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1
Q

Causes of hyperthermia

A

Infections - Sepsis, CNS infection, endocarditis, tropical disease

Environment - heat stroke

Endocrine - Thyroid/Phaeo

CNS - Hypothalamic stroke

Drugs - Serotonin, NMS, e, cocaine, Salicylate, benzo withdrawal

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2
Q

Hyperthermia effects on the CVS

A

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

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3
Q

Features of Serotonin syndrome

A

triad of:

Neuromuscular excitability - clonus, hyper reflex is, rigid

Autonomic dysfunction - hyperthermia, tachy, sweat, flushing

CNS dysfunction - anxiety agitation, confusion coma

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4
Q

Diagnosis of Serotonin syndrome

A

Clinical - features emerge when starting or raising the dose of a serotonergic drug, or second drug added

Also - Hunter criteria

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5
Q

Drugs (and catergories) causing Serotonin syndrome

A

Prevent Re-Uptake - SSRI, SNRIs, MAOI, TCA, tramadol/pet hiding

Stimulate release - Tramadol, MDMA, amphetamine

Other - Lithium, Tryptothan

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6
Q

Treatment of Serotonin Syndrome

A

Stop the drug

Sedation/control agitation

Active Cooling

Control HR/BP

Monitor coag/renal

Antedotes: Cyproheptadine (oral 5HT2a)
Chlorpromazine

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7
Q

cooling methods

A

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

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8
Q

Fever, hyperthermia and hyper pyrexia

A

Fever - hypothalamic upreguation of set point - cytokine mediated, responds to NSAIDS

Hyperthermia - failure of temperature regulation, does not respond

Hyperpyrex - >41C

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9
Q

Types of Lactic Acidosis

A

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

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10
Q

Causes of a raised CK

A 
Muscular dystrophies
Myosotis, Polymyositis,
MH
Acute MI
Cerebrovascular disease
Neurosurgery

Rhabodomyolysis, hypothyroidism (muscle loss)

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11
Q

Metabolic features of PRIS

A

Bradycardia
RBBB

Met acidosis
Raised lactate
Hepatic and renal failure

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12
Q

Definition of PRIS

A

Acute refractory bradycardia

Plus

Met acidosis (BE >10)
Rhabdo
Hyperlipidaemia
Fatty liver

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13
Q

Mechanism of PRIS

A

Direct mitochondrial resp chain inhibition

Impaired fatty acid metabolism at mitochondria

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14
Q

Risks of PRIS

A

Young (paeds)

Severe critical illness (CNS or Resp origin)

TBI

Excess catecholamines

Excess glucocorticoids

Poor carbohydrate intake

Subliminal mitochondrial disease

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15
Q

Tests for PRIS

A

Consider a serum triglyceride level

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16
Q

Dose range of PRIS

A

4mg/kg/hour

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17
Q

Treat PRIS

A

Stop propofol
Switch to alternative sedation agent

HD/HF with CVS support

Early awareness, monitoring

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18
Q

CSF finding of GBS

A

Raised protein

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19
Q

Differential of weakness

A

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

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20
Q

Ix of GBS

A

CSF - protein
NCS - demyelination from atonal types

MRI brain and spine - cord compression, stem lesions

Anti ganglioside antibodies

Infection - campylobacter, mycoplasma, HIV

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21
Q

When to tube GBS

A

Vital capacity <15ml/Kg

Bulbar weakness, can’t protect airway

Autonomic instability - haemodynamic and cardiac arrhythmia

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22
Q

Drugs to tube GBS

A

Carefully titration induction agent

Vasopressin and atropine (Brady/autonomic

AVOID SUX - hyperkalaemia

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23
Q

Treatment of GBS

A

IvIG
PLex

Equally effective, ivig more expensive but easier

NO ROLE FOR STEROIDS

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24
Q

Other issues for GBS management

A 
Tracheostomy
DVT
Pressure sores
Physio
Pain particularly neuropathic
Psych
VAP bundles
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25
Mortality of GBS
5%
26
Features of poor outcome in GBS
Elderly MV Poor neurology at start and persisting Prolonged MV
27
SCoring system for CAP
CURB 65 ``` Confusion (new) Urea > 7 RR >30 BP <90 sys Age over 65 ```
28
CURB score mortality
``` 0 0.7% 1 3.2% 2 13% 3 17% 4 41.5% 5 57% ```
29
First line ABx for CAP
Penicillin plus macrolide Ben pen/clindamcin
30
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
31
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
32
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
33
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
34
Components of q-sofa score
RR > 22 Altered mental state BP sys < 100 Helps
35
Define sepsis
A life threatening organ dysfunction caused by a dysregulated host response to infection
36
In the sepsis definitions, how is “organ dysfunction” defined
Acute change in total SOFA > 2 points
37
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
38
Variables of the SOFA score
``` Resp : PF ratio Neuro: GCS GI: bilirubin Renal: Creatinine/Urine Haem: Plts CVS: MAP or vasopressor use ```
39
Definition of VAP
Pneumonia occur in patients ventilated for 48 hours / within 48 hours of onset of infection
40
Diagnosis of VAP
Vented 48 hours Clinical signs, changes in lab tests, CXR CPIS scoring or HELICS
41
CPIS elements
``` Temperature WCC CXR changes PF ratio Type of secretions ```
42
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
43
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
44
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
45
Treatment of VAP with MRSA in sputum
Glycopeptides - vancomycin Oxazolidinone - Linezolid Linez - better lung penetrence but not convincing evidence of superiority Vanc - renal monitor
46
Treatment of VAP
Tazocin Gentamicin for MDR Vanc if MRSA Teic if VRE colonised
47
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
48
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
49
Energy from protein, carbs and fat
Protein 4kcal/g Carb 4kcal/g Fat 9 kcal/g
50
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
51
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
52
Life threatening features of refeeding
``` muscle weakness resp failure Cardiac dysrhythmias Hypotension Heart failure Coma Death ```
53
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
54
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)
55
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
56
Evidence of haemoloysis
Low Hb Film - schistocyes (fragments) Spherocytes (rounder smaller) Reticulocyte count LDH high Low Haptoglobins Raised bilirubin and urobilinogen
57
Test for TTP
ADAMTS 13 reduced Coombs test - negative
58
How does TTP differe from HUS
TTP less likely to have renal failure But more likely to have Neuro abnormalities
59
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
60
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.
61
Name some indications for plasma exchange
GBS MG Chronic inflammatory deyelinating poly Renal: Goodpastures, ANCA vasculitis
62
Process of plasma exchange
Blood drawn Cellular components separated from plasma Done by centrifuge or filter Substitute patients plasma with done FFP, or HAS
63
Complications of PLEX
``` Bleeding Infection Allergic reaction Fluid overload Hypocalcaemia (infused citrate) ```
64
Causes of SAH
85% aneurysm 10% non-aneurysmal 5% trauma, AV malformation
65
Grading severity of SAH
WFNS Score - based on GCS and deficit Fisher - 4 point radiological scale Hunt and Hess - 5 point clinical scale
66
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 ```
67
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
68
Diagnosis of vasospasm
Clinical - Neuro - reduced GCS +/- focal neurology CVS - Hypertension, brady, arrhythmia Cerebral angiography - gold standard CT/MR angio TCD - Lundegaard Ratio
69
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
70
BP target in initial SAH tx
Aim of <180 until coiled/clipped
71
Secondary measures in SAH
``` Ventilate to normocapnoea PaO2>10 Normal BM Treat seizures Get to Neuro centre Sit up, loose ties etc ```
72
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
73
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
74
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
75
Diagnose HIT
4 T’s score (Thrombocytopenia, timing, thrombosis, oTher) Specific ELISA testing for antibodies
76
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
77
4 T’s score
0-3 low prob 4-5 intermediate 6-8 high risk
78
Criterial for brain stem death - pre-conditions
Cause of coma known (CT) Irreversible Deeply unconscious needing mechanical vent Cardiovascularly stable
79
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
80
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)
81
Who does BSD
2 doctors 1 more than 5 years GMC registered 1 consultant
82
Time of death in BSD
Completion of first set of test
83
When might you not be able to do tests
High cervical cord injury - affects apnoea test Facial trauma - can’t examine cranial nerves
84
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??
85
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
86
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 ```
87
Why do ECG changes happen in TCA overdose
Blocks fast Na channels —> wide QRS Blocking of K —> long QTc interval
88
Biochemical features of TCA od
Metabolic acidosis
89
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
90
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)
91
Why does bicarb work on TCA overdose
Aim pH 7.5 Alkalinization reduces the affinity for the drug to the sodium channel
92
Drugs to avoid in TCA
Anything potentiating a Na block | Phenytoin/flecanide, disopyramide
93
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
94
Why do type A need repairing
Typically involve it aortic valve - incompetent Valve needs repair/reseat Thoracic aorta is grafted
95
Management features of type B dissections
Uncomplicated - BP reduction Complicated - left thoracotomy Complex endovascular procedures
96
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
97
Goal of SSD
Prevent or eradicate oro-pharyngeal/gastric carriage of Potentially Pathogenic Microorganisms. Thought to preserve non-pathological flora, which protect against overgrowth
98
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
99
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
100
Problems with SDD
Resistance Diarrhoea
101
Examples of nocosomial infections
UTI HAP Line infections/bloodstream SSI MRSA/VRE/C.diff
102
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
103
Risk factors for c.diff
Use of broad spec ABx Increasing length of stay in hospital Use of PPIs Poor infection control processes
104
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
105
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
106
When to do a colectomy in c diff
Caecal dilation 10cm
107
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) ```
108
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
109
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
110
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 ```
111
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
112
Poor prognostic features in critical illness of HSCT
``` MOF MV RRT GvHD Relapse of malignancy ```

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