OSCE Facts / Questions Flashcards
Causes of hyperthermia
Infections - Sepsis, CNS infection, endocarditis, tropical disease
Environment - heat stroke
Endocrine - Thyroid/Phaeo
CNS - Hypothalamic stroke
Drugs - Serotonin, NMS, e, cocaine, Salicylate, benzo withdrawal
Hyperthermia effects on the CVS
Tachy and increased SV, along with vasodilation
Decreases MAP
Fluid compartment shift - dehydration, situation worsens, CVP falls
Worsening tachy, met acidosis —> reduced contractility, SV and MAP
Hypotension and infarct
Features of Serotonin syndrome
triad of:
Neuromuscular excitability - clonus, hyper reflex is, rigid
Autonomic dysfunction - hyperthermia, tachy, sweat, flushing
CNS dysfunction - anxiety agitation, confusion coma
Diagnosis of Serotonin syndrome
Clinical - features emerge when starting or raising the dose of a serotonergic drug, or second drug added
Also - Hunter criteria
Drugs (and catergories) causing Serotonin syndrome
Prevent Re-Uptake - SSRI, SNRIs, MAOI, TCA, tramadol/pet hiding
Stimulate release - Tramadol, MDMA, amphetamine
Other - Lithium, Tryptothan
Treatment of Serotonin Syndrome
Stop the drug
Sedation/control agitation
Active Cooling
Control HR/BP
Monitor coag/renal
Antedotes: Cyproheptadine (oral 5HT2a)
Chlorpromazine
cooling methods
Passive - Cool the room, take clothes off
Active external - wet towels, ice pack, fan, pads
Active interval - Cool if fluids, Cavity lovage, RRT, CPB, ECMO
Fever, hyperthermia and hyper pyrexia
Fever - hypothalamic upreguation of set point - cytokine mediated, responds to NSAIDS
Hyperthermia - failure of temperature regulation, does not respond
Hyperpyrex - >41C
Types of Lactic Acidosis
Type A - hypoperfusional
B - normal perfusion
B1 - underlying disease (ketoacidosis, leukaemia, lymphoma)
B2 - Drugs (cyanide, beta-agonists, methanol, ethanol, methanol)
B3 - Inborn errors of metabolism
Causes of a raised CK
Muscular dystrophies Myosotis, Polymyositis, MH Acute MI Cerebrovascular disease Neurosurgery
Rhabodomyolysis, hypothyroidism (muscle loss)
Metabolic features of PRIS
Bradycardia
RBBB
Met acidosis
Raised lactate
Hepatic and renal failure
Definition of PRIS
Acute refractory bradycardia
Plus
Met acidosis (BE >10)
Rhabdo
Hyperlipidaemia
Fatty liver
Mechanism of PRIS
Direct mitochondrial resp chain inhibition
Impaired fatty acid metabolism at mitochondria
Risks of PRIS
Young (paeds)
Severe critical illness (CNS or Resp origin)
TBI
Excess catecholamines
Excess glucocorticoids
Poor carbohydrate intake
Subliminal mitochondrial disease
Tests for PRIS
Consider a serum triglyceride level
Dose range of PRIS
4mg/kg/hour
Treat PRIS
Stop propofol
Switch to alternative sedation agent
HD/HF with CVS support
Early awareness, monitoring
CSF finding of GBS
Raised protein
Differential of weakness
Brain stem lesions - Acute disseminated encephalomyelitis
Spinal Cord - transverse myelitis
Polyneuropathy - Infectious - Polio Diptheria, Lyme
Polyneuropathy - Non infection - porphyria
NMJ - Myasthenia, botulism
Muscle - rhabdo, myosotis
Electrolytes - low K, PO3
Ix of GBS
CSF - protein
NCS - demyelination from atonal types
MRI brain and spine - cord compression, stem lesions
Anti ganglioside antibodies
Infection - campylobacter, mycoplasma, HIV
When to tube GBS
Vital capacity <15ml/Kg
Bulbar weakness, can’t protect airway
Autonomic instability - haemodynamic and cardiac arrhythmia
Drugs to tube GBS
Carefully titration induction agent
Vasopressin and atropine (Brady/autonomic
AVOID SUX - hyperkalaemia
Treatment of GBS
IvIG
PLex
Equally effective, ivig more expensive but easier
NO ROLE FOR STEROIDS
Other issues for GBS management
Tracheostomy DVT Pressure sores Physio Pain particularly neuropathic Psych VAP bundles
Mortality of GBS
5%
Features of poor outcome in GBS
Elderly
MV
Poor neurology at start and persisting
Prolonged MV
SCoring system for CAP
CURB 65
Confusion (new) Urea > 7 RR >30 BP <90 sys Age over 65
CURB score mortality
0 0.7% 1 3.2% 2 13% 3 17% 4 41.5% 5 57%
First line ABx for CAP
Penicillin plus macrolide
Ben pen/clindamcin
Ix for CAP in immunocomp
Try and get BAL
MC&S
Acid Fast Bacilli (TB)
PCP
Aspergillosis
Galactomannan, beta D glucan (blood), IgG/E assessment
Causes of cavitatinig lung lesions
Bacterial pneumonia - Klebsiella and S.aureus
(PVL producing strains of aureus)
TB
Aspiration
Immunodeficiency - HIV - infective: TB, atypical, mycobacterium, aspergillosis
Non infective: NHL, Kaposi’
Non infective - vasculitis, sarcoidosis, rheumatoid, malig, pulmonary infarct
What is PVL
Extra cellular cytotoxic made by S.aureus
Leuocidal - lytic pores in the cell membrane
Associated with skin/soft tissue infections but can be pneumonia
Treatment of PVL
DoH guidance
Linezolid 600mg 12 hourly
Clindamicin 1.2-1.8g 6 hourly
Consider addition of rifampicin
Consider MRSA cover
Micro involvement
IvIG - toxin continues after bacteria killed
Components of q-sofa score
RR > 22
Altered mental state
BP sys < 100
Helps
Define sepsis
A life threatening organ dysfunction caused by a dysregulated host response to infection
In the sepsis definitions, how is “organ dysfunction” defined
Acute change in total SOFA > 2 points
Define sepsis shock
Subset of sepsis
Underlying circulatory, and cellular/metabolic abnormalities are profound enough to cause mortality
Clinically:
Hypotension requiring vasopressors to maintain MAP >65
AND
Lactate > 2mmol/L
DESPITE volume resus
Variables of the SOFA score
Resp : PF ratio Neuro: GCS GI: bilirubin Renal: Creatinine/Urine Haem: Plts CVS: MAP or vasopressor use
Definition of VAP
Pneumonia occur in patients ventilated for 48 hours / within 48 hours of onset of infection
Diagnosis of VAP
Vented 48 hours
Clinical signs, changes in lab tests, CXR
CPIS scoring or HELICS
CPIS elements
Temperature WCC CXR changes PF ratio Type of secretions
What is a ventilator associated event?
Significant event that can be infective or not, leading to a deterioration in oxygenation
20% increase in daily lowest FiO2
Increase in PEEP of at least 3 cm from stable baseline
Organisms for a VAP
Less than 48 hours in hospital - similar to CAP
More than 5 days - hospital multi-resistant:
Pseudomonas,
Klebsiella
Enterobacter
Acinetobacter
Haemophilia
Gram positives. - s. aureus, streptococcus
Fungi - rare
Preventative measures of VAP
Bundles:
Daily sedation hold 30 degree nursing Chloe hex mouth care Suction (sub glottis) Humidification Maintain cuff pressure 20-30cmH20
?SSD
Stress ulcer prophylaxis
Silver ETT
Treatment of VAP with MRSA in sputum
Glycopeptides - vancomycin
Oxazolidinone - Linezolid
Linez - better lung penetrence but not convincing evidence of superiority
Vanc - renal monitor
Treatment of VAP
Tazocin
Gentamicin for MDR
Vanc if MRSA
Teic if VRE colonised
Factors for consideration for VAP
Local policy
Local pathogens
Prevalence of MDR, ESBL, MRSA
Prior therapies, allergy status
Duration of ventilation
Micro results and BALs
Methods of working out daily energy requirements
Weight based - 25-30kcal/kg/day (IBW)
20-25 in acute illness
Protein - 1.2-1.5G/kg/day
Indirect calorimetry
Eqns - Schofield, Benedict Harris equation based on age, sex, height, weight
Energy from protein, carbs and fat
Protein 4kcal/g
Carb 4kcal/g
Fat 9 kcal/g
What is the RQ, and what is it for carbs, fat and protein
Ratio of CO2 produced to Oxygen consumed
Carbs 1
Fat 0.7
Protein 0.8
What is refeeding syndrome
A collection of features that describe the rapid re-institution of feed in patients who have been starved.
Starvation - carbs metabolism switches to fat and protein breakdown.
Start feed. Insulin surge.
Shift of electrolytes - K, PO3, Mg intra cellular
Also altered sugar homeostasis, thiamine deficiency and salt/water retention
Life threatening features of refeeding
muscle weakness resp failure Cardiac dysrhythmias Hypotension Heart failure Coma Death
Prevent refeeding
Establish who is at risk (NICE guidelines)
Careful re-establish feed at 10kcal/kg/day
Gradually increase
Monitor electrolytes and replace
Multivit replacement, thiamine
Dietician input
Risk for refeeding
1 of: 2 of:
BMI<16. BMI <18.5
Weight loss >15% in 3-6/12. 10% weight loss
Little/no intake for 10 days. 5 days
Low K/PO3/Mg prior to feed. Hx of alcohol, drugs (insulin, chemo)
Differential for low platelets and renal failure +/- neurological changes
MAHA - TTP/ HUS
Pre-eclampsia
HELLP
DIC
Autoimmune disease
Vasculitis
Infection - CMV, HSV, HIV, Hep B, sepsis
Evidence of haemoloysis
Low Hb
Film - schistocyes (fragments)
Spherocytes (rounder smaller)
Reticulocyte count
LDH high
Low Haptoglobins
Raised bilirubin and urobilinogen
Test for TTP
ADAMTS 13 reduced
Coombs test - negative
How does TTP differe from HUS
TTP less likely to have renal failure
But more likely to have Neuro abnormalities
Pathophys of TTP
ADAMTS 13 cleaves vWF
Reduction in ADAMTS means less cleavage
Large vWF factor - platelets aggregation and shearing, haemolysis
Triggers - congenital OR, acquired e.g. haemorrhagic colitis - e.coli, shigella
Treatment of TTP in pregnancy
Involve haem and obs
Early delivery of foetus (+/- steroids for lung maturation)
FFP infusions as a temporary measure
DO NOT GIVE PLATELETS
Plasma exchange (removes auto-antibodies and replenish enzymes)
IV methyl-pred.
Name some indications for plasma exchange
GBS
MG
Chronic inflammatory deyelinating poly
Renal: Goodpastures, ANCA vasculitis
Process of plasma exchange
Blood drawn
Cellular components separated from plasma
Done by centrifuge or filter
Substitute patients plasma with done FFP, or HAS
Complications of PLEX
Bleeding Infection Allergic reaction Fluid overload Hypocalcaemia (infused citrate)
Causes of SAH
85% aneurysm
10% non-aneurysmal
5% trauma, AV malformation
Grading severity of SAH
WFNS Score - based on GCS and deficit
Fisher - 4 point radiological scale
Hunt and Hess - 5 point clinical scale
WFNS class for SAH
1 - GCS 15, no def 2 - 13-14, no def 3 13-14, def 4- 12-7 +/- def 5 3-6 +/- def
Neurological complications of SAH
Rebleed - 24 hours - Coil or clip
Risk of intra cerebral haematoma
Hydrocephalus - EVD
DCI due to vasospasm - 5 to 10 days
Diagnosis of vasospasm
Clinical - Neuro - reduced GCS +/- focal neurology
CVS - Hypertension, brady, arrhythmia
Cerebral angiography - gold standard
CT/MR angio
TCD - Lundegaard Ratio
Treatment of vasospasm
Nimodipine, both prophylactic and tx
Mg - little evidence
IR - Balloon angio/intra arterial injections
HHH - (though not hypervol) drive the MAP, and haemodilute
BP target in initial SAH tx
Aim of <180 until coiled/clipped
Secondary measures in SAH
Ventilate to normocapnoea PaO2>10 Normal BM Treat seizures Get to Neuro centre Sit up, loose ties etc
Causes of thrombocytopenia
Reduced prodcuction
Increased destruction
Increased sequestration
Reduced: Bone marrow hypoplasia Alcoholism B12 loss Methotrexate/valproate
Destructions
Immune - ITP/SLE/penicillin
Non - TTP/HUS/DIC
Sepsis/CVVH
Sequestration
Hypersplenism
What is heparin
Where is it made
What does it do
Naturally occurring glycosaminoglycan
Made by mast cells and basophils from tissues rich in mast cells
Increases antithrobmin 3, in turn inhibit thrombin and Xa
Pathophysiology of HIT
Type 1 and 2
1 - non immune, 2 immune
1 - more common
1 - 3 days, 2 5-10 days
IgG antibodies form to the heparin/platelet factor 4 complex
Causes platelets activation and thrombosis, subsequent depletion
Diagnose HIT
4 T’s score (Thrombocytopenia, timing, thrombosis, oTher)
Specific ELISA testing for antibodies
Management of HIT
STOP HEPARIN
Change to something else - argatroban
Or fondaparinux/danaparoid
Avoid warfarin until platelets recover
DO NOT GIVE PLATELETS
Avoid hep for 100 days
4 T’s score
0-3 low prob
4-5 intermediate
6-8 high risk
Criterial for brain stem death - pre-conditions
Cause of coma known (CT)
Irreversible
Deeply unconscious needing mechanical vent
Cardiovascularly stable
BSD criteria - exclusions
No muscle relaxants or sedatives (may need to do benzo/thio levels)
Normal temp (34C)
Na 115-160
K>2
Mg/PO3>0.5
BM 3-20
What should you do if there is benzos/thio on board
Observe for 2-3x the half like of the drug
Give antagonists
Plasma analysis (>10ug/L midaz, >5mg/L thio)
Who does BSD
2 doctors
1 more than 5 years GMC registered
1 consultant
Time of death in BSD
Completion of first set of test
When might you not be able to do tests
High cervical cord injury - affects apnoea test
Facial trauma - can’t examine cranial nerves
If you can’t do BSD, what other tests are there
Consider ancillary tests
Two types - electrical and flow
Electrical - EEG and SSEP
Flow - Cerebral angio (four vessel test)
TCD
PET scan??
Describe the apnoea test
Increase FiO2 to 1.0
ABG - check PaCO2 and SaO2 similar to monitored value
Change ventilation to get an etCO2> 6.0 and pH < 7.4
Place suction catheter at 5l/m O2 into tube or CPAP
Leave for 5 minutes
Observe
Do another gas
CO2 rise by 0.5
ECG features of a TCA overdose
Prolonged QTc Wide QRS Arrhythmia R/S ratio > 0.7 in aVR Terminal R wave > 3mm in aVR Right axis deviation Sinus tachy
Why do ECG changes happen in TCA overdose
Blocks fast Na channels —> wide QRS
Blocking of K —> long QTc interval
Biochemical features of TCA od
Metabolic acidosis
Features of TCA overdose
Neuro and Cardiac
Neuro - Reduced GCS, seizures, coma
CVS - sinus tachy, hypotension, prolonged QRS
Sympathetic - pupillary dilation, dry mouth and skin, retention and agitation
Tx of TCA od
ABC
Tube if low GCS
Activated charcoal in 1 hour - needs an airway
Sodium bicarbonate
Seizures - benzo’s AVOID Phenytoin
Lipid emulsion
Treat hypotension - fluid/vasopressors (adrenaline over norad)
Why does bicarb work on TCA overdose
Aim pH 7.5
Alkalinization reduces the affinity for the drug to the sodium channel
Drugs to avoid in TCA
Anything potentiating a Na block
Phenytoin/flecanide, disopyramide
Classify aortic dissections
Stanford
A - Ascending aorta +/- arch
B - Descending aorta distal to left subclavian
DeBakey
1 - Starts in ascending and propogates into arch
2 - ascending only
3 - descending only
IIIA - above diaphragm
IIIB - extends below
ESC groupings
Why do type A need repairing
Typically involve it aortic valve - incompetent
Valve needs repair/reseat
Thoracic aorta is grafted
Management features of type B dissections
Uncomplicated - BP reduction
Complicated - left thoracotomy
Complex endovascular procedures
Convservative tx of a dissection
BP control - beta-block (verapamil if CI)
GTN/SNP (reduce BP but reflex tachy alone)
Aim MAP 60-65 (or lowest MAP to maintain perfusion)
If no joy:
Treat pain and anxiety
Consider clonidine
Consider dissection to renal vessels
Goal of SSD
Prevent or eradicate oro-pharyngeal/gastric carriage of Potentially Pathogenic Microorganisms.
Thought to preserve non-pathological flora, which protect against overgrowth
Four components of SSD
1 - selective eradication of PPM, use of orobase and NG ABx
2 - Systemic prophylaxis - cefotaxime - prevent resp infections from commensuals
3 - Hygiene and cross-contamination
4 - Regular throat swabs and faeces cultures
Benefits of SDD
Reduce risk of nocosomial infection
Most ICU infections are opportunistic, aerobic, gram neg, bacilli.
Klebsiella, proteus, pseudomonas, these are present already and proceeded by colonisation
Problems with SDD
Resistance
Diarrhoea
Examples of nocosomial infections
UTI
HAP
Line infections/bloodstream
SSI
MRSA/VRE/C.diff
What is C.diff
Gram pos
Spore forming
Bacteria
Causes illness when competitions bacteria wiped out by Abx
Normal component of gut flora
Causes pseudomembranous colitis —> toxic mega
Risk factors for c.diff
Use of broad spec ABx
Increasing length of stay in hospital
Use of PPIs
Poor infection control processes
Severity of c diff
Mild - normal WCC, 3 stools of type 5-7/day
Mod - WCC raised, 3-5 stools/day
Severe - WCC > 15, Temperature 38, Creatinine 50% rise, abdominal/radiology
Life threatening - Hypotension, ileus, megacolon, CT evidence
Tx of C diff
Mild/mod - 14 days oral metronidazole
Severe - vancomycin oral. Refractory - oral plus iv metronidazole.
Conisder IvIG or rifampicin
Surgical input, bloo lactate, colectomy
When to do a colectomy in c diff
Caecal dilation 10cm
Causes of alveolar infiltration/ground glass
Infective - pneumonia, bacterial/viral/fungal
Non-infective Cardiac - pulmonary oedema Idiopathic pneumonia syndrome Diffuse alveolar haemorrhage Bronciolitis obliterans (pulm complication of graft vs host)
Investigate patient with alveolar ground glass from stem cell transplant
Culture/infection: Blood, sputum, urine, BAL - MC&S Throat swabs, viral screen (adeno/rhino, EBV, influenza, RSV, HSV, CMV) Atypical Aspergillosis: galactomannan/ PCR PCP from sputum
Cardiac causes:
12 lead ECG
TTE
HRCT thorax
Causes of deranged LFTs in stem cell transplant
Sepsis
Drugs - anti virals/anti fungal/abx
Viral - EBV
Fungal
GvHD (hepatitis, dermatitis, enteritis)
Veno-occlusive disease (thrombosis after chemo)
CCF - hepatic engorgement
Cause of low platelets in stem cell transplant
Reduced survival: Sepsis GvHD Veno-occlusive HIT TTP
Decreased production: Insufficient transplant Poor marrow, made worse by drugs Marrow fibrosis Persistent/recurrent malignancy
Classify haemopoetic stem cell transplants
Source of donor - autologous (own), allogenic
Matched or unmatched to HLA (human leukocyte antigens)
Source of cells (peripheral, bone marrow or cord blood)
Intensive of pre-transplant chemo regime:
Myeloblative (total destruction of patients marrow)
Reduced intensity conditioning
Poor prognostic features in critical illness of HSCT
MOF MV RRT GvHD Relapse of malignancy
