MRC CARDS CLINICAL (16)

Question 1

PSYCH PATIENT SEDATION USING THE COUNTRY HEALTH TRAFFIC LIGHT PROTOCOL

Answer 1

24/7 psych advice is avail on 13 78 27 and many country psych patients can be managed locally, or RFDS tranferred, using COUNTRY HEALTH’s ‘TRAFFIC LIGHT’ SEDATION PROTOCOL:

GREEN (if accepting orals, LMO to give):

• LORAZEPAM 1-2mg O (max 3x/6h) & 1 of:
• HALOPERIDOL* 10mg O (max 3x/24h), or
• OLANZAPINE 10mg O (max 3x in 24h), or
• QUETIAPINE 100mg O (max 3x in 24h)

AMBER (if refusing orals, LMO to give):

• CLONAZEPAM 1-2mg IM (max 8mg/24h) + 1 of:
• HALOPERIDOL 10mg IM, or
• OLANZAPINE 10mg IM (max 2x in 24h), or
• MIDAZOLAM 2.5mg IV/IM prn (max 20mg/24h)

RED: RRMHS, to advise re

• DROPERIDOL 10mg IM or
• PHENERGAN 50mg IMI

BLACK: RETRIEVAL under KETAMINE & NETTING

• KETAMINE 200mg/50mls (4mg/ml):
• LD 0.5 mg/kg slow IV, then 20-40mls/h

* have BENZTROPINE 1-2mg O/IV/IM avail for DYSTONIA

Question 2

INITIAL MANAGEMENT OF ACUTE CORONARY SYNDROMES

Answer 2

ACS is caused by an acute fall in coronary blood flow, producing chest pain, SOB and arrhythmia. Patients with suspected ACS should be seen within 10m and receive:

• O2 only if hypoxic or shocked
• ASPIRIN 325mg
• GTN (400mcg spray or 300-600mcg tab s/l)
• MORPHINE & Anti-emetic if reqd
• ECG & blood tests, esp [Trop-T], which, together with clinical course, are used to stream into 1 of 3 protocols:

1. LOW RISK PROTOCOL: (settles, ECG & Enz N): admit to ward for serial ECGs & Enz
2. ANGINA/NON STEMI PROTOCOL: (ECG changes but not diagnostic*, [Trop-T] +): admit to CCU and add:
   
   • CLOPIDOGREL 300mg O
   • GTN infusn
   • CLEXANE 1mgkg SC
   • discuss STATINS, B Blockers etc with ICCnet
   • for RFDS T/F for ANGIO within 48h if settles, otherwise retrieve.
3. STEMI PROTOCOL: (Diagnositc ST changes present*) as per NON STEMI plus
   
   • IV CLEXANE 30mg if<75y: and
   • PCI within 60m of presentation and 120m of pain if possible, otherwise:
   • LYSE with TNK 0.5mgkg within 30m unless CI**, then wait 60m. For urgent RFDS T/F if LYSIS successful, urgent retrieval if LYSIS FAILS

• * Diagnostic ST changes = ST Elevn >2mm in 2 ANTERIOR CHEST leads, or >1mm in 2 contiguous LIMB leads.* ST depression does not count as ST Elevn (except in V1-2, where it = POSTERIOR MI) nor does T Inversion
• ** otherwise consider urgent PCI*

Question 3

ACUTE AF MANAGEMENT

Answer 3

• if compromised: sync cardioversion with 100J
• if not, or failed cardioversion
  
  • check for low K+/Mg++
  • seek RATE CONTROL with:
    
    • DIGOXIN 250 mcg slow IV or
    • AMIODARONE 300mg slow IV
  • Avoid Beta & Ca channel blockers, except on cardiologist advice, as these are negative inotropes

Question 4

APO MANAGEMENT GUIDELINES

Answer 4

• acute SOB, particularly nocturnal, often represents Heart failure, although all 10 causes should be considered: (bronchospasm, PT, PE, effusion, ischaemia, arrhythmia, failure, anaemia, infection & exacc COAD).
• Where APO is the diagnosis, Rx =
  
  • O2 (only if needed)
  • Posture
  • CPAP
  • GTN
  • Lasix 40-80 slow IV*
  • consider precipitating causes, esp ischaemia, arrhythmia and anaemia
• Pts who are alert & hypertensive often settle rapidly locally, whereas those who are obtunded and hypotensive generally require retrieval.
• ** over 10m, or risks ototoxicity

Question 5

SIGNIFICANCE OF S1Q3T3* IN PE?

*(or more accurately: S I, Q III T III)

Answer 5

Whilst most patients with PE will show only a non specific SINUS TACHYCARDIA, some will show the classic S1Q3T3 pattern of R heart strain, where:

• S1 = deep S wave in Lead I
• Q3 = Q wave in Lead III
• T3 = T inversion in Lead III

Question 6

INITIAL MANAGEMENT OF COAD PATIENTS

Answer 6

Increasing SOB in COAD may = exaccerbation of COAD, but all 10 causes should be considered (bronchospasm, PT, PE, effusion, ischaemia, arrhythmia, failure, anaemia, infection, exac COAD). Where exac of COAD is the Dx, local treatment options include:

• O2 only if needed (SpO2 88-92%)
• CPAP*
• bronchodilators (salbutamol and atrovent)
• antibiotics: CEFTRIAXONE 1g IV daily + AZITHROMYCIN 500mg IV daily
• Steroids

* but less likely to settle on this without intubation than APO pts

Question 7

ACUTE ASTHMA TREATMENT: 9 steps

Answer 7

1. All that wheezes is not asthma: review the ‘10 causes’, and add FB in children & tumour in adults
2. give Oxygen only if needed (to SpO2 >92%)
3. give SALBUTAMOL, either:
   
   • MDI: puff 100 mcg into spacer & inhale 4x, rpt 16x, or
   • Neb: 5mg initially, can be continuous, or
   • IV: 3mg/50mls (60mcg/ml): LD 4mls slow IV (240mcg) then 1-20ml/h
4. give ATROVENT*: 500mcg neb
5. give HYDROCORT 250mg IV (kids 4mg/kg)
6. consider MgSO4 10mmol slow IV (5mls x 49%) ** (kids 1/100th amp per kg)
7. if B Blockers contributing, consider AMINOPHYLLINE 6mg/kg slow IV or GLUCAGON 1-5mg IV
8. in EXTREMIS, but before intubation, consider ADREN 500mcg IM or IV***
9. if INTUBATING -
   
   • induce with KETAMINE (bronchodilates) or PROPOFOL (suppresses reflexes)
   • Accept hypercarbia: use small volumes, slow rates and long exp times, minimal PEEP, disconnect frequently to avoid breath stacking
   • consider compression assisted exhalation but evidence scant
   • consider VOLATILES as bronchodilators, empirically SEVO
   • if deteriorates suddenly on vent, check for PT and mucous obstruction of ETT/bronchus

• * = IPRATROPIUM, an anticholinergic bronchodilator related to atropine*
• ** slowly, hurts, more effective in paeds, beware incr muscle weakness in fatigued adults*
• *** usually well tolerated despite acidosis and cardiac irritability*

Question 8

SALBUTAMOL AS A CAUSE OF HYPOXIA

Answer 8

• Because salbutamol is both a broncho and a vaso-dilator, it can cause hypoxia by increasing V/Q mismatch, particularly:
  
  • initially - as bronchospasm cracks, or
  • if continued inappropriately long after bronchospasm settles

Question 9

ACUTE STROKE CLINICAL MANAGEMENT

Answer 9

The goal in acute stroke is lysis of suitable lesions within 4.5h (and/or clot retrieval at the RAH within 24h)

• Address the ABCs and expedite transfer to a STROKE HOSPITAL for clot lysis unless C/I by:
  
  • no lyseable lesion on CT
  • onset >4.5 h or unknown (eg woke with it)
  • minor symptoms, and resolving
  • major CVA, comatose
  • seizures (likely indicates bleed)
  • recent bleeding (esp intracranial)
  • already anticoagulated (incl Clexane* but antiplatelets OK)
  • BP >185/110
  • significant dementia or terminal illness

* in contrast to the STEMI lysis guidelines, perhaps remember as ‘brain more likely to bleed than heart’

Question 10

STATUS* EPILEPTICUS MANAGEMENT

Answer 10

‘Status’ = continuing >10m: most seizures stop spontaneously and need nothing more than first aid

Management:

• address the ABCs, but immediate intubation not usually reqd
• address reversible causes: hypoxia, hypoglycaemia, fever, head injury
• gain IV access and draw bloods for EUCGluc, CBE, drug levels & screen
• if still fitting after 10m, give MIDAZ 5-10mg IV (IMI OK)
• if still fitting after 10m, give SODIUM VALPROATE 15 mgkg slow IV UNLESS PREGNANCY POSSIBLE*
• if still fitting after 10m, give KEPPRA 20mgkg slow IV
• if still fitting after 10m, consider GA with THIO or PROPOFOL infusion but continuous EEG then mandatory to detect occult seizures whilst paralysed

* “VE before VE”

Question 11

TRADE NAMES FOR ANTICONVULSANTS?

Answer 11

• VALPROATE = EPILIM (‘VE’)
• PHENYTOIN = DILANTIN (‘PD’)
• CARBEMAZEPINE = TEGRETOL (‘CT’)

Question 12

KEPPRA

Answer 12

• KEPPRA (LEVITIRACETAM) is a new anticonvulsant with unclear mechanism of action which is replacing
  
  • VALPROATE (because its safer in pregnancy)
  • PHENYTOIN (because it doesnt req levels)
• DOSE
  
  • LD in acute seizures = 20mg/kg slow IV
  • neurosurg prophylaxis = 500mg

Question 13

THE DREADED EBOLA

Answer 13

• EBOLA is a VIRAL HAEMORRHAGIC FEVER from West Africa. Natural hosts include bats and monkeys, although pigs and dogs can also transmit it.
• Symptoms begin up to 3 weeks after exposure, initially as a general illness with headache, fever, rash, muscle pain, V&D. This progresses to lethal coagulopathy & organ failure in over 50% of cases
• the virus enters via mucous membranes or broken skin, either by direct contact with infected pts or objects, or short range DROPLET SPLASH. AIRBORNE transmission does not occur.
• Ebola survives for days when wet and hours when dried. Patients are most infectious when sickest (or dead!) and are NOT INFECTIOUS PRODROMALLY
• Required PPE = CONTACT precautions : gloves & gowns, plus eyepro & masks for DROPLET splash.
• RAH & ACH are SAs designated ebola treatment centres

Question 14

RABIES

Answer 14

• Rabies is a lethal* encephalitis caused by the Rabies virus, or other Lyssavirus.
• Globally, the principle vector is the dog, although other land mammals can carry it. The only natural host in Australia is the bat, via the Bat Lyssavirus.
• Infection usually follows exposure to saliva when licked, bitten or scratched, but could follow contact with infected neural tissue, eg after shooting a rabid dog.
• The virus then travels centrally along the nerves to the brain, causing encephalitis weeks to months later.

TREATMENT

• Prevention
  
  • avoid animal contact
  • pre-exposure vaccination (3 doses)
• Post exposure management
  
  • wash susceptible wounds with soap & water then iodine
  • consult CDC regarding
    
    • Post exposure vaccination
    • H_uman Rabies Immunoglobulin_ (HRIG)

*death is virtually certain after encephalitis develops

Question 15

PAEDIATRIC DKA INITIAL Rx (SAHS 2013)

Answer 15

DKA occurs when a relative* or absolute insulin deficiency leads to:

1. Impaired glucose utilisation, with hyperglycaemia, osmotic diuresis, and Na, K+ and water loss
2. Increased fat catabolism, with KETONE production & metabolic acidosis

DIAGNOSIS:

• polyuria, polydipsia, wt loss, nausea, vomiting and abdo pain
• [Gluc>11], [HCO3- < 15], urinalysis + for glucose and ketones

TREATMENT:

• address the ABCs & commence initial fluid resus with NS 10ml/kg x several
• determine cause: new onset, missed insulin, infection**
• admit to HDU/ICU for rehydration over 48h per protocol
• hold insulin until initial fluid resus given (gluc will fall) & K+ known (often low), then start ACTRAPID infusion at 50u in 50mls NS, 0.1u/kg/h, aiming to reduce BSL to 8-12mmol/l at 5 per hour: add 5%D to the IVT when approaching target, rather than reducing insulin
• avoid HCO3- as associated with late onset cerebral oedema: suspect if headaches, falling GCS and incr vomiting: Manage with Mannitol or Hypertonic Saline
• * 10% of paediatric DKA is now T2DM*
• ** do septic screen but note raised WCC is common and not diagnostic*

Question 16

FORMULA FOR CALCULATING FIRST 48h FLUIDS FOR PAEDIATRIC DKA

Answer 16

1. calculate current fluid deficit as % dehydrated x current wt, where
   
   • only mildly unwell* = <5%
   • very ill = 10%
2. add 48h maintenance via the 4:2:1 rule
3. subtract any initial resus fluids given
4. give evenly over 48h as NS +/- KCl, where:
   
   • if [K+] <3.5: add 40mmol/l
   • if 3.5 - 5.0: add 20mmol/l
   • if >5.0: nil

* these may settle with oral fluids and SC insulin