in contrast to herniation in which there is a surgical CN3 palsy.

Question 27

What are the stages of uncal herniation?

Answer 27

Early third nerve stage Late third nerve stage Midbrain-upper pons stage Central herniation type stage

Question 28

Cause of lid retraction (Collier's) in Parinaud's

Answer 28

Bilateral. Supranuclear inhibitory input to the CN3 nucleus is disrupted causing LPS activation

Question 29

Cause of light near dissociation in Parinaud's

Answer 29

Light and near pathways are different at the level of the midbrain. Near pathway is spared because it is more rostral and communicates directly with the EW and CN3 from above rather than via the pretectal nucleus which is more dorsally located and thus vulnerable to dorsal compression

Question 30

Cause of convergence retraction in Parinuad's

Answer 30

Loss of supranuclear inhibition of CN3 causes all of 3's EOMs to fire causing the eye to look in, combined contraction of SR and IR causes retraction. Nystagmoid rather than nystagmus as non-rhythmic

Question 31

Cause of upgaze paresis in Parinaud's

Answer 31

Upward gaze is mediated by CN3 Vertical gaze centre (the rostral interstitial nucleus of the MLF- vertical saccades; the interstitial nucleus of Cajal- gaze holding and skew deviation) is at the thalamomesencephalic junction. They both lie in close proximity to the aqueduct of Sylvius and both decussate in the posterior commissure. Their presence in the posterior commissure makes them particularly vulnerable to unilateral lesions. The downgaze pathway is bilateral so a bigger lesion is required.

Question 33

Cause of sunsetting in Parinaud's

Answer 33

Unopposed downgaze due to impairment of the upgaze centre in the dorsal midbrain.