6 May 2020 - Geriatrics, Palliative Care 

Program

10-1015hr – Welcome and recap of last week – Dale ‘stand in’ Jacqueline

1015-1100hr – How to manage your palliative patient – Hope

1100-1110hr – coffee break

1110-1140hr – Ouch – Falls in the Elderly – Marrillo

1140-1200hr – 10 min Tox Case – Khalid

1200-1215hr – ECG of the Week – Alex

1215-1230hr – *New* Xray of the week - Matt

1230-1245hr – Gas of the week – Mark

1245-1300hr –quick lunch break

1300-1345ish hr – SAQ questions – Jacqueline/Sarah

1300-1500hr – Fellowship OSCE practice – Brendan, venue TBA

 Key Learning Points

Palliative Care

Hope discussed the emergency management of common palliative symptoms. Here are some of the key learning points:

• Pain - the PRN dose of opioid should be 1/6 of the total 24 hour opiate dose

• Hydromorphone is a useful opioid in those with poor renal failure (eGFR < 40)

• Use eviQ opioid calculator to help convert doses between different opioids and routes of administration - https://www.eviq.org.au/clinical-resources/eviq-calculators/3201-opioid-conversion-calculator

• Subcutaneous doses of medications take 20-30 minutes to take effect

• Syringe drivers do not work immediately - they will need PRN medications while taking effect (up to 4 hours)

• Use haloperidol (0.5-1mg PO/SC/IM/IV) for nausea in palliative care - ondansetron will constipate!

• Opiates are first line for treatment of dyspnoea, in small doses. I.e. ordine 1-2.5mg PRN

• Always consider hypercalcaemia as a cause of altered conscious state. It can cause a whole range of different symptoms.

• Treatment of hypercalcaemia in the ED is essentially just fluids - the rest of the treatment will happen on the wards

• Always consider urinary retention in the palliative patient - get a bladder scan!

Falls in the elderly

Tox Case

Khalid presented a case of a patient with verapamil and desvenlafaxine overdose

• Verapamil

  • Resuscitate: haemodynamic support as below

  • Risk assessment: Ingestion 2-3x usual dose can lead to serious toxicity, 1-2 tablets in a child can kill, > 10 tablets in an adult is life threatening. Expect haemodynamic collapse

  • Supportive: As required

  • Investigations: ECG!

  • Decontamination: Charcoal up to 6 hours, longer if modified release

  • Enhanced elimination: Whole bowel irrigation possible in discussion with tox

  • Antidote: Calcium! 30mls Ca gluconate IV over 5 minutes. Repeat x 3 over the 1st hour. Infusions may be needed

• Atropine for bradycardia

• HIET: 50mls of 50% glucose followed by 1 unit/kg actrapid IV. Continue with 1unit/kg/hr infusion with ongoing glucose.

• Inotropes

• ECMO

• methylene blue/lipid emulsion may be indicated in refractory cases

• Disposition: Depends on dose. Prolonged observation as slow release
  

• Desvenlafaxine

  • Resuscitate: treat seizures with diazepam, inotropic support if needed

  • Risk assessment: Seizures (all ingestions > 5g), seretonin toxicity, left ventricular dysfunction (if > 8g)

  • Supportive: As required

  • Investigations: Nil specific

  • Decontamination: Charcoal up to 4hours

  • Enhanced elimination: Whole bowel irrigation possible in discussion with tox

  • Antidote: none

  • Disposition: Depends on dose. Prolonged observation as slow release

 ECG of the Week

90 yo female BIBA after being found on the floor.

This ECG is consistent with hypothermia. HR ~30, sinus bradycardia, shiver artifact, Osborne waves and a long QT

Other features of hypothermia that can be seen on ECGs include a slow AF, junctional bradycardia. Everything can be slowed - long PR, QRS, QT.

Osborne waves are small positive deflections at the J point. They are most prominent in praecordial leads. In hypothermia, the Osborne waves increase in size with decreasing temperature. Other causes of this notching include:

• Hypothermia

• Benign early repolarisation

• Hypercalcaemia

• Brugada

• Neurological insult such as SAH

 Image of the Week

Matt is going to start facilitating a radiology image of the week. Each week, have a look and have a go answering the questions anonymously below.

https://radiopaedia.org/cases/acute-subdural-haemorrhage-on-warfarin-2

Describe the key findings on the CT

1)     Right subdural haematoma (mixed density blood, cystic appearance in places)

-        Looks like acute-on-chronic but can be a hyper-acute bleed or effect of anticoagulation

-        Convex, diffuse, & crosses suture lines

2)     Significant midline shift

3)     Effacement ipsilateral lateral ventricle, dilation of the contralateral lateral ventricle

4)     Subfalcine herniation

Dilation of the contralateral ventricle

-        Implies obstructive hydrocephalus from mass effect

-        Requires urgent neurosurgical intervention

-        The patient can rapidly deteriorate (as in this case)

Subfalcine herniation

-        Implies critical raised intracranial pressure

-        Another indication for urgent neurosurgical intervention

-        Is an indication for ICP lowering treatment (mannitol, hypertonic saline, intubation with ongoing deep sedation & paralysis, and low normal PaCO2)

What are the risk factors for this pathology?

1)     Cerebral atrophy: advanced age or chronic alcohol abuse

2)     Anticoagulation

3)     Chronic liver / kidney disease 

4) Frequent falls

 Interesting Blood Gas

Look at both blog posts on gas interpretation to assist if needed.

Primary Acid/Base

• There is a severe acidaemia (pH 7.07)

• At first glance, the primary process is a metabolic acidosis (BE -22, low bicarb, low pCO2)

• If using Fencl-Stewart:

  • Measured base excess is -22.1 = severe metabolic acidosis

  • Chloride effect: SID = 120 + 2.9 - 75 = 53, should be 42 therefore hypochloraemic alkalosis which should give BE +11

  • Lactate effect: = 2.6 mmol/L therefore should give BE -1.6

  • Albumin effect: 42-38 = 4, therefore very mild hypoalbuminaemic alkalosis which should give BE +1

  • Calculated BE is 11 - 1.6 + 1 = 10.4

  • The actual BE is -22 therefore there is an unexplained severe acidosis of -32.4 (difference between +10.4 and -22). This will be due to weak acids and in this case, probably ketone bodies.

  • In summary there is a moderate hypochloraemic alkalosis, mild lactic acidosis, mild hypoalbuminaemic alkalosis and a likely severe ketoacidosis

• If using traditional approach

  • Bicarb 6 so severe metabolic acidosis

  • AG = 120 - 75 - 6 = 39, = HAGMA

  • Delta ratio = (39 - 12)/(24 - 6) = 1.5 therefore isolated HAGMA. Remember LTKR for causes.

Secondary Acid/base

• Expected PCO2 = 1.5 x HCO3 + 8 = 17

• Actual PCO2 is 22. Therefore could argue there is a secondary respiratory acidosis. However, there are limits to how far the respiratory system can compensate for an acidosis and a pCO2 of 20 is about the limit

Oxygenation

• Normal pO2

• Unknown FIO2 so cannot calculate an Aa gradient

Electrolytes and other

• Severe hyperglycaemia

• Severe hyponatraemia. But corrected for glucose it comes towards normal.

• We don’t know how high the glucose is. Assuming it is 60 then corrected Na = (60-5)/3 + 120 = 138

• Expected potassium = 6.8, therefore relative hypokalaemia and potassium replacement needed urgently

• Hypocalcaemia

Overall Interpration

This patient has marked metabolic derangement. The likely cause is DKA however it is unusual to have such a high glucose in DKA in a type two diabetic. This is probably due to anuric renal failure where the patient is unable to excrete glucose.