Standardised Case Based Discussion Flashcards
What are the typical tasks for OSCE CBD’s?
Outline your approach to the clinical situation, with rationale
Outline your priorities in the investigation and management of the patient.
Answer the examiner’s further questions as the case evolves.
What have candidates done well in the past for OSCE CBD’s?
had a structured approach to the station and expressed themselves clearly.
were able to synthesise the clinical information and consider the patient’s medical history and medications and how these would impact the patient’s current presentation.
were able to outline priorities in their initial assessment and resuscitation and to then modify and justify their approach to ongoing resuscitation based on further case information.
recognised the critical nature of the presentation and the urgency to act with a need for resuscitation and potential airway management
gave specific details of the actions they would take in assessment and management of the patient as opposed to generic resuscitation responses.
correctly identified the ECG findings, escalated their management without prompting.
What is the LIPSSS mnemonic for approaching SCBD’s?
L: Label the case ie
- 3 month old in status epilepcticus
- critically unwell septic obese man in hypoxic respiratory failure
- Unstable but already intubated polytrauma patient
I: Issues
- Rural location, ongoing pathology, need for MTP, no IV access, predicted difficult intubation etc
P: Priorities
- MTP, treat hyperK, treat low BSL, early antibiotics, NIV for delayed sequence intubation etc
S: Staff
- Resus team, specialties, retrieval services
S: Space
- resus vs theatre vs transfer etc
S: Stuff
- equipment needed (ie intubation stuff)
Approach to adult and paediatric hyperkalaemia?
Main Causes
- Too much K in (ie overdose)
- Release from cells (ie rhabdo)
- Not enough out (ie AKI, addisons)
- Pseudohyperkalaemia (usually from RBC lysis with difficult blood draw)
Adult top differentials
- Renal failure
- Rhabdomyolysis
- TLS
- DKA and HHS
- Addisons disease
- Beta blockers
- Metabolic acidosis
Paediatric
- Tumour lysis syndrome
- Rhabdomyolysis
- Accidental overdose
- Acute renal failure
- Acidosis (ie from acute sepsis)
Paediatric Doses
- Salbutamol 2.5-5mg Neb (fastest, 0.5-1mmol drop)
- Calcium gluconate 10% 0.5ml/kg (reduces ECG changes, doesnt alter serum K+)
- Sodium bicarbonate 8.4% 0.5-1ml/kg
- 5ml/kg 10% dextrose with 0.1U/Kg of insulin short acting
- Calcium resonium
- IV frusemide for hypervolaemic and non-anuric patients
- Haemodialysis
How should a rash be approached?
Non-blanching
- Palpable: Meningococcaemia, HSP, endocarditis
- Non-palpable: ITP, TTP, HUS
- Either: Leukaemia, sepsis with DIC, NAI/mechanical
Blanching
- SSSS, scarlet fever, anaphylaxis, measles, viral exanthem, Kawasakis
Sloughing
- Nikolsky +ve: TEN/SJS and pemphigus vulgaris
- Nikolsky -ve: Pemphigoid
Shock and Rash
- Anaphylaxis
- SJS/TEN
- Toxic shock syndrome (usually staph but can be strept)
- Meningococcal septicaemia and Gram Negative sepsis
- Measles (worse in adults)
- DRESS syndrome
- Heat stroke
- Others (Idiopathic Erythroderma, Leptospirosis and rocky mountain spotted fever)
Shock and Rash in children
- As for adults
- SSSS
- Kawasakis
- PIMS TS/MIS-C
- Bad viral illness with exanthem
- Scarlett fever
Erythroderma (diffuse redness) DDx
- Toxic shock syndrome (staph and strep)
- Meningiococcaemia (before purpura)
- Heat stroke
- Anaphylaxis
- SSSS
- Adenovirus, scarlet fever and measles
- Kawasakis disease/PIMS TS/MIS-C
- Drug eruptions (SJS, TEN, DRESS)
- Severe sunburn or dermal burns
Hyponatraemia SCBD?
Risk Factors for complications
- Severity of hyponatraemia
- Acuity of onset (seizures/cerebral oedema higher with acute, ODS higher with chronic)
Important points on Hx/Ex
- Volume status!
- Headache/lethargy/confusion
- Unstable gait
- New drugs
- Recent pneumonia or surgery
- GCS, neurological deficits
- Seizures, unexplained loss of time
Complications
- Seizures
- Cerebral oedema
- Osmotic demyelination syndrome aka central pontine myelinolysis
Hypovolaemic
- Acute dehydration (vomiting, diarrhoea, ALOC etc)
- Diuretic induced
- Addisons disease
- Treat intravascular volume loss, CSL has Na+ 128 so lower chance ODS
- This is the main time DDAVP is indicated, as once correcting hypovolaemia a diuresis often occurs
Euvolaemic
- SIADH
- Non-diuretic drug induced (antipsychotics, SSRI’s, amiodarone etc)
- Steroid induced adrenal insufficiency
Hypervolaemic
- CCF, renal failure, liver failure
- Psychogenic polydipsia
- Treat with fluid restriction
SIADH Definition
- Euvolaemia hypo-osmolar
- Urine Na+ >20
- Urine osmolarity >100
- Not explained by other organ disease ie liver/renal/cardiac failure
- Causes: CNS disturbance, pneumonia, surgery, drugs, malignancies, hypothyroidism, exogenous ADH
Treatment of complications
- 3ml/kg of 3% saline titrated to rise in serum Na+ of 4-6mmol (usually 100-150mls with repeat to max 300)
- If no 3% saline then use 1 amp (100mls) sodium bicarbonate
General treatment
- Fluid restriction aiming for rise in 24hrs no greater than 10-12mmol
- Saline lock the IV
- Strict fluid balance, insert IDC
- Aim for UO <100ml/hr
- If UO >100ml/hr then send urine osmolarity
- If Urine osmolarity <100 then give DDAVP 1mcg to concentrate urine
- NO WATER!!!
ODS
- Occurs due to rapid overcorrection
- Can occur up to 7 days post
- Typically the Pons, but also cerebellum and basal ganglia
- Ataxia, quadriplegia, cranial nerve palsies and lock in syndrome
- RF’s elderly, chronic low Na+, malnourished, hypokalaemia
Hypercalcaemia SCBD
Causes
- Malignancy (bone mets, MM, paraneoplastic syndromes ie NSCLC)
- Granulomatous disease (TB and Sarcoid)
- Hyperparathyroidism
- Drugs (Thiazides, lithium)
- Hyperthyroidism, Phaeo, Addisons
- Acromegaly, pagets disease
- Milk-alkali syndrome and parenteral nutrition
- Long term immoblisation
ECG
- Short QT interval
- Tall QRS complexes
- Osborn waves
- PR prolongation
- Broad T waves merging with the QRS (pseudo STE)
- VT and VF can occur
Treatment
- IV fluids 0.9% saline, titrated to normovolaemia + 1-2ml/kg/hr UO
- Bisphosphonate (IV Pamidronate 60- 90mg)
- Calcitonin 4 international units/kg
- IV hydrocortisone 1-200mg QID
- Withhold meds that cause hypercalc (ie thiazides)
- Haemodialysis if other treatments are refractory
Hypokalaemia SCBD?
Causes
- Reduced intake (malnourishment, refeeding syndrome, short gut)
- Intracellular sequestration (catecholamines, excess insulin, alkalosis)
- Increased loss (thiazide diuretics, RTA 1&2, diarrhoea, *severe vomiting, mucous secreting tumours, fistulas, hyperaldosteronism ie Cushings, burns losses and RRT)
* Vomiting doesn’t normally cause hypokalaemia, unless severe and underlying renal failure or thiazide use
ECG
- inverted T waves
- Large U waves
- Prolonged QT (QU)
- Prolonged PR
Complications
- ascending muscle weakness and respiratory failure
- Rhabdoymyolysis > myoglobin induced kidney injury
- Hypomagnesaemia
- Arrhythmias (particularly TdP)
Treatment
- Always correct Magnesium when correcting potassium
- Seek and treat hypovolaemia
- IV vs oral repalcement
- 0.25mmol/kg/hr aiming for K+>4.0
- 0.2mmols/kg bolus magnesium aiming for >1.0
ECG differentials
STEMI mimic (ELAVATION mnemonic)
E- Electrolyte abnormalities (ca+, K+)
L- LBBB
E- Electrical (Early Repolarisation, PPM)
V- ventricular hypertrophy/Aneurysm
A- Arrhythmia (Brugada, VT)
T - Takutsubos
I- Injury (myocardial contusion) and Inflammation (Peri/myocarditis)
O- Osborne waves (hypothermia)
N- Non-atherosclerotic (Coronary vasospasm, PE, TAD, global ischaemia, elevated ICP)
Q waves
- STEMI
- LBBB
- Normal in V1/2, II, III, AVF (Right and inferior facing leads)
- Dexrocardia
- L) pneumothorax
- HOCM (dagger q waves)
- LV and RV hypertrophy
- HyperK
- WPW
TWI
- Ischaemia
- Raised ICP
- Hypokalaemia
- Takutsubos
Peaked T waves
- Hyper acute T waves (ischaemia)
- Hyperkalaemia
- Coronary vasospasm
- BER
- LVH
- LBBB
- Rarely raised ICP and pericarditis
Short QT interval
- Hypercalcaemia
- Digoxin toxicity
- Hyperkalaemia
- Hyperthermia
- Short QT syndrome
- Catecholamine toxicity
- Severe acidosis
- Myocardial ischaemia
Long QT Interval
- Hypo K/Mg/Ca
- Long QT syndrome
- Many drugs
STEMI vs Pericarditis
- 15% of Pericarditis cannot be distinguished from STEMI on ECG
- Reciprocal depression in any leads except aVR and V1
- STE in lead 3 > lead 2 (3 is higher number than 2, and STEMi is higher priority than pericarditis)
- Convex or horizontal (STEMI) vs concave (pericarditis) STE
- Checkmark or RT sign
- New Q waves (not old)
- New TWI (uncommon in pericarditis unless also myocarditis)
STE in AVR causes
- Proximal LAD or LMCA STEMI
- Diffuse subendocardial ischaemia
- Large PE
- Aortic dissection
- Demand ischaemia from poor perfusion (severe sepsis, upper GI bleed, shock, dysrhythmias, severe anaemia etc)
- Na+ channel blockade
- Correlates with poorer prognosis
- Consider NO CLOPIDOGREL if ACS with STE in AVR as strongly correlated with need for CAGS
HHS vs DKA
HHS Basics
- mOsm >320 (normal 275-295)
- Often marked hyperglycaemia
- Unusual to be ketotic
HHS endpoints
- <300mOsm
- BSL <15
- UO >1ml/kg/hr
- GCS 15, neurological baseline
HHS Treatment
- IV fluids aiming for UO >1ml/kg/hr
- Drop in mOsm no greater than 4mOsm per hour
- 0.05U/kg/hr insulin
Toxic Shock Syndrome
Diagnostic criteria
- Fever >38.9
- Diffuse macular erythroderma rash
- Hypotension
- Multisystem involvement (>3 systems)
- Negative results on other microbiological/serological testing (except staph and strep)
- A comfirmed case is all 5 + the rash desquamates 1-2 weeks later
Shock with non-blanching Rash DDx
- TSS
- Sepsis
- Meningococcaemia (can have non-blanching rash first
- Anaphylaxis
- SJS/TENS or DRESS syndrome
- PIMS-TS/MIS C in children
- Kawasakis with shock in children
- Fulminant viral infection (Influenza, adenovirus, measles etc)
- Red Man syndrome (Vanc infusion)
Ventricular tachycardia SCBD?
Definition
- 3 or more VEB at >130bpm
- Sustained is >30secs
Brugada criteria
- Is RS complex present in all precordial leads? No = VT
- Is RS interval >100ms? Yes = VT
- AV dissociation present (ie capture beats and fusion beats)? yes = VT
- Morphology criteria for VT present? yes = VT
Wide Complext Tachy DDx
- Monomorphic VT
- SVT/AF/Aflutter/ST with Aberrancy
- Antidromic WPW
- AF with WPW
- Hyperkalaemia
- TCA/Na+ blocker toxicity
- Polymorphic VT
- Torsades de Pointes
- AIVR
VT Causes
- See picture
- Enhanced automaticity
- Re-entry
- Enhanced trigger acitivity
Tox Causes
- Hydrocarbon induced catecholamine sensitisation
- TCA/Na+ blocker overdose
- Sympathomimetic (speed, cocaine, meth) induced
- Channelopathy (ie brugada) + ethanol or Na+ channel blocker
Risk Factors
- Older age (>35)
- Structurally abnormal heart
- IHD and active ischaemia
- electrolyte abnormalities
- Catecholamine sensitivity (congenital vs tox/acquired)
- Channelopathies (ie Brugada) or FHx of sudden cardiac death
- Hypothermia
LBBB morphology criteria
- Absence of R wave (QS complex) V6
- R/S ratio <1 in V6 (small R wave)
- Josephson sign (notching/slurring of the S wave)
- Very wide QRS complex
RBBB morphology criteria (V1/2)
- Taller left rabbit ear (ie opposite to tox taller right rabbit ear)
- qR complex in V1
- Smooth monophasic R wave
- SVT suggested by RSR pattern
Pericarditis SCBD
Causes
Inflammatory
- Post viral
- Autoimmune
Infectious
- TB, IE
Post MI
- Dresslers syndrome
Injury
- Direct trauma, radiation, post surgery
- Aortic dissection
Medication
- Chemotherapeutics
Systemic Diseases
- Uraemia
- metastatic cancer
- Amyloidosis, sarcoidosis
Risk factors for severe disease
- Large effusion or evidence of tamponade
- Strong anticoagulant use or bleeding diathesis
- Acute trauma
- Immunosuppressed patients
- Elevated trop (suggests concomitant myocarditis)
- Failure to respond to 7 days of appropriate therapy
- Fever and subacute course
Treatment
- NSAID’s 1st line
- Colchicine 2nd line
- Glucocorticoids 3rd line
- Anti-immune agents 4th line
Pericarditis vs BER
- Both have concave STE in multiple leads
- Both can have spodicks sign
ST/T wave ratio
- Measured in V6
- STE measured from the end of the PR segment to the start of J point
- STE measurement normally relative to the TP segment, so different to normal
- Ratio <0.25 = BER
- Ratio >0.25 = pericarditis
Fish hook sign
- Notching or irregularity at the j point, suggestive of BER
Hypertension evaluation and emergenices SCBD
Life Threats
Subarachnoid Haemorrhage
- Aim SBP <160mmHg
- GTN and BB’s, Hydralazine as well
- ANALGESIA!!!
Ischaemic Stroke
- Aim SBP <180 if fibrinolysing or if evidence of other end organ damage (no need to lower otherwise as may worsen ischaemia
- BB’s +/- Clevidipine
- SNP may worsen ischaemia due to shunt
*Hypertensive Encephalopathy
- Aim 20% reduction in MAP in 1-2hrs
- BB’s +/- GTN/Hydralazine
Eclampsia
- Aim SBP <160 and DBP <100
- Labetalol, Hydralazine, Magnesium
Aortic Dissection
- Aim SBP <120
- Esmolol/Labetalol + GTN/SNP
- ANALGESIA!!!
- If aortic regurge present BB’s may worsen this
STEMI
- Aim MAP 20% reduction
- GTN +/- BB’s
- BB’s controversial as may worsen acute heart failure
- Aspirin, antiplatelet, heparin, PCI
- Acute Heart Failure
- GTN and Frusemide, NIV with PPV
- Clevidipine as CCB, BB’s are relatively contraindicated
Secondary Hypertension Causes
- Head down approach
- Raised ICP (SOL)
- Inctracranial bleed/stroke
- Amphetamine/stimulant use
- Hyperthyroid
- Cushings syndrome
- HOCM/Aortic coarctation
- Phaechromocytoma
- Reno-vascular hypertension
Antihypertensive dosing
Esmolol
- 500mcg/kg load then 50mcg/kg/min infusion
Labetalol
- 20mg bolus then 2mg/min
GTN
- 5mcg/min
Hydralazine
- 5mg bolus
Pacemaker Problems SCBD
Under-sensing
- When the PPM doesn’t sense underlying rhythms and attempts to pace over an intrinsic rhythm
- Programming issues
- Lead displacement
- New bundle branch block
- Stimulation threshold too high
ECG findings
- Pacemaker spikes within native QRS complexes
Over-sensing
- PPM interprets inappropriate signals as QRS’s and doesn’t pace
- Very large P or T waves
- Lead contact issues
- Significant skeletal muscle activity
ECG Findings
- Native rhythm with intermittent or no pacemaker spikes
Failure to Pace
- When no paced stimulus is generated
- Battery low
- Oversensing
- Lead misplacement/fracture
- Interference
ECG
- No or less than normal pacing spikes, native rhythm revealed
Failure to Capture
-When a paced stimulus reaches the myocardium but does not cause depolarisation
- Acidaemia and electrolyte abnormalities
- ischaemia
- lead displacement/fracture
- exit block
ECG
- Pacing spikes present but no P or QRS immediately post this
Twiddlers Syndrome
- When the leads are miss placed due to accidental or intentional movement of the generator by the patient
- leads to output failure, sometimes pacing of innapropriate structures (ie diaphragm and sometimes lead dysplacement arrythmias
ECG Findings
- Native rhythm +/- intermittent ventricular ectopics or VT
Pacemaker mediated tachycardia
- Usually starts with retrograde conduction of a PVC with a dual chamber system in situ
- This sets up a circus movement tachycardia using the dual chamber PPM as the accessory pathway
- Maximum rate is usually 140-150
- Can be terminated either by magnet or AV blockade (as still need AV node for circus movement)
- Occasionally it is due to a physiologic response (ie underlying sinus tach), this can only occur if the PPM is rate responsive in its programmin (ie DDDR)
Recent Pacemaker insertion
- Tension pneumo/haemothorax
- Cardiac tamponade
- Large or infected haematoma
- New VSD/ASD from pacemaker erosion
- Ischaemia
- PPM/cardiac infection
- Pulmonary embolism
Unstable
- Pacing/defibrillation pads in the AP position away from the generator
- Standard ACLS protocol
- Magnet on PPM will default it to VOO or DOO (depending on PPM) and ICD will turn off defibrillation
- Magnet can be used to check for low battery and oversensing
- May need multiple magnets in obese patients
Stable
- Interrogate using wand
- CXR, electrolytes, ECG +/- inflammatory markers, trop and thyroid function tests
STEMI SCBD
STEMI Mimics
Ischaemia
- Prinzmetals angina
- Cocaine/amphetamines
- Aortic dissection
- Myocardial contusion
- Myocarditis
- Emboli to coronaries (infective endocarditis, air embolism etc)
- Coronary vasculitis
- Congenital (ie ALCAPA)
ST elevation
- Takutsubo’s cardiomyopathy
- LVH/HCOM
- Hypercalcaemia
STEMI Equivalents
- Right sided MI
- Posterior MI
- AVR STE with widespread STD
- Sgarbossa criteria in LBBB and new onset LBBB
New onset bifascicular block
- Specifically LAFB + RBBB + ischaemic sounding chest pain
- Associated with prox LAD occlusion
Inferior wall MI
- STE of any degree in 2 of leads II/III/AVF
- STD in lead AVL +/- other leads
- Doesn’t meet normal STEMI criteria but represents and OMI
De Winters T waves
- A true STEMI equivalent, indication for both thrombolysis and cath lab
- ST/J depression that upslopes into a large T wave, often accompanied by STE in AVR
- Different from hyper acute T waves as this often persists whereas hyperacute changes to typical STEMI pattern within minutes
- Represents proximal LAD occlusion
- By definition the patient had acute angina that has now resolved and are (mostly) asymptomatic
Wellens Syndrome
- Represents a very high risk for proximal LAD occlusion in the next 24-48hrs
- Is an indication for acute but not neccesarily immediate PCI (unless symptomatic), it is NOT an indication for thrombolysis on its own
- Deep and symmetric TWI or biphasic TWI with terminal negativtity in leads V1-6
Sgarbossa criteria LBBB
- 3 or more points is 98% specific and 20% sensitive
- Concordant STE >1mm in any lead = 5 points
- Concordant STD >1mm in leads V1- V3 = 3 points
- Discordant STE > 25% of the S wave in leads with dominant S = 2 points
Sgarbossa modified for RV pacing
- No points, any of the 3 in isolation or combined are of equal value
- Approx 80% sensitive and specific
- Concordant STE >1mm in any lead
- Concordant STD >1mm in V1-V6
- Discordant STE >25% in the lead with the greatest STE/S wave ratio
COVID SCBD
Life threats
- PIMS-TS in children
- ARDS
- Secondary bacterial Sepsis
- PE and myocarditis
Differentials
- CAP/HAP
- Other viruses
- Autoimmune disease
- COPD/Asthma
Severity Grading
Mild
- Viral symptoms
- No SOBOE, no dyspnoea at rest
- Normal imaging, normal sats
Moderate
- Evidence of LRTI clinically or on imaging
- Sats >94% on room air
Severe
- Sats <94% on RA, RR >30, lung infiltrates >50% or Pa02/Fi02 <300mmHg
Life Threatening
- ARDS, septic shock, cardiogenic shock, severe VTE
- Usually intubated
High risk groups
- Immunocompromised
- Age >75
- Age >65 and unvaccinated
- Poorly controlled diabetes
- Renal/cardiac/liver failure
Treatment
Mild
- Simple analgesics and supportive care, monitor for deterioration
Moderate Outpatient
- As above, also for mild but at risk of deterioration
- Paxlovid (oral 5 day course) and Remdesevir (IV 3 day course) 1st line
- Molnupiravir 2nd line (oral 5 days)
Severe Inpatient
- Remdesevir 1st line
- Dexamethasone if needing 02
- Prophylactic vs therapeutic anticoagulation based on VTE risk
Critical
- As above
- Add PO baracitinibb if can swallow
- Add IV Tocilizumab if intubated or cant swallow
Subarachnoid haemorrhage SCBD
Risk Factors
- Hypertension
- Smoking and alcohol
- FHx of cerebral aneurysms/SAH
- PCKD, connective tissue disorders
- Alpha 1 antitrypsin deficiency
- Amphetamine/cocaine use
- Older age
Scoring Systems
WFNS + Hunt and Hess
- Both score severity and likely outcome
- Incorporates the initial GCS and symptoms/signs
- see picture
Fisher Grading scale
- uses CT findings to predict risk of vasospasm
CTB Findings
Atraumatic
- Blood often pools centrally near the circle of Willis and gravity dependent will pool in the basal cisterns
Traumatic
- Peripherally near site of impact or contrecoup distribution, blood extends into the sulci
CT rule out
- Within 6hrs approx 98.5% sensitive and 99.5% specific
- Still very sensitive at 86% after this, and the baseline rate of people presenting with SAH after 6hrs is lower leading to a combined post test probability of 0.8%
- Small volume bleed, severe anaemia, non-neuro radiologist and increased time all decrease sensitivity
- CT angio COW is 99%
sensitive/specific even after 6hrs
Lumbar Puncture
- Essentially 100% sensitive but poorly specific, SNout but high rate of false positives
Ottawa SAH score
- 100% sensitive but 15% specific, SNout
Management
- Urgent NSx referral
- Intubate, avoid hypoxia, hypercapnoea and hypotension during the intubation
- Neuroprotective ventilation, aim CO2 35-40
- Neuroprotective strategies such as head up 30 degrees, avoid pressure on neck, avoid cough and straining, keep paralysed and well sedated, prevent hyperthermia
- Nimodipine 60mg Q4hr to prevent vasospasm
- Aim SBP <160/110 if raised ICP, aim SBP <140 if no RICP
- Reverse any anticoagulation, 1 apheresis unit of platelets for Plates <100 or antiplatelet use +/- give TXA (controversial)
- Aim SBP <140mmHg, can use labetalol 20mg, hydralazine 5mg etc
- Consider mannitol 1gm/kg and 3% saline 3ml/kg
- Consider repeat CTB for re-bleed or vasospasm
- Seizure prophylaxis 40-60mg/kg Keppra
Induction agent
- Ketamine controversial
- Likely use Fentanyl and Propofol, but with close monitoing of BP and early use of metaraminol to maintain SBP in normal range
- Avoid both hyper and hypotension
- Minimize stimulation during laryngoscopy, use V/L and senior operator
1st seizure management
Life threats
Neuro
- SAH/ICH/Stroke
- Head trauma/TBI
- Meningoencephalitis
Not-Neuro
- Cardiac arrhythmia
- Hypoglycaemia
- Electrolyte disturbance (HypoNa+)
- Drug/Toxin overdose
- Hypertensive encephalopathy
- Eclampsia
- Wernickes encephalopthy and alcohol withdrawal
DDx
- Brain tumour
- Structural lesion
- PNES
- Breath holding spell (kids)
- Vasovagal syncope
Red Flags
- Non-blanching rash
- Fevers
- Headache just prior to seizure
- Pregnant
- Drug/alcohol use
- Ongoing neurology
- Head injury
Initial Assessment
- Confirm patient has stopped seizing (ie not non-convulsive status)
- Screen for life threats ie RICP, purpuric rash, significant head trauma, evidence of Wernickes
- If no life threats and seizures stopped then proceed to HEI
- Primary (more common kids and adolescents) vs secondary (ie stroke, tumour, more common in adults and geriatrics)
- True seizure vs mimic (ie cardiac)
- Type of seizure (partial, GTC, absence etc)
History
- Aura, focal features
- Recent head trauma
- Medications, drug use
- Focal vs general seizure
- Any ongoing neurology
- Post ictal phase, hemiparesis
- FHx epilepsy, cardiac disorders, sudden death
- Developmental history
- History of possible myoclonic jerks or absence seizures
No need to start anticonvulsant
- Normal neuro exam
- No major acute or chronic medical conditions
- Normal initial diagnostic testing
- Normal mental status
When to start anticonvulsant
- If identifiable cause ie a brain tumour or lesion
- Abnormal neuro exam
Discharge Advice
- No driving until cleared by neurology, may need to report to road authorities if non-compliant
- If job involves driving or use of heavy machinery then will need to mandatory report to licensing authority
- No climbing ladders or heights, no swimming, avoid power tools
- Try and avoid alcohol, stimulants or anything patients knows brings on own seizures
- Give handout on first seizures
- if present discuss with family or at least patient regarding first aid if another seizure occurs
- F/U with neurology or trained GP
- Risk for recurrent seizure is greatest within the first 2 years (21-45%)
Seizure 1st aid
- see pic
Basics of Pacemakers and ICD’s?
Indications for PPM?
- Any cause of 3rd degree or unstable (MBII) 2nd degree AV block
- Symptomatic bradycardia or ventricular dysrhythmia not manageable by another method
- Cardiac resynchronizartion for HFrEF (biventricular pacing)
- Symptomatic bradycardia in context of drugs required for dysrhythmia management
- Chronic bi/trifascicular block with intermittent 3rd/MB II 2nd degree AV block
Indications for ICD?
- Cardiac arrest from VT/VF not caused by reversible pathology
- Spontaneous sustained VT
- Syncope with induced VF/VT in EP lab, when drug therapy will not work or is not desired
- NSVT with ischaemic or structural heart disease and induced or recorded VF/VT that is not treatable with class 1 antiarrhythmic
Common PPM modes?
Slow Atrial Fibrillation
- VVI (+/-R)
- VVIR rate responsive, but requires advanced programming
Complete Heart block
- DDD best, or VAT
- VAT works if 3rd degree heart block but normal SA node, allows AV synchronisation (essentially acts as new His-Purkinje system)
- DDD same as above but use if dysfunctional SA node as well or intermittent AV block
- AV synchronicity restores normal physiology and prevents pace maker syndrome, also reduces risk of AF, but not rate responsive (unless DDDR) and requires 2 leads/advanced program
Sick Sinus Syndrome
- DDDR or AAI
- DDDR Universal pacing with rate responsiveness, but high cost, difficult trouble shooting, 2 leads and regular re-evaluation
- AAI works if no tachy-brady syndrome and AV node fully intact
AOO, VOO and DOO
- Usually the default rates when a magnet is placed on the corresponding PPM (AAI, DDD or VVI)
- DOO or VOO (usually VOO) used for emergent transvenous or transcutaneous pacing
Post ICD/PPM insert complications
Infection
- Overlying cellulitis, pain, swelling, fevers, tenderness to PPM/ICD
- Isolated bacteraemia with systemic symptoms
Vein Occlusion/Thrombophlebitis
- SVC syndrome
- ipsilateral arm venous engorgement and swelling
Pacemaker Syndrome
- Mostly with VVI
- Worsening of fatigue/syncope, CHF and exercise intolerance
- Loss of AV synchrony and ventriculo-atrial conduction
- From PPM firing out of sync with intrinsic atrial function, ie atrial contraction when TV/MV closed, get cannon A waves, retrograde p waves
AICD trouble shooting?
1” Appropriately firing?
- Seek and treat cause of underlying ventricular dysrhythmia
- Haemydnamic and resp support
2: Inappropriately firing?
- place magnet on AICD to turn off
- Seek and treat underlying cause ie sinus tachy, SVT or AICD malfunction
3: inappropriately NOT firing?
- WCT that isn’t VT
- Malfunction of sensing
- Battery low
- Malposition/fracture of leads
- Over-impedence
Simplified management of ventricular arrhythmias?
> 3 of episodes VT/VF/Appropriate AICD shock in 24hrs is deemed significant and defines STORM
LSGB = left stellate ganglion block
Consider
- 3x stacked shocks
- ECMO
- Vector change shocks
If an AICD/PPM is in situ then place the lease in the Anterior Posterior position
Hyper and Hypothyroidism
Transplant medicine
Typical infections
Early (0-4 weeks)
- nosocomial infections ie c diff or MRSA
- donor derived infections ie candida, HIV, HB/CV, tuberculosis, CMV
- Recipient dormant ie TB, HSV, EBV, CMV, HepB/C, candida, aspergillus and pseudmonoas
Intermediate (1-6 months)
- HZV, HSV, EBV, CMV, resp viruses
- Pneumocystis jirovecii
- Mycobacterium and fungal species
Late (>6months)
- All of the above + UTI’s, community acquired infections, resp viruses
Other non-infectious casues
- Graft rejection
- Graft vs host disease
- Transplant associated malignancies
- Drug toxicity
- Recurrence of primary disease (ie infection or autoimmune cause etc)
- Other pathology same as non-transplant patients ie pregnancy, appendicitis etc
Liver complications
- Most common is hepatic artery thrombosis
- Portal vein thrombosis and biliary tract obctruction
Pneumothorax SCBD
Pleural effusion SCBD
Hyperemesis Gravidarum
RF’s
- Predisposition to N/V
- Multiple gestation
- Previous HG
- Hydatid mole
- GI disorders/reflux
Definition
- Pregnant with ongoing N/V
- >5% weight loss pre-pregnancy
- Ketonuria with no other cause
Evaluations
- Weight, postural BP, fluid status
- Foetal wellbeing/viability
- U/S for foetal number and hydatiform molar pregnancy
- Laboratory studies (BSL, ketones, VBG, electrolytes, UEC, LFT’s, TFT’s, lipase)
- Urine for ketonuria, UTI and proteinuria
- H. pyloria breath test
DDx
- N/V of pregnancy
- Gastritis/h. pylori
- Gastro, UTI
- Pancreatitis
- HELLP, Pre-eclampsia, acute fatty liver of pregnancy
- DKA, thyrotoxicosis, adrenal crisis
- Mechanical cause
- Appendicitis
- Drug overdose
Complications
- Severe dehydration
- Starvation ketosis
- Electrolyte derangement
- Long QT and TdP from electrolytes
- Malnutrition and Wernickes
- Mallory-Weiss tear and Boerhaves
- Aspiration
- Premature labour, foetal distress
Management
- IV normal saline
- Seek and treat hypoglycaemia
- IV pyridoxine and Thiamine
- Assess baby with CTG
- Ondansetron, maxalon, cyclizine
- May need NGT if vomiting severe
- Seek and treat ketosis
- Inpatient vs outpatient based on response to treatment and PUQE score
Scoring system (PUQE 24)
- >13 points is severe and likely admit, 3 questions, 1-5 points
- Hours of nausea in last 24hrs (>6hrs = 5 points)
- Vomiting episodes last 24hrs (>7 = 5 points)
- Dry heaving episodes 24hrs (>7 = 5 points)
Special Points
- beware nutritional deficiency and Wernickes encephlaopthay
Disaster SCBD
Concepts
- Greatest good for greatest number
Sieve: Airway patency (if not patent, considered dead)
- HR, RR CRT
vs
Sort: Order of transportation out and where on scene interventions will be performed
METHANE (communication)
- Major incident declared
- Exact location
- Type of incident (chemical, fire etc)
- Hazards present
- Access/Egress
- Number of casualties
- EMS needed and already there
CSCATT (structure)
- Command (allocate and delegate)
- Safety
- Communication
- Assessment
- Triage
- Treatment
- Transfer
Triage
Black = Dead or unlikely to survive
Red= Critical injury requiring immediate care
Yellow= Significant but not immediately life threatening injuries
Green= Walking wounded
Stake Holders
ED Medical + nursing director
Bed co-ordinator
Blood bank/Haem
Heads of anaesthesia/surgery/Radiology/ICU
Hospital CEO
Security
Media department
ED Actions
- Contact stakeholders
- code brown/Hospital disaster plan
- Set up decontamination zone if needed (ie chemical disaster)
- Altered triage (trauma triage vs ATS triage system)
- Call in extra staff
- Ask current staff to stay late
- Discharge as able current patients (allocate senior Dr)
- Move other patients to the ward (Med team and bed coordinator)
- Setup up a large triage bay
- Minimise any investigations
- Rationalise interventions
- Empower nursing staff to initiate treatment without Dr oversight
- Take stock of equipment/drugs
Hospital Actions
- No new surgical cases, activate all theatres
- Call in extra staff, current stay late
- Inpatient teams discharge as able
- Clear outpatients, use for walking wounded
- All hospital visitors leave
- Establish central point of contact aka a command centre
- Notify morgue (multiple bodies)
5 phases ED response
Prevention
Mitigation
Preparedness
Response
Recovery
ECG Approach
Always check for PACING SPIKES!!!
- PMT
- dysrythmias, faulty
Rate
- 300/big squares
Rhythm
- Sinus
- AV dissociation
Axis
Intervals
- PR, QRS, QT,
Size
- LVH, Sokolov-Lyon
- Small complexes (fat, fluid, asthma, hypothyroidism)
Syncope
- HOCM
- Brugada, long QT,
Ischaemia
- STEMI
- Equivalents
- Sgarbossa
Anaemia SCBD
Resuscitation first
Compensated vs Decompensated
- Asymptomatic
- Still able to function but fatigued
- Dissociative shock
Key Differentials
- Blood loss
- Chronic disorders (inflammatory vs organ failure vs malignancy)
- Nutritional deficiency (Fe, B12, folate and alcohol)
- Haemolytic anaemia
- Bone marrow failure
Classification
Morphology
- Micro, normo, macrocytic (MCV)
- Hypochromic, normochromic or hyperchromic (MCHC)
Causes
- Decrease production, increased destruction, increased loss
Severity
- Mild 130-100Hb
- <Moderate 100-70
- Severe <70 or 70-100 with evidence of decompensation (almost always needs transfusion)
Decreased Production
Bone marrow failure
- parvovirus B19, leukaemia, drugs, radiation, aplastic anaemia)
Bone marrow infiltration
- leukaemia/lymphoma, myelofibrosis, myeloma
Lack of subtrates
- iron, B12 and folate
Other
- sepsis related suppression, Hereditary, pregnancy, anemia of chronic disease
Increased Destruction
- Splenic sequestration
- Coombs negative vs positive
Haemolysis screen
- Reticulocyte count
- Peripheral smear (Spherocytes in immune, schistocytes in non immune)
- Haptoglobin (low)
- Unconjugated bilirubin
- LDH (high)
- Haemoglobinuria
Increased Loss
- GI losses (malaena, haematochezia, haematemesis)
- menstruation
- Haemorrhage
- Haemptysis, epistaxis
- Hereditary bleeding disorders
Examination
- Instability, shock
- Cardiac failure
- Organomegaly
- Lymphadenopathy
- Wasting, weight loss
- Jaundice
Complications
- High output cardiac failure (Vasodilated, bounding pulse with wide pulse pressure)
- Low output cardiac failure (LV dysfunction from relative ischaemia)
- Dissociative shock
Thrombocytopaenia SCBD
Life Threats
- Meningococcaemia
- NAI/trauma
- Leukaemia
- SLE/Autoimmune
- DIC/TTP
- HUS
- Bone marrow failure (aplastic anaemia ie parvovirus)
More Common
- Viral induced ITP (EBV and adenovirus most common)
- Drug induced
- Mechanical destruction (marching or jogging, valve replacements, hypersplenism)
- Nutritional deficiencies (B12, folate and iron)
- vW disease
ITP Classification
Life threatening
- Large GI Haemorrhage or ICH
Severe
- Significant bleeding but not immediately catastrophic
Moderate
- Minor bleeding ie from gums, self limiting epistaxis, haematuria etc
Low
- Essentially no bleeding
ITP Management
- Management always in discussion with haematologist
- Needs FBE film reviewed before discharge
Low RIsk
- Repeat FBE in 1 week, outpatient
- Can forego medications unless psychosocial or safety concerns
Moderate
- Admission
- Prednisolone 2mg/kg
- IVIG 1gm/kg
- +/- TXA
Severe/Life threatening
- All of above, Methylpred 30mg/kg
- Platelet transfusion
ITP restrictions
- Avoid contact sports
VTE assessment and treatment?
Key History
- Recent surgery
- Previous VTE
- Immobility
- Malignancy
Other points
- Smoking
- Pregnancy
- Flights
Wells score DVT
Score 0 (5% risk) = low, score 1-2 = moderate (14% risk), score 3 or more = highr risk (50+%)
- -ve 2 points if alternate diagnosis just as likely
- +1 point for immobilisation, cast, recent surgery, local tenderness over deep vein system, unilateral oedema, affected leg >3cm bigger than asymptomatic leg
Wells score PE
- Low risk <2 (1.3% PE)
- Moderate risk 2-6 (16% PE)
- High risk 7 or more (40% chance PE)
- 1 point Malignancy or haemoptysis
- 1.5 points previous VTE, Hr >100 or immobilisation 3 days/surgery within 1 month
- 3 points signs/symtpoms DVT or PE number 1 diagnsosis
PERC score
- 0 points = <2% risk PE
- Used to rule out PE
- Age >50, Hr >100, sats <95%
- Unilateral leg swelling, haemoptysis
- Prior VTE, oestrogen hormone use
- recent surgery/trauma last month needing general anaesthesia
Isolated distal (below knee) DVT
- See algorithm for treatment
Anticoagulation
- Warfarin aiming INR 2-3
- BD Enoxaparin 1mg/kg
- Rivaroxaban/Apixaban
Implications of anticoagulation
- High risk sporting activities
- No effect on menstruation expect
- Employment affected if involves physical tasks
- Pregnancy (only safe one is Clexane, need to cease others)
- Travel (need doses, cant miss)
- Modify risks
Pregnancy
- Heparin and Enoxaparin safe
- Warfarin contraindicated, others unclear
- Usually change to clexane during pregnancy then Heparin in the peripartum period (risk of PPH)
- Need to continue for at least 6 weeks post partum and 6 months in total
Pneumonia SCBD
Scoring Systems
PSI
- Most well validated, accurate and safest
- Complex score with lots of factors
CURB 65
- Less well validated, not preferred
- Much simpler score and easier to implement
SMART COP
- Somewhere in between, not preferred
Pneumonia Severity index
- 5 classes based on points
- Age and sex
- Co-morbidities and nursing home
- Physical findings of reduced GCS, SBP <90, tachycardia, tachypnoea, febrile
- Blood tests pH, elevated urea, low Na+, high BSL, Anaemia, hypoxia
- Pleural effusion on CXR
Pancytopaenia
Emergencies
- Febrile neutropaenia
- Severe neutropaenia (<0.5)
- Severe anaemia
- Severe thrombocytopaenia (<10) with bleeding (<50)
- DIC
- Acute Leukaemia
- Acute aplastic anaemia
- Haemophagocytic lymphohistiocytosis
- Hypeuricaemia
- Acute renal failure
Acute Kidney Injury SCBD
- Rule out life threats
- Severe acidosis
- Hyperkalaemia
- Severe overload
- Uraemia/Uraemic serositis - Assess for adequate perfusion
- Shock assessment
- Hx, Ex and Ix
- Pocus - Assess for overload
- Pulmonary oedema and peripheral oedema
- If neither present then give a fluid challenge - Remember the golden rules
- Measure post void residual (neurogenic bladder, BPH etc)
- Urine dipstick for blood and urine (nephritic syndrome, intra-renal)
- Monitor urine output (ideally catheter)
- Avoid nephrotoxins (ACE, ARB, NSAID’s, Gentamicin) - Consider renal tract imaging
- Stones, tumours, strictures
- Post-renal causes
Classification
Pre-Renal
- Shock and hypovolaemia
Intrarenal
- Vasculitidies
- Diabetes
- Deposition (myoglobin, rhabo etc)
Post renal
- Stones, tumours, strictures
- BPH, neurogenic bladder etc
- Anticholinergics, alpha agonists etc
3rd term vaginal bleeding
