ICU & FICM Flashcards

1
Q

What is the MACOCHA score?

A

Predicts difficult airway in critical ill patients?

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2
Q

What does the MACOCHA score comprise?

A
Mallampati class III/IV (=score of 5)
Apnoea (OSA) (= 2)
C-spine mobility (= 1)
Opening of mouth <3cm (= 1)
Coma (=1)
Hypoxaemia (SpO2 <80%)(=1)
Anaesthetist (or not)(=1)
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3
Q

What MOCACHA score predicts difficult airway?

A

A score of >3

Max score of 12

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4
Q

What are the signs of PRIS?

A
Arrhythmias
Rhabdomyolysis - high CK
High K
Metabolic acidosis
Lipidaemia from high triglycerides
Enlarged liver/fatty liver
Cardiac failure/myocardial collapse
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5
Q

What is the maximum rate of infusion of propofol?

A

4mg/kg/hr

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6
Q

List risk factors for developing PRIS

A
High infusion rate
Severe head injury
Sepsis
Pancreatitis
High catecholamine/glucocorticoid levels - high stress
Low carbohydrate supply - starvation e.g. burns/trauma
Inborn errors of metabolism
Paediatric populations
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7
Q

What might you see on blood tests for PRIS?

A
Acidaemia
Raised lactate
Raised CK
Myoglobinuria
Hyperkalaemia
Hypertriglyceridaemia
Raised Cr
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8
Q

How do you manage PRIS?

A

Stop propofol
Maintain sedation with other drugs
Inotropic/vasopressor support
Cardiac pacing for refractory bradycardia
IHD to resolve renal failure
Carbohydrate administration (and AVOID TPN)
ECMO

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9
Q

Explain why HFNO is so good?

A

Warmed/Humidified O2 - improved clearance of secretions, decreased atelectasis
High flow rate (up to 60L/min) - washout of dead space/CO2, allows FiO2 of 100%
PEEP - increased FRC, alveolar recruitment

Can be used for: difficult airway, post-op hypoxaemia, procedural oxygenation, maintenance of oxygenation at extubation

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10
Q

What are the contraindications to HFNO?

A
Unconscious patient
Uncooperative/combatant patients
Basal skull fracture
Epistaxis
Facial injury
Laser surgery
Airway/nasal obstruction
T2RF
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11
Q

What is the Parkland formula?

A

Used for fluid replacement in burn patients:
Weight x % burn BSA x 4ml
First half in 8 hours, second half in 16 hours

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12
Q

What are the criteria for sending a burn to a specialist centre?

A
>40% BSA burn (>5% in children)
Age <5 or >60
Full thickness
Site of burn: hands/feet/perineum
Circumferential burn
Inhalational injury
Mechanism of burn: steam, chemical, ionising radiation
Significant associated injuries
NAI
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13
Q

Who sets the information about tracheostomies?

A

National Tracheostomy Safety Project set standards

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14
Q

What % of difficult airways occurred on ICU during NAP 4

A

25%

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15
Q

List 6 patient related factors that increase the risk of complications during the intubation of critical care patients

A
Unfasted, emergency intubation
May already be hypoxaemic
Unable to pre-oxygenate
Airway assessment difficult
Agitation/confusion
Respiratory pathology e.g. shunt
CVS instability
Difficult patient positioning
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16
Q

List some environmental factors that may increase the likelihood of a difficult airway in critical care patients

A

Not in the theatre environment
Staff not trained as airway assistants
High stress environment

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17
Q

List some indications for tracheostomy in a critical care patient

A

Long term ventilation (e.g. C spine injuries) & long term respiratory wean (Guillain Barre)
Avoid complications of long term tracheal intubation (vocal cord stenosis)
To stop sedation
Facilitate tracheal suctioning/respiratory toilet
FONA - difficult airway
Upper airway obstruction
Poor airway reflexes - MND, bulbar palsies

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18
Q

What are the contraindications to tracheostomy?

A
Absolute:
-Unstable C-spine
-Infection over site of trache
Relative:
-High FiO2 >0.6
-High PEEP required >10cmH2O
-Difficult anatomy
-Previous radiotherapy
-Coagulopathy
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19
Q

List some early complications of tracheostomy

A
Loss of airway
Damage to airway
Derecruitment
Pneumothorax
Surgical emphysema
Bleeding
Damage to RLN
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20
Q

List some late complications of tracheostomy

A
Displaced tube causing loss of airway
Tracheal stenosis
Tracheomalacia
Erosion into blood vessel - tracheoarterial fistula
Infection
Scarring/permanent stoma
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21
Q

What are the criteria for diagnosing ARDS?

A

Berlin criteria:
1. Timing - within 1 week of clinical insult
2. Chest imaging - bilateral opacities not fully explained by other cause
3. Origin of oedema - not fluid overload or cardiogenic oedema
4. Oxygenation PF ratio <39.9kPa:
—Mild PaO2/FiO2 ratio = 26.6-39.9kPa
—Mod P/F ratio = 13.3 - 26.6kPa
—Severe P/F ratio = < 13.3
With PEEP 5cmH2O

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22
Q

Describe the pathophysiology of ARDS

A

Increased permeability of alveolo-capillary membrane
Increased non-aerated lung tissue -> lower compliance
Increased deadspace and venous admixture -> hypoxaemia/hypercapnoea

Inflammatory mediators
Diffuse alveolar damage
Non-cardiogenic pulmonary oedema
Surfactant dysfunction
Atelectasis
Fibrosis
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23
Q

What are the 3 phases of ARDS?

A

Acute/exudative - hypoxia and reduced compliance from protein rich fluid in alveoli

Proliferative/subacute - micro vascular thrombi with further reduced compliance and hypoxaemia

Chronic/fibrotic - widespread fibrosis and lung remodelling

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24
Q

What are the strategies used for management of ARDS?

A
Lung protective ventilation 6ml/kg Vt
Avoid peak plateau pressure of >30kPa
Permissive hypercapnoea
Prone positioning
Using PEEP, increasing with increasing O2 requirements
Avoid hyperoxia
Recruitment maneouvres
ECMO
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25
What constitutes the Murray score?
Score for ECMO referral: - PF ratio on 100% - PEEP in cmH2O - Compliance in ml/cmH2O - CXR quadrants infiltrated Each component scored 0 - 4 Score >3 = severe resp failure
26
What are the benefits of the prone position in severe ARDS?
Reduction in V/Q mismatch Increase in FRC Recruitment of atelectatic lung PROSEVA trial showed NNT of 6
27
What is the alveolar gas equation?
PAO2 = PiO2 - PACO2/RQ
28
How is oxygen harmful?
Reactive oxygen species created when there is hyperoxia —OH* + 1O2 Damage DNA & RNA Impairs DNA repair Exposure time and PO2 will determine cumulative O2 dose
29
What are the stages of pulmonary toxicity from excess O2?
1. Increase in Reactive Oxygen Species & reduction in anti-inflammatory levels 2. Inflammatory stage - destruction of pulmonary lining and migration of inflammatory mediators 3. Proliferative phase - cellular hypertrophy & increased secretions from alveolar type II cells 4. Fibrotic phase - collagen deposition and interstitial thickening Irreversible changes Decreased Vital Capacity is first change in lung function seen Acute Lung Injury
30
What are the physiological effects of hyperoxia?
- Hypoxic pulmonary vasoconstriction affected - Altered V/Q relationships from HPV changes - causes increased perfusion to hypoxic lung regions and increasing alveolar dead space (increasing CO2) - Absorption atelectasis - Systemic vasoconstriction - important in coronary/cerebral circulation: - Retinopathy in neonates - Bronchopulmonary dysplasia in neonates - Increased infarct size of MI/Stroke
31
What are the therapeutic uses of hyperoxia?
``` CO poisoning Pneumothorax Cluster headache Hyperbaric O2 for wound healing Hyperbaric O2 for decompression sickness Possibly improved wound healing post surgery ```
32
What is post cardiac arrest management??
2021 Resuscitation Council Guidelines Update state: MAP >65mmHg Targeted temperature management for all adults if unresponsive post-ROSC: -Aim 32-36 first 24 hours -Avoid pyrexia for 72 hours post ROSC Not for routine anticonvulsants but Keppra now first line (or valproate) ``` Neuroprognostication - poor outcome if: -Motor score <3 post arrest with no other reason PLUS -Absent corneal reflexes at 72 hours -Bilateral absent SSEPs at 24 hours -Highly malignant EEG at 24 hours -Neuro-specific enolase -Status myoclonus -Diffuse anoxic brain injury on CT/MRI ```
33
What is APRV? What are the indications/benefits?
Extreme inverse ratio of BiPAP (I:E ratio 10:1) High pressure almost all the time; short period of Tlow means not enough time for alveoli to collapse Aids recruitment and maintains it Atelectetrauma reduced as alveoli remain splinted open
34
What are the problems encountered with APRV?
``` High Paw: -pneumothorax risk -impedes venous return Increased PVR High CO2 (think neuro patients) Staff and unit unfamiliarity ```
35
What are the practical settings for APRV?
PHigh - set at current plateau pressure (25-30cmH2O) PLow - ALWAYS ZERO THigh - 5 seconds is a good place to start TLow - 0.5secs (This means I:E ratio is 10:1; each cycle taking 5.5secs) The main parameter to fine tune is TLow - find the peak flow at 75% of peak and set TLow there
36
How would you adjust the APRV if a patient became: 1. Hypoxaemic 2. Hypercapnoeic
1. Increase PHigh +/- THigh Check TLow = 75% of PEFR (derecruitment if TLow is too long) 2. Increase alveolar ventilation: increase PHigh +/- THigh Increase MV: decrease THigh and increase PHigh
37
How would you wean someone on APRV?
Decrease PHigh while increasing THigh (eventually becomes CPAP) Once PHigh is ~20 then it is basically CPAP
38
What are the NICE guidelines for treating someone with COVID?
—Steroids: Only for people on O2 Dex for 10 days —Tocilizumab: For patients on steroids Cannot have had any other IL-6 therapy on this admission No evidence of bacterial infection NEED to have: -A need for O2 with a CRP >75 OR are within 48 hours of starting NIV/HFNO/I&V Cannot use CRP for monitoring if have had Toci —Remdesivir: Not unless in a trial —VTE: If on HFNO/CPAP/NIV/I&V - double normal dose considered (“intermediate dose”)
39
What are some possible indications for the use of ancillary tests in diagnosis of death following cessation of brainstem function?
Severe resp disease with raised CO2 High C spine injury Extensive facial trauma Thiopentone level >12mg/L
40
What are the indications for intubation in a patient with Guillain Barre?
``` Vital Capacity of <15ml/kg Reduced inspiratory pressure (<30cmH2O) Reduced expiratory pressure (<40cmH2O) Rising PaCO2 Autonomic instability Bulbar involvement Poor cough ```
41
What are the features associated with a poorer outcome in Guillain Barre?
``` Older age Ventilatory support required Anti-GM1 Anti-ganglioside antibody (?) Upper limb involvement Campylobacter infection ```
42
What are the risk factors for prolonged post op ventilation in a patient with myasthenia gravis?
MG history >6years No concurrent respiratory disease Pyridostigmine <750mg/day FVC >2.9L
43
What are the effects of myasthenia gravis on: 1. Depolarising muscle relaxants 2. Non-depolarising muscle relaxants?
1. Increased resistance to Sux 2. Increased sensitivity to NDMR
44
What are the 4 categories of fluid replacement to be considered in any surgical patient?
Resuscitation Redistribution Replacement & reassessment Routine (maintenance) fluid (20-30ml/kg in an adult)
45
Which NAP project focused on peri-operative anaphylaxis?
NAP 6
46
What is the four step grading scale used to describe the severity of anaphylaxis?
Ring & Messmer Grade I & II - non life threatening (non-allergic) —Grade I - mucocutaneous signs —Grade II - moderate multi visceral signs - moderate hypotension/tachycardia with or without bronchospasm/GI upset Grade III & IV - life threatening IgE mediated anaphylaxis —Grade III - CVS compromise from vasodilatation and hypovolaemia —Grave IV - cardiac arrest
47
What are the common causative agents in anaphylaxis?
``` Antibiotics (Teicoplanin or Co-Amoxiclav) NMBDs Dyes - patent blue, methylene blue Chlorhexidine Povidone iodine Colloids Iodinated contrast agents Sugammadex ```
48
What are the benefits of prone position ventilation?
Reduced V/Q mismatch Improved FRC Recruitment of atelectatic lung PROSEVA - reduced 28 day mortality with NNT of 6
49
Describe the mechanism of action of oral hypoglycaemic agents
Biguanides (Metformin): increase insulin sensitivity in hepatic/peripheral tissues; decrease hepatic glucose output Sulphonylureas (Gliclazide): stimulates insulin release from pancreas; decrease insulin resistance in peripheral tissues Thizolidinediones (Pioglitazone): improve peripheral uptake/use of glucose in muscle & fat; decrease liver glucose production SGLT-2 inhibitors (Flozins): increase urinary glucose excretion; (sodium/glucose co-transporter type 2 inhibitors) DPP-4 inhibitors (Sitagliptin): stimulate insulin secretion/inhibit glucagon secretion Incretin analogues (Exenatide): reduce carb absorption, stimulate insulin secretion/inhibit glucagon secretion Meglitinides: stimulate insulin release Alpha-glucosidase inhibitors: slow/limit absorption of glucose
50
What are the effects of malnutrition on the critical care patient?
``` Poor wound healing Lower immunity - increased risk of infection Muscle wasting - respiratory muscle Impaired ventilatory drive Low mood ```
51
What are the risk factors for developing refeeding syndrome?
No oral intake for 5-10 days Unintentional weight loss of >10% over <3months Low BMI (<16 or <18 with other risk factors) Low electrolytes on admission Alcohol/chemotherapy
52
What are the metabolic changes that occur in refeeding syndrome?
Free fatty acid metabolism changes back to carbohydrates Increased phosphate/thiamine requirements Release of insulin Acute thiamine deficiency Intracellular shift of K, Mg, Phosphate
53
What are some features of refeeding syndrome?
``` Arrhythmia Hypotension Cardiac arrest Pulmonary oedema Lactic acidosis Respiratory muscle weakness/fatigue Confusion - Wernicke’s/Korsakoff’s Seizures, coma Immune dysfunction ```
54
What are the NICE recommendations for nutrition in patients at high risk of developing refeeding syndrome?
Thiamine - high dose either Pabrinex or PO Start feed at 10kcal/kg/day with slow increase over 5-7 days Monitor fluid status Monitor K/Mg/Phos and replace as required Trace element supplementation
55
What are the causes of ARDS?
Direct: - Pneumonia - Aspiration - Lung contusion - Fat embolism - Drowning - Inhalational injury Indirect: - Pancreatitis - Sepsis - Major trauma - Massive transfusion - CPB
56
What is the pathophysiology behind paracetamol overdose?
Normally metabolised by the liver NAPQI (minor metabolite) normally conjugated by glutathione Glutathione stores depleted in OD NAPQI binds to cellular proteins causing hepatocellular damage NAC is precursor of glutathione
57
What are the patient risk factors that increase the risk of hepatic damage following paracetamol OD?
``` Chronic liver disease Chronic kidney disease Malnourished Eating disorder Alcoholism Hepatic enzyme induction ```
58
What is the prediction model used to identify liver transplant candidates in hepatotoxicity?
Acute: King’s College Criteria: Paracetamol OD: —pH <7.3 OR —INR >6 (or PT>100) —Creatinine >300 —Encephalopathy 3 or 4 (Think ICE) —lactate >3 after resuscitation Non-paracetamol cause: —PT >100 OR 3 of: —Age <10 or >40 —PT >50 —Bilirubin >300 —Encephalopathy >7 days after jaundice —Disease aetiology: non-hep A/B hepatitis; drug induced; halothane hepatitis Chronic: UK MELD score (generally needs to be >49 to be eligible) - INR, bilirubin, Na, Creatinine (BINC)
59
What are the risk factors that increase the risk of VAP?
Being ventilated NG tube Enteral feed Nasal intubation Immunodeficiency (from critical illness - decreased salivary fibronectin) Severe burns Supine position Excessive sedation Enteral feeding Long duration of mechanical ventilation
60
How can you reduce the incidence of VAP?
``` Avoid intubation Reduce duration of ventilation Hand hygiene Closed loop suction Limit disconnections in circuit Do not allow water pooling in circuit to run into patient Subglottic suction Antimicrobial coating on ETT Ventilator Care Bundle: -Head up -Sedation hold -Histamine H2 receptor blocker -Thromboprophylaxis (Reduce risk of aspiration or number of ventilated days and therefore risk of VAP) Oral hygiene ``` Recent study - PROPHY VAP - showed that one dose ceftriaxone reduced VAP in TBI patients
61
What are the causes of weakness in an ICU patient?
Common: ICU acquired weakness Pharmacological: NMBDs; steroids Nutritional: poor intake; low magnesium; low phosphate; refeeding syndrome Vascular: stroke Neuromuscular: Guillain Barre; Myasthenia Gravis Muscular: myositis
62
What are the features and types of ICU Acquired Weakness?
Definition: clinically detectable weakness where no other aetiology can be found ``` Features: After onset of critical illness Symmetrical Flaccid weakness Peripheral Cranial nerve sparing/autonomic sparing Muscle power weakness noted on >2 occasions 24 hours apart ``` Types: Critical illness polyneuropathy CIP Critical illness myopathy CIM: —cachectic myopathy, thick filament myopathy or necrotising myopathy —reduced CMAP amplitude, normal sensory function, normal conduction velocity & latency, reduced direct muscle CMAP on direct stimulation; abnormal muscle biopsy Critical illness neuromyopathy CINM
63
What are the risk factors of ICU Acquired Weakness?
BEING UNWELL Elderly Female Severity of illness Mechanical ventilation - prolonged course Use of muscle relaxation (prolonged) Use of corticosteroids Use of RRT High dose vasopressors/inotropes
64
How is ICU acquired weakness diagnosed?
Diagnosis of exclusion Clinical diagnosis EMG Nerve conduction Nerve biopsy Muscle biopsy Imaging: CT/MRI
65
What problems does ICU acquired weakness cause?
Slow mechanical wean Ventilator dependence Longer ICU stay Increased risk of VTE Increased risk of pressure damage Increased risk of pneumonia
66
Define the stress response
Physiological and pathophysiological changes occurring in response to stimulus (e.g. of surgery) 1. Metabolic response 2. Immune response
67
How does the stress response occur? (Neuroendocrine)
Hypothalamic stimulation from ascending nociceptive pathways: - Release of ACTH from pituitary (HPA axis) - Release of adrenaline from adrenal medulla (SNS stimulated by hypothalamus) - Increased GH - Increased ADH - Stimulation of RAAS by SNS
68
How does the immune part of the stress response occur?
Both innate and acquired immune systems used - Local response to tissue damage (neutrophils, macrophages, NK cells) release pro-inflammatory cytokines (IL-1, IL-6, IL-8, TNFa) and acute phase reactants - Systemic response to tissue damage causes suppression of T cell response
69
How can we try to reduce the stress response to surgery?
- Propofol and TIVA may reduce cortisol secretion - Etomidate will suppress adrenals - Volatiles have more of an effect than TIVA on immune function - Benzos inhibit HPA - a2-adrenergic agonists inhibit SNS - Systemic opioids - REGIONAL ANAESTHESIA - Surgical technique - minimally invasive - Good nutrition and enteral feeding; short fasting times
70
What is the stress response?
A process whereby pituitary and sympathetic nervous system activation leads to a number of predictable metabolic changes Co-ordinated by the hypothalamus (neural (ascending pathways) and endocrine (cytokines) activation) Pituitary - increased GH/ACTH/ADH Sympathetic - increased catecholamines/RAAS/glucagon Including: - Hyperglycaemia - Nitrogen/protein loss - Lipolysis - SIRS from cytokine - Increased circulating catecholamines - Fluid overload - Decreased CD4 and T helper cell activity
71
What are the causes of ARDS?
Pulmonary Extra-pulmonary
72
What is the pathway for synthesis of catecholamines?
Secreted in response to SNS activation Action potential in pre-ganglionic sympathetic neurones terminate directly on chromaffin cells ACh released -> nicotinic receptors which increase Na/K permeability and depolarisation. Depolarisation opens Ca channels and triggers exocytosis of catecholamine containing granules Phenylalanine -> Tyrosine ->(rate limiting step) L Dopa -> Dopamine -> Noradrenaline -> Adrenaline (in the presence of PNMT, which is only functional in very steroid rich areas - hence why Addison’s patients collapse)
73
What is the pathophysiology of Covid pneumonitis?
``` SARS-CoV-2 enters cells through Angiotensin Converting Enzyme 2 Causes: —ARDS —Thrombophilia and VTE —PTX —AKI/MOF ``` Diffuse alveolar damage: - Exudation - Proliferation - Fibrosis
74
What are the benefits of prone positioning in ARDS?
—Reduces V/Q mismatch —Increases FRC —Allows recruitment of posterior alveoli Evidence from PROSEVA study
75
What are the complications of prone positioning?
``` —Extubation —Endobronchial intubation —Pressure damage/areas —Oedema —Brachial plexus injury (& others) —Cardiac instability (e.g. if underfilled while proning) ```
76
What is RASS?
Agitation/Sedation score used in ICU From -5 to +4 Aim is for a RASS of -2 to +2
77
What are the nutritional requirements for a patient on ICU?
25kCal/kg/day Carb: 2g/kg/day Protein: 1.5g/kg/day Fat: 1g/kg/day Trace elements Vitamins ``` Water: 30ml/kg Na: 1mmol/kg K: 1mmol/kg Mg: 0.1mmol/kg Ca: 0.1mmol/kg ```
78
What is tetanus?
Caused by Clostridium tetani - releasing a neurotoxin that binds irreversibly to neuromuscular junction and prevents release of inhibitory neurotransmitters - Muscle rigidity - Muscle spasms - Autonomic instability ``` Management: —Wound debridement —Antibiotics —Immunisation (immunoglobulin) —Monitoring/sedation +/- ICU ```
79
What is refeeding syndrome?
Metabolic disturbances occuring after reinstitution of nutrition in a patient who is malnourished or prolonged fasting Characterised by severe hypophosphataemia and arrhythmias/seizures/rhabdomyolysis
80
What features of OOH cardiac arrest might affect prognosis?
Prognosis After Resuscitation score: - Metastatic malignancy - Non-metastatic malignancy - Sepsis - Dependent functional status - Pneumonia - Cr >130 - Age>70 - Acute MI
81
What factors are used for prognostication after OOHCA?
—Clinical: corneal blink reflex, pupil response, myoclonus, ongoing seizures —Radiological: CT, MRI —EEG —SSEPs
82
What scoring systems are used for prognosis following OOHCA?
``` ERC and ESICM 2021 guidelines: —after 72 hours of Targeted Temp Management in unconscious patient M <3 Need 2 of: -No pupillary/corneal reflex -Absent SSEP -Malignant EEG -NSE (blood test) high -Myoclonus -MRI/CT DAI/anoxic injury ``` MIRACLE study to determine who should go for PPCI Cerebral Performance Categories 1 - 5 mRS 0 - 6 Glasgow Outcome Scale Scoring System MIRACLE 2:
83
What spectrum of light is used in a pulse oximeter?
660nm (red) & 940nm (infrared) Isobestic point - 840nm
84
What happens in a quinine overdose?
Prolonged QTc VF resistant to amiodarone Blindness Hypoglycaemia Not removed by CVVh
85
What are the categories used to calculate the HIT score?
The 4 Ts: —Thrombocytopenia —Timing of platelet fall —Thrombosis —Exclusion of any other potential cause Max score of 8: 0-3 low probability; 4-5 intermediate (10-30%); 6-8 high pre-test probability for HIT (20-80%) Thrombocytopenia with >50% fall or down to 20 = 2 points
86
What is acute graft vs host disease?
Complication of allogeneic haematopoietic stem cell transplant caused by T cells from donor attacking host tissue Involves skin, liver and gut: -Rash starts on palms/soles -Diarrhoea can become TEN -Jaundice and cholestasis Rx with steroids/immunosuppression
87
What is the management of GvHD?
Steroids T-cell immunosuppression Anti-TNF antibodies MMF Prophylaxis: calcineurin inhibitors
88
What is the typical course of Heparin induced thrombocytopenia? What is the pathophysiology?
Platelet count falls by 30-50% within 5-10days of starting heparin More common with UFH than LMWH More common in women Complex forms between heparin antigen and platelet factor 4, which is immunogenic. IgG antibodies attach to platelet/heparin complex causing consumptive coagulopathy Stop heparin. Use direct thrombin inhibitors or Factor Xa inhibitors to prevent thromboses
89
Describe the classification for aortic dissection
Stanford Classification: —Type A (ascending aorta) —Type B (descending) European Society Cardiology: —Types 1-5 DeBakey: —Types I-III
90
What is the management of aortic dissection?
BP control - systolic 100-120mmHg Beta blockers Once blocked, SNP/GTN/hydralazine to vasodilate
91
When does an intra-aortic balloon pump inflate?
Onset of diastole Timed against the middle of the T wave on the ECG/dichrotic notch on the A-line Deflates at onset of systole - the peak of the R wave on the ECG
92
What variables does the Child-Pugh score use?
Bilirubin Albumin INR Ascites Encephalopathy
93
What is the MELD score?
UK Model for End stage Liver Disease Used for prognosis of liver disease and prioritising liver transplants If score >15 - suitable for transplant Vs (unclear books) If score >49, mortality without transplant = 9% at 1 year Uses: -Bilirubin -Creatinine -INR -Na
94
How can you classify ACUTE liver failure?
O’Grady: —Hyperacute (<1 week) —Acute (<1 month) —Subacute (<3 months) From jaundice to encephalopathy Bernuau: —Fulminant (1-2 weeks) —Subfulminant (>2 weeks) Jaundice to encephalopathy Japanese: —Fulminant (acute up to 9 days, subacute to 8 weeks) —Late-onset (8-24 weeks) Jaundice to encephalopathy
95
Describe the blood group compatibilities
O - universal RBC donor AB - universal FFP donor Rh +ve can receive Rh -ve blood Rh -ve women should not receive Rh +ve blood
96
What are the APLS weight calculations?
1 - 12 months = (0.5 x age in months) + 4 1 - 5 years = (2 x age) + 8 6 - 12 years = (3 x age) + 7
97
For paediatric trauma, what are the doses of the following: Adrenaline? Blood? Glucose?
Adrenaline = 10mcg/kg Blood = 5ml/kg Glucose = 2ml/kg of 10% solution
98
What are the characteristics of a drug that results in their increased clearance by RRT?
—Small Vd —Low protein binding —High water solubility —Molecular weight (smaller molecules for IHD (500Da), larger for CVVH (40kDa)) —Low endogenous clearance —Extraction ratio exceeding endogenous elimination
99
What are the risk factors for developing bleeding from stress ulceration, and which is most important?
Respiratory failure requiring I&V for >48 hours (most important) Coagulopathy Head injury Major burns (>35%) Spinal trauma Polytrauma Renal failure Liver failure Severe sepsis Shock Organ transplant Steroids Prev PUD
100
What is the composition of CSF?
Osmolality is 280mOsm/kg Specific gravity = 1.005 Glucose = 1.5-4 mmol/L Cl- = 120-130mmol/L Bicarbonate = 25-30mmol/L Protein = 0.15-0.3g/L
101
What are the contraindications to Peritoneal Dialysis being performed on the unit?
Absolute: —abdominal adhesions —lack of trained staff —uncorrected mechanical defects (hernias) Relative: —intra-abdominal sepsis —wound infections —PD catheter leak —malnutrition —inflammatory/ischaemic colitis —newly placed foreign body in abdomen (e.g. clips)
102
What are the likely organisms in peritonitis in Peritoneal dialysis patients?
Coagulase negative Staph Staph aureus Non-Pseudomonas Gram -ves
103
How do you decide that a spinal cord injury patient is ready for respiratory weaning?
FiO2 <0.4 PEEP ~5cmH2O Patient is awake Patient is co-operative Not in pain but not overly sedated No ongoing infection Pulmonary compliance >50ml/cmH2O
104
What factors affect circulating drug levels?
If high hepatic clearance - hepatic blood flow is determining factor If low hepatic clearance - protein binding and hepatic enzyme activity AKI will affect drugs metabolised by the kidneys Ileus will affect enteric absorption of drugs
105
What is the management of PJP?
Co-trimoxazole Prednisolone
106
List some causes of a normal anion gap metabolic acidosis
HCO3 loss replaced by Cl- so anion gap normal Excess Chloride Renal: -Renal tubular acidosis Types I, II & IV -Drugs that reduce ability to acidify urine (acetazolamide or spironolactone) Extra-renal: -Iatrogenic acids - TPN; 0.9% NaCl -Loss of alkaline - diarrhoea/fistulae -Ileal conduit; ileostomies
107
Describe the difference between botulism and tetanus
They are both spore forming Gram +ve anaerobic bacteria Botulism = flaccid paralysis -Blocks ACh release -descending paralysis -often early cranial nerve involvement -supportive treatment Tetanus = spastic paralysis -blocks GABA release -over 2 weeks - lockjaw/autonomic/respiratory/rigidity -tetanus immune toxin/supportive
108
What types of necrotising fasciitis do you know?
Types I-IV I - 70% of cases; polymicrobial II - Group A Strep +/- Staph; Toxic Shock Syndrome III & IV - rare but high mortality
109
What is a toxin?
An enzyme-like protein with biological activity Gram -ve organisms often release ENDOtoxins (part of their cell structure) ->profound inflammatory response EXOtoxins are secreted by bacteria (Strep/Staph/Clostridium) Linezolid and Clindamycin have toxin-suppressing properties
110
How are new UK ICUs built?
According to the DoH’s ‘Health Building Note 04-02’ (2013)
111
What is the minimum bed space area on an ICU?
20m2 or 25m2 for side rooms One washbasin per 2 beds at least
112
What are the minimum standards for an ICU bed space?
Electricity/heating etc Bed that can do Trendelenburg and chair Pressure relieving mattress Dual pendants with 28 single socket outlets, at least some with uninterrupted power supply Gas supply: 3-4 O2 outlets; 2 air outlets (4bar); 2-4 medical vacuum outlets 4 data outlets Emergency call system Telephone and TV outlet for patient use Equipment: -Computer -Monitoring -3-6 infusion pumps -4-10 syringe pumps -blood warmer -feeding pump -ventilation and humidification equipment
113
What is the minimum recommended number of side rooms on an ICU?
20% of beds should be side rooms Ideally with lobby
114
What are the nurse:patient ratios for ICU?
Level 1 patients = 1:4 Level 2 patients = 1:2.5 Level 3 patients = 1:1 May be higher e.g. for ECMO (2:1) There should also be a lead nurse supernumerary to assist (a 2nd if >10 beds occupied) Not more than 20% should be from agency bank nurses
115
What are the medical staffing requirements for an ICU?
Consultant 24 hour on call cover Ward round x2 per day at least Consultant:patient ratio of 1:8 - 1:15 Trainee:patient ratio 1:8 An appropriate airway skilled doctor is available to attend at all times
116
What are the roles of the critical care outreach team?
Identify deteriorating patients on wards Follow up of recent ICU discharges Rehab of ICU discharges Support ward nursing staff to deliver care beyond their normal Institute palliative care where appropriate
117
What studies are there relating to critical care outreach/recognition of deteriorating patients?
MERIT study Priestly study showed significant reduction in hospital mortality with CCOT intervention
118
What scoring systems do you know?
Organ/disease specific (e.g. GCS, MELD) Generic scores (e.g. SOFA, MODS, APACHE)
119
What is the purpose of scoring systems?
Common language for discussion Comparator in clinical trials Quantification of severity of illness which may dictate resource allocation Estimators of prognosis
120
How can a scoring system be assessed?
Predictive - predicts what it needs to predict (mortality, severity etc) Applicable - to a wide group of patients Calibrated - is a higher score worse than a lower score etc Easy to perform Discriminatory - reasonable level of detail (ideal = 1.0; accepted >0.7) Discrimination: —how effective a system is at predicting which patients will die vs which will survive —receiver operator curve (ROC) - constructed by plotting the true-positive rate (sensitivity) against the false positive rate (1-specificity) for a range of score cut offs. Analysis of area under ROC provides an indication of the ability of the scoring system to discriminate between 2 outcomes -1.0 represents perfect discrimination -0.5 suggests the scoring system is no better than a coin toss ->0.7 is accepted as adequate discrimination for a clinical score or test Calibration: —Examines the correlation between predicted and actual outcome over a range of probabilities —e.g. if a score predicts 60% mortality, comparing actual and predicted outcomes will determine the calibration —Simplified Acute Physiology Score (SAPS) is calibrated to different geographical regions Validity(?)
121
What scoring systems do you know (detail)?
Admission scores: Acute Physiology and Chronic Health Evalutation (APACHE I-IV) Simplified Acute Physiology Score (SAPS) Injury Severity Score (ISS) Severity of illness scores: Sequential organ failure assessment (SOFA) Multiple organ dysfunction score (MODS) Nursing workload scores: Therapeutic intervention scoring system (TISS) Organ- or disease-specific scores: GCS MELD RASS CURB 65 Child-Pugh etc etc etc
122
How can we compare ICU performance?
Hospital mortality Standardised mortality ratio - score >1 is worse than expected; <1 is better than expected Early death (within 4 hours of ICU admission) Late death (within 7 days of ICU admission) Out of hours discharge (between 2200 and 0700) Delayed discharge (>4 hours) Unit acquired infections
123
What is ICNARC?
Intensive Care National Audit and Research Centre
124
What is intra-hospital transfer associated with?
Higher risk of: -VAO -pneumothorax -atelectasis -hypoglycaemia -hyperglycaemia -hypernatraemia -increased length of stay Overall mortality was NOT affected
125
What is trans-pulmonary pressure?
TPP = airway pressure - pleural pressure TPP is associated with ventilator-induced lung injury, rather than airway pressure alone Oesophageal pressure is a good surrogate for pleural pressure
126
What is the post-intensive care syndrome?
Up to 50% of ICU survivors will experience cognitive, psychological and physical changes following discharge
127
What is Cardiac Output?
SV x HR Normal value = 4.5-8L/min
128
What is Cardiac Index?
CO/BSA Normal value = 2.7-4L/min/m2
129
What is stroke volume?
(CO/HR) x 1000 60-130ml/beat
130
What is Systemic Vascular Resistance?
80 x (MAP-CVP)/CO Normal value = 770-1500dynes/s/cm5
131
What is Pulmonary Vascular Resistance?
80 x (PAP - PCWP)/CO Normal value = 100-250dynes/sec/cm5
132
What is Ejection Fraction?
(EDV-ESV)/EDV Normally >0.6
133
What is Mean Arterial Pressure?
MAP = CO x SVR Normal = 80-90mmHg
134
What is the normal value for Flow Time corrected (FTc) on oesophageal Doppler?
330-360ms
135
Describe Lundberg waves
Refer to the ICP over time rather than individual waves A = slow vasogenic waves seen in patients with critical cerebral perfusion. Mean ICP 50-100mmHg! A = ALWAYS PATHOLOGICAL Longer lasting - 5-20 minutes) B = cycles of 30s - 120s; transient increases of ICP to 20-30mmHg = evidence of normal autoregulation. Absence is a bad sign C = doesn’t matter. No clinical relevance
136
Describe the normal intracranial pressure waveform
P1 >P2 >P3 P1 = percussion wave; transmitted arterial pressure from choroid plexus to ventricle P2 = tidal wave; reflection of the pressure waves from the skull. This can be affected by brain compliance P3 = dicrotic wave secondary to aortic valve closure
137
What are the indications for invasive ICP monitoring in TBI?
Moderate to severe head injury in those unable to be assessed Severe head injury (GCS<8) and abnormal CT head Severe head injury with normal CT head but 2/3 of: >40yrs, BP<90, abnormal motor GCS EVD may be the best choice (can measure and treat), but if ventricles squished may need intraparenchymal
138
What are your ICP targets in TBI?
ICP <20mmHg CPP >60mmHg
139
What factors are associated with poor outcome in TBI?
Increased age Poor motor GCS Lack of pupil reactivity CT head showing subarachnoid blood Increased Marshall CT grade (oedema/midline shift/extra-axial blood) Hypoxia or hypotension Co-morbidities
140
What forms of neurological monitoring do you know?
Invasive: ICP bolt EVD SjVO2 Brain tissue oxygenation Micro-dialysis catheter Non-invasive: CT head Transcranial Doppler NIRS
141
When should invasive ICP monitoring be performed?
TBI with moderate/severe injury (=GCS<9) in those unable to be assessed Severe TBI and abnormal CT head (haematoma/contusion/swelling/compression) Severe TBI With normal CT head but 2/3 of >40yrs, BP <90, abnormal motor GCS Non trauma: Spontaneous ICH with coma Anoxic brain injury Hepatic encephalopathy and cerebral oedema associated with fulminant liver failure Intracranial infections
142
How do you insert a Sengstaken Blakemore tube?
Insert to 50cm or so Confirm gastric placement Inflate gastric balloon with 250ml of air/saline Apply traction using 500ml or 1L bag (but lower preferred). If bleeding ongoing, inflate oesophageal balloon to manometer of 35-40mmHg, then deflate until bleeding restarts and keep it just above that. Deflate oesophageal balloon every few hours; leave gastric balloon for 12-24 hours
143
When should ICP be monitored in brain injury?
All who have an acceptable chance of survival, a GCS <9 and CT evidence of TBI Normal CT head if they ALSO have >1 of: age >40, motor score <4, hypotension <90 Ventricular site is the most accurate readings with reduced chance of drift/can be recalibrated
144
How would you calculate predicted body weight?
Males = 50 + 0.91 (height in cm - 152.4) Females = 45.4 + 0.91 (height in cm - 152.4)
145
How do we i. measure ii. calculate energy requirements on ICU?
Indirect calorimetry = gold standard —based on O2 consumption; difficult to do Measurement of CO2 production Estimate: —Schofield formula states: <65years = 25kcal/kg/day >65years = 20kcal/kg/day
146
What nutritional requirements does an ICU patient have?
Energy: -if <65years = 25kcal/kg/day -if >65years = 20kcal/kg/day Carbs: -3-4g/kg/day Protein: -1-1.5g/kg/day; increased in burns/major trauma/massive catabolism -essential and non-essential amino acids Lipid: -0.7-1.5g/kg/day Electrolytes: -Water 30ml/kg/day -Na+ 1-2mmol/kg/day -K+ 0.7-1mmol/kg/day -Ca 0.1mmol/kg/day -Mg 0.1mmol/kg/day -Phos 0.4mmol/kg/day Trace elements - selenium, copper, manganese, zinc, iron - unknown role
147
What role do vitamins play in the ICU patient?
Vitamins a —Fat soluble vitamins: -A (eyes) -D -E (anaemia) -K —Water soluble vitamins: -B1 Thiamine (beri beri; Wernicke/Korsakoff) -B2 Riboflavin -B3 Niacin (pellagra) -B6 Pyridoxine (periph neuropathy) -Folic acid -B12 cyanocobalamin
148
What BP are you aiming for with an unsecured aneurysm that has caused SAH?
<140mmHg Use beta blockers
149
Describe the management of aneurysmal SAH
BP <140mmHg Maintain MAP Neuroprotection Coiling preferred to clipping if possible Prophylactic nimodipine 60mg QDS for 21 days reduces delayed cerebral ischaemia/vasospasm
150
How are patients monitored for delayed cerebral ischaemia post SAH?
Clinical: -drop in GCS/neurology Digital subtraction angiography: -gold standard -allows treatment at same time if detected CT angiogram: Transcranial Doppler: -velocity in middle cerebral artery >200cm/s suggests DCI; confirmed using Lindegaard index (index >3 = DCI) EEG: -not as reliable
151
How would you manage a patient confirmed to have delayed cerebral ischaemia?
Hypertension - titrate to clinical response Hydration - euvolaemia Nimodipine - intra-arterial during angiography - should also be started on day 1 diagnosis to prevent DCI (60mg QDS) Balloon angioplasty Drugs still under investigation
152
What is the differential diagnosis for weakness on ICU?
Cerebral cortex: vascular event, encephalopathy Brainstem: stroke, compression Anterior horn cells/spinal cord: transverse myelitis, compression, ischaemia, infection, motor neurone disease, polio Peripheral nerves: Guillain Barre, critical illness polyneuropathy, Eaton-Lambert, uraemia, mononeuropathies NMJ: MG, botulism, NMBDs Muscle fibre: steroids, electrolytes, critical illness myopathy, disuse atrophy, polymyositis
153
What is the definition of pulmonary hypertension?
2022 definition: Mean PASP >20mmHg at rest PVR >2 Wood units PAWP <15mmHg
154
What is the initial test for pulmonary hypertension?
TTE Tricuspid regurgitation velocity is used to estimate the PASP
155
Describe the pathophysiology of TTP
Thrombotic Thrombocytopaenic Purpura Inhibition of ADAMTS13 (enzyme that cleaves vWF), causing increased platelet adhesion and microthrombi Neurological symptoms, microangiopathic haemolytic anaemia and renal failure
156
What is the treatment for TTP?
Plasma exchange —Removal of autoantibody against ADAMTS13 and replacing it with the normal enzyme from donor plasma Glucocorticoids Rituximab if severe
157
What is Hepatorenal Syndrome?
-Loss of renal function related to chronic hepatic failure -Probably due to inappropriate splanchnic vasodilation and decreased renal perfusion -Associated with poorly controlled ascites -High mortality Type 1 = x2 increase in Cr in <2 weeks (higher mortality) Type 2 = more slow
158
How is Hepato-Renal Syndrome diagnosed?
Cirrhosis with ascites Cr >133 No improvement in Cr after stopping diuretics and expanding with albumin (1g/kg up to 100g per day) Absence of shock No recent nephrotoxics Absence of parenchymal kidney disease
159
What is the management of organophosphate toxicity?
Atropine 1-2mg doubled every 5 mins until resp secretions and bronchospasm cleared Pralidoxime antidote - given early but NOT BEFORE atropine (OP can be absorbed through skin/lung/GIT. Bind to AChE and after time the enzyme is then irreversibly resistant to reactivation by oxime antidote)
160
How do you manage a failing RV?
1. Optimise RV preload - closely monitored fluid/diuretic/RRT 2. Augment the RV - milrinone strengthens RV contraction and reduces PVR; (also dobutamine, adrenaline, levosimendan) 3. Reduce RV afterload - optimise HPV factors; inhaled NO, milrinone, prostacyclin 4. Maintain systemic BP/coronary perfusion - noradrenaline/vasopressin (may cause pulm vasodilatation too and improve PVR/SVR ratio)
161
What are the clinical signs of alcoholic hepatitis?
Jaundice Pyrexia Tender hepatomegaly
162
What are the lab findings in alcoholic hepatitis?
Moderate AST & ALT rise with AST:ALT ratio >2 Bilirubin and GGR raised Leukocytosis with neutrophils
163
What drugs might you give in alcoholic hepatitis?
Steroids if Maddrey discriminate function score >32 Pentoxifylline (?)
164
What are the effects on the denervated heart of: 1. Adrenaline 2. Noradrenaline 3. Dobutamine 4. Isoprenaline 5. Ephedrine 6. Atropine 7. Glycopyrrolate 8. Digoxin
1. Increased response 2. Increased response 3. Normal response 4. Normal response 5. Decreased response 6. No response 7. No response 8. No response
165
How does serotonin syndrome classically present?
A triad of: -change in mental state -neuromuscular abnormality -autonomic hyperactivity Treat with Benzos and Dexmedetomidine Cyproheptadine for severe cases
166
What is the mechanism of action of Vitamin C?
-Direct free radical scavenger, reducing production of radical oxygen species -Reduces cytokine release from B cells -Promote bacterial killing, lymphocyte proliferation and production of interferon -Co-factor in synthesis of vasopressin and catecholamines -Promotes wound healing, protects endothelial barrier and maintains microcirculatory patency Absorbed by Na-dependent transporters Trials have not shown benefit in sepsis yet (?)
167
What is the purpose of thiamine?
-Thiamine is a necessary co-factor for the Krebs cycle -essential in neuronal signalling -works synergistically with Vit C
168
Signs of baclofen OD?
Rapid onset of: -delirium -respiratory depression -coma -seizures Synthetic derivative of GABA (actually quite similar to GHB) At therapeutic dose it works on spinal GABAb, but in excess it inhibits excitatory neurotransmission in all the CNS Can appear brain dead if OD is large enough
169
What is prothrombin complex?
Concentrated factors II, IX and X at significantly higher levels than FFP
170
What is the BP management post haemorrhaging stroke?
Aim systolic <140mmHg (INTERACT2 & ATACH trials)
171
When do you think about intubating a myasthenia patient having a crisis?
If vital capacity falls <20ml/kg Negative inspiratory force <30cmH2O
172
What is Panton-Valentine leukocidin?
Refers to a strain of Staph aureus Causes a necrotising, cavitating pneumonia in association with skin/soft tissue infection Low WBC Treatment: -Linezolid & Clindamycin -IVIG and Rifampicin if it gets really bad
173
How do you differentiate between SIADH and CSWS?
Low Na in both CSWS: -diuresis and natriuresis -hypovolaemic Resuscitate with Na-containing fluids SIADH: -hypervolaemic Fluid restrict
174
What is the management of calcium channel blocker overdose?
Mainly diltiazem/verapamil - myocardial depressants (verapamil in particular) -Supportive; charcoal if MR -Glucagon will increase calcium entry into myocytes -Insulin - similar mechanism -Intralipid (CCBs are highly lipid soluble, highly protein bound) -Calcium!
175
What on earth is haemophagocytic lymphohistiocytosis (HLH)?
—Hyperinflammatory state characterised by pathological macrophage and T cell activation from cytokine production -Can mimic severe sepsis without a source -Excess production of cytokines -Inflammatory dysregulation -End organ damage Can be familial Triggered by infection - often virus (EBV, CMV, HIV) Can be triggered as part of CAR-T therapy
176
What are the characteristic features of HLH?
3 Fs: —Fever —Falling blood counts —Ferritin High fever Hepatosplenomegaly Cytopaenia VERY high ferritin (>10,000) High triglycerides Liver transaminitis Low fibrinogen
177
What is the management of HLH?
H-score >169 Steroids Anakinra (recombinant IL-1 receptor antagonist) IVIG Etoposide Treat the underlying trigger
178
How do you manage raised intra-abdominal pressure?
Assess for end organ damage (if present, likely compartment syndrome) Evacuate intraluminal contents 1. NG 2. Prokinetics 3. Enemas Evacuate intra-abdominal SOLs 1. Drain abscesses Improve abdominal wall compliance 1. Sedation/analgesia 2. Remove constrictive dressings; change position 3. Neuromuscular blockade Optimise fluid balance: 1. Aim negative fluid balance by day 3 2. Consider fluid removal/CVVH
179
What are the features of anti-NMDA receptor encephalitis?
Prodromal flu-like syndrome Psychotic episodes Seizures “” 60% of patients have associated malignancy (teratoma) Diagnosis by positive NR1 & NR2 antibodies in CSF + clinical picture Differentials = paraneoplastic encephalitis; voltage gated K+ channel antibody associated limbic encephalitis Treatment is with immunotherapy and removing tumour
180
What is the normal value for SVR?
900 - 1400 dynes/sec/cm5 — SVR = ((MAP - CVP)/CO) x 80dynes/s/cm5 —
181
What risk factors do you know for refeeding syndrome?
~MAJOR: -BMI <16 -Weight loss 15% in last 3-6 months ->10 days without food -Low Mg/K/PO4 already ~MINOR: -BMI <18.5 -Weight loss 10% last 3-6 months ->5 days without food -Alcohol abuse, insulin, chemotherapy, diuretics
182
QUORUM
Quality of Reporting of Meta-analyses
183
SQUIRE
Standards for Quality Improvement Reporting Excellence
184
CONSORT
Consolidated Standards of Reporting Trials (Most common for all RCTs)
185
MOOSE
Meta-analysis Of Observational Studies in Epidemiology
186
STROBE
Strengthening the Reporting of Observational Studies in Epidemiology
187
What are the minimum staffing standards in ICU?
1x consultant per 8-15 patients 1x junior doctor per 8 patients Level 3 patients: 1:1 nursing Level 2 patients: 1:2 nursing 1x supernumerary coordinating nurse 1x additional nurse for every 10 patients E.g. a 12 bedded ICU will need a nurse for every L3 patient, 1 nurse for every 2 L2 patients, 1 consultant, 2 junior doctors plus a supernumerary coordinating nurse
188
How do you diagnose vasospasm in Doppler?
Measures flow velocities in cerebral arteries. Vasospasm indicated if: Flow velocity >120cm/s ——OR—— Ratio of flows >3 between middle cerebral artery and ipsilateral internal carotid artery
189
Describe autonomic dysreflexia
Loss of co-ordinated autonomic response below level of injury Uninhibited sympathetic response causes profound VASOCONSTRICTION BELOW the level of injury ->hypertension VASODILATATION ABOVE the level of injury and bradycardia from the baroreceptor response
190
Where is the commonest site of aortic injury in trauma?
Proximal descending aorta, at the site of the ligamentum arteriosum (just distal to the origin of the L subclavian artery)
191
How can traumatic aortic injury be defined?
Grading on imaging: -Grade I - intimal tear -Grade II - intramural haematoma -Grade III - pseudoaneurysm -Grade IV - rupture
192
How do you classify lactate?
1. Type A - tissue hypoxia (shock, anaemia, COHb) 2. Type B1 - underlying disease (renal, liver, diabetes) 3. Type B2 - drug/toxin (salbutamol, NRTIs) 4. Type B3 - inborn errors of metabolism (G6PD etc)
193
What do you target in patients with a high lactate?
Target a decrease in 20% over 2 hour - reduce in hospital mortality in those with septic shock & lactate >3
194
How do you declare a major incident?
M - major incident declared E - exact location of incident T - type of incident H - hazards A - access routes N - number/nature of casualties E - emergency services present/required
195
How is a major incident managed pre-hospitally?
CSCATTT Command & Control Safety - of self/rescuers/scene/survivors Communications Assessment of scene Triage - sieve on scene, sort at hospital Treatment Transport
196
How many air changes should happen on ICU?
>10/hr Theatres = 25/hr Anaesthetic room = 15/hr Recovery = 10/hr
197
What fire safety precautions should be taken when designing an ICU?
Well marked fire call points Fire extinguishers O2 shut off valves Isolation of zones of O2 cut off Small bays or side rooms Air changes (>10/hr) Ground floor location Interconnecting with theatres Separate clinical and non clinical areas Wide doors for bariatric patients Smoke control system; smoke lighting Sprinkler system ICU pendants reduce fire risk
198
What are the aims of prone position ventilation?
1. Improve oxygenation 2. Improve respiratory mechanics 3. Homogenise pleural pressure gradient, alveolar inflation & ventilation distribution 4. Increase lung volume & decrease atelectatic regions 5. Facilitate drainage of secretions 6. Reduce VALI
199
What are some causes of a HIGH anion gap metabolic acidosis?
= unmeasured anions (-ve charged) Lactate Ketoacidosis - diabetes/starvation/alcohol Acids - salicylates/methanol/ethylene glycol Pyroglutamic acid Isoniazid Cyanide Renal failure
200
What are some causes of a NORMAL anion gap metabolic acidosis?
GI loss - vomiting, diarrhoea, ileostomy Chloride Renal Tubular Acidosis (kidney unable to acidify urine -> acid retention) Addisons Acetazolamide
201
Management of eclamptic seizure?
-4g bolus Mg -1g/hr for 24 hours -if further seizure, further 2g -deliver foetus once patient stable if possible
202
What is the classification of SAH according to the WFNS?
I - GCS 15; motor deficit absent II - GCS 13-14; motor deficit absent III - GCS 13-14; motor deficit present IV - GCS 7-12; motor deficit present OR absent V - GCS <7; motor deficit present OR absent
203
What are the acceptable warm ischaemic times for transplant post cardiac death?
The duration of time following a sustained decrease in BP <50mmHg for >2mins until the organs have been cooled with cold perfusate in theatre <20mins ideally for liver 30 mins - liver & pancreas 60 mins - lungs 120 mins - kidneys Heart is not transplanted from DCD
204
What is the management of severe traumatic brain injury?
PaO2 >10-13kPa PaCO2 4.5-5kPa MAP 80-90mmHg (if ICP unknown) CPP 60-70mmHg (CPP = MAP - ICP) Head up 30degrees Unobstructed venous drainage Glucose 6-10mmol Na 145-150 Normothermia/avoid pyrexia Hb >10g Sedation Antiepileptics
205
What is the management if ICP rises >20mmHg in TBI?
Sedation bolus +/- paralyse Osmotherapy: —hypertonic saline e.g. 100ml 5% bolus; aim to increase serum Na (but <155) —mannitol 1g/kg bolus; aim osmolality <320mOsm Further imaging - repeat CT Insert EVD (or drain CSF if already in situ) Strict temp control Hyperventilate to PaCO2 of 4kPa Consider surgery - decompressive craniectomy Consider thiopentone coma
206
What is intra-abdominal hypertension?
Sustained increase in intra-abdominal pressure. Normal = <12mmHg. IAH graded 1-4: 1. 12-15mmHg 2. 16-20mmHg 3. 21-25mmHg 4. >25mmHg Abdominal compartment syndrome = IAP>20mmHg with new organ dysfunction
207
How do you start a COPD T2RF on NIV?
Using BTS guidelines: -initial IPAP of 10cmH2O -initial EPAP of 4-5cmH2O -IPAP can be increased 5cmH2O every 10 mins until response or tolerability reached (Most will need IPAP of 20cmH2O; keep EPAP at 5)
208
What pressure should we keep ETT cuff at and why?
<25cmH2O; checked every 8 hours Ideally 20-25cmH2O Trachea capillary pressure is roughly 20cmH2O
209
What is basal metabolic rate?
The metabolic rate of a subject under standardised conditions at mental and physical rest, in a comfortable environmental temperature and fasted for 12 hours Amount of energy expended per unit time during a period of rest Normally 40cal/m2/hr
210
How do you measure Basal Metabolic Rate?
Directly: -Under steady-state conditions, can be measured by whole body calorimetry. (Heat produced per hour is measured) Indirectly: -Measure O2 consumptions of a subject at rest. O2 consumption is multiplied by 4.8kcal of heat produced per L of O2, to give heat produced per hour. Measured using a modified spirometer.
211
How do you treat hypertriglyceridaemia causing pancreatitis?
Insulin-dextrose infusion Stop precipitant Give a fibrate (?)
212
What do you know about short gut syndrome?
If <2m bowel left, need parenteral nutrition support If <50cm bowel, need TPN as nutrition If in between, may also have enteral but will definitely need parenteral support too
213
What can cause a raised PCT?
Infection Burns Trauma Pancreatitis ICH Cardiac arrest Rheumatoid arthritis does NOT raise PCT, so useful in determining if joint is septic or not
214
In pituitary apoplexy, what do you replace first?
1. Cortisol 2. ADH 3. Thyroxine
215
How do you manage tumour lysis syndrome?
Prompt rasburicase and IV fluid therapy Rasburicase CONTRAINDICATED in G6PD Benefit can be seen within hours of starting treatment
216
How is cytokine release syndrome treated?
Steroids Tocilizumab/siltuximab/anakinra - suppress cytokine (IL-6)
217
Which immunosuppressants cause the most renal damage?
Ciclosporin Azathioprine may rarely Tacrolimus and MMF are fine MMF may cause bowel perforation; if unwell can stop MMF
218
What are the pillars of damage control resuscitation?
Permissive hypotension Haemostatic resuscitation Damage control surgery
219
Which types of drugs need adjustment in renal failure?
Antifungals: Fluconazole > voriconazole > Amphoteracin Antibiotics: beta-lactams; quinolones Anti-coagulation
220
Which drugs are most nephrotoxic?
NSAIDs Calcineurin inhibitors - Cyclosporin Contrast HAART Acyclovir Ciprofloxacin Antibiotics Anticonvulsants
221
How can TBI be classified?
By CT - Marshall Classification: I - no visible intracranial pathology II - midline shift 0-5mm; basal cisterns remain visible; no high or mixed density lesions >25cm3 III - midline shift 0-5mm; basal cisterns compressed or completely effaced; no high or mixed density lesions >25cm3 IV - midline >5mm; no high or mixed density lesions >25cm3 V - any lesion evacuated surgically VI - high or mixed density lesions >25cm3; not surgically evacuated
222
What are the contra-indications for liver transplant?
Absolute: -Alcohol consumption (if disease caused by alcohol) -Illicit drug use Relative: -Dependence on drugs but engaging with programme -Poor social support
223
What are the contra-indications to renal transplant?
There aren’t many! Absolute: -Uncontrolled cancer -Active infection -Life expectancy <2 years Relative: -Life expectancy <5 years -Risk of graft loss >50% -Poor adherence -Likely to have problems with immunosuppression
224
What is severe C. difficile infection and how do you treat it?
WCC >15 AKI with Cr >50% above baseline T >38.5 Severe colitis on imaging Rx with PO Vancomycin
225
What is the treatment for: -uncomplicated malaria -severe malaria -malaria in pregnancy?
1. Artemisinin-based combination therapy (ACT) if falciparum; chloroquine if vivax/ovale/malariae 2. IV artesunate until can take oral ACT 3. 1st trimester: artmether-lumefantrine. 2nd trimester: ACT Pregnant or G6PD should NOT get primaquine
226
Which bug causes an alkaline empyema?
Proteus mirabilus
227
What diseases are notifiable?
Meningitis & encephalitis Polio Hep A/B/C (acute) Anthrax Botulism Brucellosis Cholera Diphtheria Enteric fever (typhoid/paratyphoid) Haemolytic Uraemic Syndrome Infectious bloody diarrhoea Group A strep Scarlet fever Legionella Leprosy Malaria Measles Meningococcal sepsis Mumps Plague Rabies Rubella SARS Smallpox Tetanus TB Typhus Viral haemorrhagic fever Whooping cough Yellow fever
228
What is CAR-T?
Chimeric antigen receptor therapy Artificial T cells that can target a specific antigen Used in B cell derived malignancy (myeloma, B cell lymphoma, ALL)
229
What is CRS?
Cytokine release syndrome; usually happens a few days after CAR-T (2-3 days) Occurs in 80-90%(!) of patients Fever +/- hypotension +/- low SpO2 Rx = Tocilizumab (if no concurrent ICANS) Dexamethasone Supportive care 80-90% CRS 75% ICANS 2-4% may develop HLH
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What is HLH?
Haemophagocytic lymphohistiocytosis Usually with diffuse large B-cell lymphoma or B-cell ALL; caused by malignancy but exacerbated by CAR-T Massively high ferritin Rx: -Tocilizumab -Dexamethasone -Anakinra
231
What is ICANS?
Immune effector cell-associated neurotoxicity syndrome Encephalopathy from systemic inflammation; usually with CRS Occurs in 70%, usually 4-6 days after treatment Language abnormalities, especially word-finding; evolving aphasia “Encephalopathy with preserved alertness” Fluctuating course Rx= -thiamine supplements -Dexamethasone -anakinra
232
What is the BODE index score?
Body mass index (0-1) (< or > 21) airflow Obstruction (0-3) (FEV1 % predicted) Dyspnoea (0-3) (MRC score 0-4) Exercise (0-3) (6 min walk test) Predicts long term outcomes in COPD patients Need score >7 for lung transplant
233
What is the injury severity score?
Calculated once all injuries known (so can only be done in hospital) Max score = 75 >15 = major trauma
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Describe TEG/ROTEM
R time/CT - speed of fibrin formation; time taken to reach 2mm K time/CFT - kinetics of fibrin binding to platelets; time between 2mm and 20mm Alpha angle Max ampl/max clot firmness Lysis time - clot stability
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How would you treat a problem with: 1. R time/CT 2. K time/CFT 3. MA/MCF 4. LY30?
1. FFP; PCC or reverse anticoagulation 2. Cryoprecipitate; fibrinogen concentrate 3. Cryoprecipitate; platelets; DDAVP; fibrinogen concentrate 4. TXA
236
How do you assess spinal cord injuries?
Using ASIA impairment scale A = complete B = sensation but no motor below level C = some motor function below level, but most have MRC <3 D = some motor function below level, but most have MRC>3 E = normal sensory/motor Neurological level = lowest level of cord with normal sensation/motor bilaterally
237
What is tetraplegia vs paraplegia?
Tetraplegia = injury within c-spine Paraplegia = injury within thoracic, lumbar or sacral plexus; arm function preserved
238
Why do you need to replace Mg when your K is low?
Mg/K exchange pump, where K is lost to retain Mg. Mg needs to be replaced to turn this pump off and prevent further loss of K
239
What are the goals when treating a TCA OD?
Alkalinisation I&V for low GCS Aim pH 7.5-7.55 Giving sodium to support cardiac cell function - sodium bicarb 1-2mmol/kg (100-150ml) 8.4%; Consider hypertonic saline if BP low despite NaHCO & fluid & pressors Mg if arrhythmia persists post NaHCO; lidocaine; lipid emulsion
240
What is the KDIGO definition of AKI?
Stage 1: -Increase in Cr by >26.5 within 48 hours -Increase in Cr by >1.5x within 7 days -UO <0.5ml/kg/hr for 6 hours Stage 2: -Increase in Cr by >2-3x baseline -UO <0.5ml/kg/hr for >12 hours Stage 3: -Increase in Cr by >3x baseline -UO <0.3ml/kg/hr for >24 hours or anuria for 12 hours -Cr >254 -Initiation of dialysis
241
What does SOFA score use?
6 organs, scoring 0-4 Resp: PaO2:FiO2 ratio CVS: BP +/- pharmacological support Neuro: GCS Liver: Bilirubin Renal: Cr or UO Coag: Platelets Can be modified for chronic liver failure (CLIF-SOFA) to be more accurate for cirrhotics
242
Which pathogen are you more likely to grow in: 1. Early VAP 2. Later VAP?
Early = <72 hours -Strep pneumoniae -H. Influenzae -Staph aureus -Klebsiella pneumoniae -E coli Later = >72 hours: -Pseudomonas -MRSA -Aceinetobacter -Stenotrophomonas maltophilia
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What is SDD?
Selective Digestive Decontamination: 1. Enteral antimicrobials e.g. in gel form to mouth/NG 2. IV abx that covers pseudomonas 3. Strict hygiene 4. Regular surveillance cultures of rectum and throat Potentially decreases VAP but concern about resistance
244
What are the KDIGO guidelines for referrals to Renal in patients with CKD?
AKI GFR <30 Albuminuria ACr >300mg/g Urinary red cell casts CKD plus HTN despite 4 agents K abnormalities persisting Hereditary kidney disease Nephrolithiasis recurrent CKD progressing >5 GFR per year
245
What are the KDIGO recommendations for CT with contrast?
Oral NAC with IV fluid filling - isotonic crystalloids (e.g. isotonic sodium bicarbonate) in at risk patients
246
What is the management of PCP?
Co-trimoxazole (If significant hypoxia (PaO2 <9.2kPa on air), add in prednisolone 40mg BD for 5 days) Alternatives: Dapsone Clindamycin/primaquine Pentamidine
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How do you treat: 1. Aspergillosis 2. Candidiasis 3. Cryptococcus 4. Histoplasmosis 5. Pneumocystis
1. Voriconazole or liposomal amphotericin B 2. superficial - clotrimazole/nystatin -systemic - caspofungin/anidulafungin or liposomal amphotericin B 3. Liposomal amphotericin B 4. Liposomal amphotericin B 5. Co-trimoxazole
248
What is the Child Pugh score?
Used to determine the prognosis of Chronic Liver Disease Ascites Albumin Bilirubin Hepatic encephalopathy INR A = 5-6 points B = 7-9 points C = >10 points (45% 1 year survival)
249
How do you manage oesophageal rupture?
Primary repair is gold standard Fluid resuscitation and broad antibiotic cover (anaerobic and aerobic Gram -ve) NBM PPI TPN Conservative management if small tear and no leak Stent if iatrogenic and no sepsis
250
What comprises SOFA?
6 organ systems scored 0-4 For each organ: -1-2 organ dysfunction -3-4 organ failure Resp: PF ratio CVS: MAP & pharmacological support CNS: GCS Renal: Cr or UO Liver: bilirubin Haem: Plt count
251
What is the qSOFA score?
Sepsis screening tool -RR >22 -SBP <100mmHg -GCS <15 If 2 out of 3 present with infection, then increased risk of mortality
252
Describe the cell-based model of coagulation
1. Initiation: -Plasma exposure to Tissue Factor -TF binds Factor VII -> activates Factor X ->Factor V 2. Amplification -Factor Xa/Factor Va produce Thrombin (Factor II) -Thrombin activates & aggregates platelets -Activated platelets bind vWF and activate VIII 3. Propagation -TF/VIIa activate Factor IX -IX & VIII bind on the platelet surface to form a complex, activating Xa further -Xa & Va bind, producing a burst of Thrombin for a clot
253
What are the indications for filgrastrim?
If Neutrophils <0.1 & evidence of infection Continued until neutrophils >0.5
254
What types of Ehlers Danlos do you know?
Classic type - dislocations, hernias, bruising Hypermobile type - benign really; generally minor problems Vascular type - bruising and dissections/ruptures Kyphoscoliosis type - significant kyphoscoliosis from birth, joint dislocations, poor wound healing & blindness
255
What are the treatments for IPF?
Pharm: -Perfenidone -Nintedanib -treat GORD aggressively Non-pharm: -pulmonary rehab -O2
256
What is the definition of sepsis?
Life threatening organ dysfunction caused by dysregulated host response to infection
257
How is electrical safety classified?
Equipment classified into whether it is designed to prevent: —Macroshock: -Class I - earthed -Class II - double insulated -Class III - battery or transformer to reduce voltage from mains —Microshock: -Type B - max leakage of 500microamps (class I) or 100microamps (class II) -Type BF - same as B, but floating -Type CF - max leakage of 50microamps (class I) or 10microamps (class II) (only one allowed to use in direct contact with heart)
258
How do beta-lactams work?
Bind to transpeptidase active site, interrupting cross linking & prevent cell wall synthesis Act on penicillin-binding proteins (different penicillin = different PBP affinity) Better at treating Gram positive as they have to get through the cell wall in order to work (Gram negative have got a thick cell wall)
259
How many penicillin binding proteins are there in a bacterium?
4 - 8
260
What are the mechanisms of action of antimicrobial agents?
1. Inhibit cell wall synthesis - penicillin, glycopeptides 2. Inhibit protein synthesis (ribosomes) - tetracyclines, aminoglycosides, macrolides 3. Inhibit DNA synthesis/function - quinolones 4. Inhibition of THF synthesis - trimethoprim
261
Give some examples of Gram staining of bacteria
Gram +ve cocci - Strep, Staph Gram -ve cocci - Neisseria, Moraxella Gram +ve bacilli - Clostridium, Listeria, Diptheria Gram -ve bacilli - everything else
262
By what mechanism are bacteria resistant to antibiotics?
1. Intrinsic (Gram -ve thick wall) 2. Acquired drug inactivation (beta-lactamase) 3. Acquired reduced permeability 4. Acquired efflux of drugs (pump out antibiotic) 5. Acquired alteration of molecular target (low affinity binding site - penicillin binding proteins) 6. Reduced number of pores
263
How do bacteria acquire resistance to antibiotics?
Intrinsic: —thick call wall —biofilm —lack of penicillin-binding proteins Acquired resistance mechanisms: —lack/reduce pores —decreased permeability Sporadic mutation Horizontal gene transfer -transformation - free DNA from dead bacteria -transduction - transferred by virus -conjugation - plasmids -transposition MRSA reduces its Penicillin Binding Proteins - making it resistant
264
How do you classify causes of weakness?
Brainstorm - stroke, ADEM Spinal cord pathology - MS/TM, GBS Polyneuropathy - polio, AIP, diphtheria Neuromuscular junction - MG, botulism Muscle - rhabdo, myosotis
265
What is constipation? What is ileus?
Failure of the bowel to open for 3 days Intestinal blockage in the absence of physical obstruction
266
What are the risk factors for constipation?
Modifiable: -Delayed enteral nutrition (>24hours) -Reduced mobility -Sedation -Opiates -Electrolyte derangement -Anticholinergics/calcium channel blockers -Dehydration -Hypotension -Hypoxia Non-modifiable -Abdo surgery -Severe illness -Paralysis (of spinal cord) -Alcohol/cannabis use -Nicotine withdrawal
267
What are the consequences of constipation?
Longer ICU stay Slower weaning Delirium Increased mortality (?!!!) Vomiting/aspiration Reduced nutrition Bowel obstruction/perforation Translocation of bacteria
268
What are the management strategies for constipation/ileus?
Constipation: -stool softeners -stimulant laxatives -soluble fibres -osmotic laxatives -enemas Ileus: -prokinetics -opiate antagonists Neostigmine
269
What is the mechanism behind acute traumatic coagulopathy?
Activated protein C causes anticoagulation Endothelial glycocalyx releases heparin when disrupted Loss of fibrinogen Platelet dysfunction from initial hyper activation as a result of widespread ADP release from endothelial cells
270
How do we classify severity in pancreatitis?
Atlanta classification: Mild - no organ failure/complications Moderate - transient organ failure or local complications Severe - persistent organ failure >48 hours
271
What is the diagnostic test for pancreatitis?
Lipase
272
Define maternal sepsis
WHO 2017: Life threatening condition defined as organ dysfunction resulting from infection during pregnancy, childbirth, post-abortion or post-partum period
273
How is VAP diagnosed?
Clinical Pulmonary Infection Score: -Temp -Leucocytosis -PF ratio -CXR -Tracheal secretions -Cultures
274
How do you calculate fluid deficit in children?
Body weight x % dehydration x 10
275
What are the principles underlying confidentiality?
1. Use minimum necessary personal info 2. Manage and protect information 3. Be aware of responsibilities 4. Comply with the law 5. Share relevant information for direct care in appropriate manner 6. Ask for consent to disclose 7. Tell patients when you disclose 8. Support patients to access their information
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What is the pathophysiology of sepsis?
Disruption of the glycocalyx causes endothelial dysfunction. Results in: 1. Vasodilatation 2. Loss of barrier function 3. Increased leukocyte adhesion 4. Procoagulant state Causes release of cytokines - IL-1, IL-6, TNF-a Reactive oxygen species damage DNA and impair mitochondrial function
277
Definition of neutropenia
Neuts <0.5 Neuts <0.5 plus Temp >38 or signs of infection = neutropaenic sepsis
278
What are the causes of thrombocytopaenia?
1. Dilution —massive transfusion/fluid administration 2. Sequestration —hypersplenism; extreme hypothermia 3. Decreased production - bone marrow suppression —Drugs: alcohol, Linezolid, chemo —Bone marrow: myelofibrosis, anaemias —Viral: HV, Hep C, EBV —Nutrition: B12, folate —Liver disease - decreased TPO 4. Increased destruction —Drugs: Heparin —Autoimmune: TTP, HUS, ITP, MAHA, Anti-phospholipid, SLE —Haem: DIC, HELLP —Machinery - CPB, IABP, RRT
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How would you investigate thrombocytopenia?
Blood film - platelet clumping Coagulation profile with XDP & fibrinogen (DIC) FBC - macrocytosis B12 HITTS screen - anti-platelet factor 4 antibody and platelet aggregation tests (ELISA for anti-PF4) Autoimmune screen - ESR, ANA, ENA, dsDNA, anti-cardiolipin, RF, anti-CCP, ANCA, complement ADAMTS13 level - if low = TTP
280
How would you recognise citrate toxicity?
1. High anion gap metabolic acidosis OR ALKALOSIS (due to an increased strong ion difference) 2. Low Ca2+ with high/normal total calcium (if acidotic you should normally have a high ionised calcium) Pre-disposing risks: —Liver disease —Coagulopathy —HITTS —Hypocalcaemia —Decreased hepatic blood flow
281
How do you reduce CVC infections?
Hand hygiene Asepsis 2% chlorhex/alcohol prep Avoid femoral Daily review and removal if not needed
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How do you assess severity of VAP?
Clinical pulmonary infection score 1. Tracheal secretions 2. CXR infiltrates 3. Temp 4. WCC 5. PF ratio 6. Micro Score >6 - likely VAP
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What is the evidence for: 1. HFNO 2. Transfusion thresholds 3. Albumin 4. Malignant MCA surgery 5. TBI surgery 6. ARDS 7. Covid 8. Prone ventilation 9. TXA 10. ECMO 11. PA catheters 12. Glucose targets 13. Septic shock/fluids 14. Tracheostomy timing 15. Temp management 16. Vasopressin 17. Timing of CRRT 18. Blood resuscitation in trauma 19. Clipping vs coiling 20. PCV vs VCV 21. CCOT 22. Steroids in ICU 23. PPI against stress ulcers 24. Fluid choice
1. FLORALI 2. TRISS/TRICC/TRICS III 3. ALBIOS/SAFE 4. DESTINY/DECIMAL/HAMLET 5. RESCUE ICP/DECRA 6. ARDSNet 7. RECOVERY 8. PROSEVA 9. CRASH II/WOMAN/PATCH 10. CESAR/EOLIA 11. PAC-Man 12. NICE-SUGAR 13. ProCESS/ProMISe/ARISE/PROWESS-SHOCK (ProtC) 14. TracMan 15. TTM/TTM2 or cardiac arrest; EUROTHERM for TBI 16. VASST/VANISH 17. AKIKI 1+2 18. PROPPR 19. ISATf 20. Cochrane review 2015 - improved mortality on ICU (just); no improved hospital mortality 21. MERIT/Priestly - reduced mortality 22. ADRENAL/CORTICUS/APPROCCHSS 23. REVISE 24. SMART, SPLIT, BaSICS, PLUS
284
What are the causes of fever after major surgery?
Early <48 hours: —hyper metabolic causes: sepsis, thyroid, SS/NMS/MH —drugs: transfusion reaction, withdrawal, beta-lactams, anti-epileptics —post op - normal healing process —adrenal insufficiency Late >48 hours (operation-related vs ICU-related?): —infection - HAP, wound etc —anastomotic leak —VTE —pancreatitis —drugs —alcohol/drug withdrawal
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Define: 1. Fever 2. Hyperthermia 3. Hyperpyrexia
1. Upward resetting of hypothalamus from PGE2 2. Core body temp >37.5 without hypothalamic involvement (unresponsive to anti-pyretics) 3. Temp >41
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Which acts are involved in capacity assessment etc?
Mental Capacity Act 2005 Mental Health Act 1983/2007 Human Rights Act 1998 Equalities Act 2010
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What do you do differently in paediatric major trauma?
Blood 5ml/kg & FFP 5ml/kg —after 15ml/kg of FFP and RBC, give 5ml/kg plt and 5ml/kg cryo TXA 15mg/kg Aim for normal BP Check blood glucose more Calcium chloride 0.1ml/kg after each MHP cycle Be even more avid for hypothermia Think of NAI
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What is the post-intensive care syndrome?
Complex constellation of physical, cognitive and mental dysfunctions that severely impact patients’ lives after hospital discharge
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What is antibiotic stewardship?
Hospital wide practice that links infection control measures with judicious antibiotic management
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What are some examples of increasingly resistant bacteria?
E - enterococcus faecium S - Staph aureus C - C diff A - Acinetobacter P - Pseudomonas E - enterobacteriaceae
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What are the hypertensive emergencies?
Cardiac - acute MI, cardiogenic shock/pulmonary oedema Vascular - aortic dissection; pre-eclampsia CNS - PRES; SAH, ICH; malignant hypertension Renal - AKI; sclerodermic renal crisis
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What are some causes of status epilepticus?
Epilepsy Vascular - stroke; eclampsia Infection - meningitis/encephalitis Neoplasm - SOL Drugs - withdrawal (alcohol, benzo) or excess (TCAs, cocaine) Trauma - post traumatic Endocrine - low electrolytes
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What are the causes of pulmonary haemorrhage?
Diffuse Alveolar Haemorrhage —from pulmonary microvasculature -autoimmune - vasculitides, connective tissue disease -infection -CCF -DIC/thrombocytopaenia -drugs like cocaine Focal Haemorrhage —from bronchial circulation or lung parenchyma -PE -Neoplasm -trauma (bronchoscopy) -suppurative lung disease -AV malformation, vascular erosion
294
How do you manage pulmonary haemorrhage?
ABCDE -prevent asphyxia -treat haemorrhage -DLT or large ETT -bronchoscopy -thoracic surgery opinion Ix: -CT angio -flexible bronchoscopy
295
How do you classify TBI?
Mild: GCS 13 - 15 Moderate: GCS 8 - 12 Severe: GCS <8
296
What are the mechanisms of secondary brain injury?
Intracranial: —seizures - CMRO2 —haematoma - ICP —hydrocephalus - ICP —infection - CMRO2 & ICP Extracranial: —hypoxia —hypercapnoea —hypocarbia —pyrexia —hyponatraemia —hypoglycaemia (impaired cerebral metabolism)
297
How are thyroid hormones produced?
In response to TSH Iodine + Tyrosine + thyroid peroxidase enzyme = T3 and T4 Stored on thyroglobulin; cleaved and released when TSH binds to G protein receptors; bind to albumin or globulin
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How do thyroid hormones exert their effects?
-Enter target cell via membrane transporter proteins -Enter nucleus to bind receptor -Effect on DNA (T4 -> T3 in liver and kidneys)
299
What are the scoring systems for: 1. GvHD 2. Fat embolism syndrome 3. TEN/SJS 4. Skin integrity risk 5. Burn mortality 6. DIC 7. HLH
1. Seattle - predict survival at 100 days; grades I - IV 2. Gurd - 1 major (rash/resp/CNS signs) + 4 minor criteria to diagnose FES 3. ScoreTEN/ABCD-10 - predict mortality 4. Braden 5. Baux - mortality; age, burn size +/- inhalational injury (also modified AIS) 6. ISTH - >5 = DIC (uses disease trigger, plts, PT, D-dimer & fibrinogen) 7. H-score - if >169, likely HLH
300
How can we do respiratory monitoring?
1. Gas exchange —PaO2 / PaCO2 2. Capnography 3. Lung volumes —ventilator waveforms - asynchrony —auto triggering 4. Lung mechanics —oesophageal balloon —measure PEEP -> end expiratory hold = static iPEEP 5. P0.1 (negative pressure in first 100ms of inspiration) —on a patient on support mode it gives an idea of the work of breathing —normal = 1-5cmH2O 6. Airway occlusion pressure 7. Diaphragm ultrasound
301
Define acute liver failure
Rapid decline in liver failure with jaundice, coagulopathy and encephalopathy in a patient with a previously healthy liver Acute liver injury = coagulopathy without encephalopathy
302
What investigations would you perform in a suspected acute liver failure?
Intra-hepatic/Assess liver function: -ALT -AST -Bili -Albumin -GGT -Coagulation - INR -Lactate -Blood sugar -Blood gas -Ammonia level Extra-hepatic: -U&Es -FBC -Blood group -Amylase/lipase Causes: -Paracetamol levels, other drug screen -PREGNANCY TEST -Viral screen - Hepatitis, EBV/CMV etc -Autoimmune screen - ANA, SMA, AMA, copper levels
303
How are outcomes measured following TBI?
Glasgow Outcome Scale (Extended) 1 - 8 (1 being dead; 1-4 unfavourable) 4 - 8 favourable
304
How is DIC diagnosed?
International Society of Thrombosis and Haemostasis uses a table that comprises: 1. Underlying predisposing clinical condition 2. Platelet count 3. FDP/D-dimer 4. Fibrinogen level 5. Prothrombin time prolongation Score >5 = DIC
305
What is DIC?
Acquired syndrome characterised by the intravascular activation of coagulation with loss of localisation arising from different causes Usually caused by sepsis
306
What is DKA?
Blood sugar >11 Blood ketones > 3 Bicarbonate <15 or pH <7.3
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What are the goals of treatment in DKA?
1. Fluid/electrolyte replacement as per Joint British Diabetes Societies 2. Insulin therapy to stop ketogenesis —Blood ketones 0.5mmol/hr —Venous bicarbonate 3mmol/hr —Blood sugar 3mmol/hr 3. Treat underlying cause 4. Prophylaxis (VTE, ulcer)
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How do you treat DKA differently in children?
Only fluid if proper shocked Delay insulin by 1 hour Give fluid over 48 hours rather than 24 hours
309
What is HHS?
Hyperosmolar hyperglycaemic state -Serum osmolarity >320mosm/kg -Serum glucose >30 but without significant ketones/acidosis -Severe fluid deficit Often type 2 diabetics
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What are the goals when treating HHS?
1. Normalise osmolality: —how do you calculate osmolality? 2. Replace fluid and electrolytes as per JBDS 3. Reduce blood sugars (only add in insulin once blood sugars stop dropping with rehydration) 4. Treat underlying cause 5. Prevent thrombotic events
311
How would you intubate and ventilate a severe asthma exacerbation?
Carefully -Ketamine for induction and maintenance -Prepare for haemodynamic instability at induction - preload with fluid (high losses from high RR) -Volume control (SIMV) with volumes low-ish e.g. 400ml -Monitor plateau pressure (aiming <35cmH2O) -Low or no PEEP (or 1/3 intrinsic PEEP) -Low RR 10-12 -I:E ratio - prolong expiratory time; 1:4 or 5
312
What is VAP?
Nosocomial infection occurring 48-72 hours after intubation Common - 25% Mortality can be up to 50%
313
What are some complications post: 1. Renal transplant 2. Liver transplant 3. Lung transplant 4. Heart transplant
ALL have risk of: -haemorrhage -ischaemia-reperfusion injury -infection -AKI -Complications from immunosuppression incl. renal failure, liver failure, malignancy, infections 1. —Primary graft dysfunction - hyperkalaemia, poor UO —hypovolaemia 2. —Primary graft dysfunction - lactate, clotting —hepatic artery/vein/IVC thrombosis —biliary tree obstruction 3. —Primary graft dysfunction in 30% (grades 0 - 3) - poor oxygenation, diffuse alveolar opacities —MODS, haemothorax, pneumothorax, anastamotic leak —CVS - RV dysfunction; vasoplegia —Dynamic hyperinflation —aspergillus —post transplant lymphoproliferative disease 4. —Primary graft dysfunction - LVEF <40% despite inotropes —Secondary graft dysfunction —Cardiac allograft vasculopathy (accelerated IHD) —Arrhythmias —tamponade, pulmonary hypertension
314
Who would you recommend have post ICU clinic follow up?
>3 days length of stay (although RVI only offers if >7 days) Postpartum patients Post-anaphylaxis Should be offered to everyone 30-45mins, 2-3 months post hospital discharge
315
What are some causes of stress in ICU patients?
1. Psychological stress: —Pain —Lack of sleep —Noise —Lights —Delirium —Change in personal identity 2. Physical stress: —Weakness —Pain —Deconditioning —Restriction in movement 3. Physiological stress: —Cortisol and effects …
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How could you screen ICU patients for psychological consequences post-discharge?
Use of tools such as HADS or PTSS score Predisposition: -substance abuse -alcohol abuse -pre-existing cognitive impairment/disease -pre-existing anxiety/depression
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What is weaning?
Generally means reducing support of ventilator with aim to liberate the patient from mechanical ventilation Occupies 40% of the time a patient spends on mechanical ventilation Need: —SBTs with insp pressure support —minimal sedation —NIV post extubation —weaning protocols —cuff leak test
318
What prokinetic agents do you know and how do they work? What are their side effects?
Metoclopramide —dopamine & muscarinic antagonist —5HT agonist —dystonic reactions; tachyphylaxis Erythromycin —motilin receptor —prolong QTc; tachyphylaxis Naltrexone: —mu opioid antagonist —only works in opioid induced Neostigmine: —acetylcholinesterase inhibitor (causes increased parasympathetic tone) —bradycardia
319
Define liver failure
(from GPICS) Onset of hepatic encephalopathy 1. Acute 2. Acute on chronic liver failure (in those with cirrhosis) 3. Following liver resection 4. From multi-system illness (sepsis, low CO, malaria, dengue, HLH or malignancy)
320
By what mechanisms do patients become hypothermic?
1. Increased heat loss Trauma, surgery, GA, immersion, burns 2. Decreased thermogenesis Hypothyroidism, elderly 3. Impaired thermoregulation Drugs - either directly or by impairing behaviour 4. Altered hypothalamic set point Burns
321
What are the complications of stem cell transplant??
Acute: —infection —haemorrhage —acute GvHD —interstitial pneumonitis —aplastic anaemia Chronic (>100 days): —chronic GvHD —chronic pulmonary disease —infections —autoimmune disorders
322
How do you reduce catheter related blood stream infections?
Using care bundles (such as shown in Matching Michigan programme) 1. Hand hygiene 2. Strict asepsis with barrier precautions 3. 2% chlorhex in 70% alcohol 4. Avoid femoral 5. Daily review and removal asap
323
What investigations should you do in a patient presenting with severe hypertension?
Bloods: —FBC; U&E; glucose; cholesterol/triglycerides —TFTs —Aldosterone & Renin —Cortisol Urine: —blood/protein —casts —metanephrines Radiology: —CXR —CT head —Renal USS ECG Echo
324
How would you manage malignant hypertension?
(Evidence of retinopathy, encephalopathy, MAHA, nephropathy) —Lower diastolic BP to 100mmHg over 2-6 hours —Slow reduction - 25% MAP over 24 hours vs reduce by 25% in first hour (conflicting books!?!?!) Use labetalol, GTN, SNP IV nicardipine also a possible Alpha blockers ACEi - caution if renal artery stenosis
325
What is PRES?
Abrupt increase in BP causes acute confusion & visual disturbance MRI - hyperintense white matter on T2 in parietal and occipital
326
What is HIV?
RNA retrovirus causing destruction of CD4
327
How is HIV classified? How is AIDS diagnosed?
HIV: —Stage 0 - early infection, normal CD4 —Stage 1 - acute infection, CD4 >500 —Stage 2 - chronic infection, CD4 200-500 —Stage 3 - AIDS, CD4 <200
328
What is compliance? What does lung compliance comprise?
The measure of distensibility or the ease with which something can be stretched Lung compliance = change in lung volume per unit change in transpulmonary pressure Specific compliance is compliance divided by FRC (compensates for different body sizes) Relastance = reciprocal of compliance Static: -Chest wall compliance -Lung tissue compliance Dynamic: -includes airways resistance
329
What is hysteresis?
The term used to describe the difference between inspiratory and expiratory compliance The energy applied to the lung during inspiration is not recovered in expiration Compliance is greater during expiration than inspiration Due to: -surfactant -alveoli recruitment -gas absorption during measurement
330
How do antibiotics work?
Generally they inhibit: 1. Bacterial cell wall synthesis —Beta lactams —Glycopeptides (Teic/Vanc) 2. Bacterial protein synthesis —30S - aminoglycosides, tetracyclines, tigecycline —50S - macrolides, lincosamide (Clindamycin), oxazolidinone (Linezolid), chloramphenicol 3. Bacterial DNA synthesis —fluroquinolones - cipro —anti-folates —imadazoles - metronidazole
331
Classify cytotoxic drugs used in malignancy
Alkylating agents - platins Anti metabolites - MTX Anti-tumour antibiotics - rubicin Hormones - tamoxifen Monoclonal antibodies - rituximab Topoisomerase inhibitors
332
What are common side effects of chemotherapy drugs?
Pulmonary toxicity —pneumonitis —fibrosis Cardiac: —arrhythmias, MI, CCF —cardiomyopathy Renal: —CKD Liver: —fatty change, hepatocellular necrosis Neuro: —peripheral and cranial neuropathies, autonomic dysfunction, seizures
333
What happens at a cellular and molecular level in sepsis?
-Pathogen-associated molecular patterns and damage-associated molecular patterns (PAMPs & DAMPs) are detected by innate immune system -triggers release of pro-inflammatory cytokines (TNFa, IL-1, IL-6) -trigger widespread cell death -trigger complement & acute phase protein synthesis -trigger increased expression of tissue factor - high risk of thrombus This leads on to systemic injury when: -ROS damage cell components/DNA/mitochondria -Complement increases ROS etc
334
What monitoring and supportive care considerations are there when treating a patient with sepsis?
B - LPV, HFNC rather than NIV C - lactate, CRT D - insulin if >10mmol/L E - feed within 72 hours, stress ulcer prophylaxis, VTE prophylaxis Hb 70 as transfusion threshold Rehab referral if I&V >48 hours or in ICU >72 hours
335
What are the important trials regarding sepsis?
Fluids - ARISE, ProMISe, ProCESS BP target - SEPSISPAM & 65 Vasopressin - VASST Steroids - ADRENAL, CORTICUS Transfusion thresholds - TRISS, TRICC Fluids - FEAST, 6S, ALBIOS, SPLIT BM - NICE-SUGAR
336
What is multi-organ dysfunction syndrome?
2 or more organ systems have altered function during an acute illness such that homeostasis cannot be maintained without intervention
337
What is the sepsis care bundle?
3 hour bundle: -lactate -blood cultures -antibiotics -30ml/kg for hypotension or lactate >4 6 hour bundle: -vasopressors if MAP <65 after fluids -re measure lactate if elevated
338
What is the glycocalyx?
Protein/glycoprotein web on top of cell wall Regulates: -permeability -vascular tone -leukocyte recruitment -coagulation If disrupted, it activates pro-inflammatory pathways and disrupts starling forces across cell membrane
339
What are the causes of hypomagnesaemia?
Decreased intake: —starvation —alcohol dependence —TPN Redistribution: —treating DKA —refeeding syndrome —pancreatitis —alcohol withdrawal Loss: —D&V —renal
340
Do you know of any scoring system for necrotising fasciitis?
Laboratory Risk Indicator for Nec Fasc (LRINEC) score Score >6 has high PPV Variables: -CRP -WCC -Hb -Na -Cr -Gluc
341
1. What dose of alteplase would you use in PE? 2. What does of alteplase would you use in acute stroke?
1. If CVS unstable: 10mg bolus then 90mg over 2 hours If arrest: 50mg bolus, further 50mg if 15 mins and no ROSC 2. If no contraindications & within 4.5 hours, calculate dose and give 10% as bolus, followed by the rest over 60 mins
342
What are the indications for bronchoscopy?
Diagnostic, therapeutic or combined Aspiration Infection Lobar collapse/mucus plug Airway assessment/management Foreign body Strictures/stenosis Haemoptysis
343
What are some complications from bronchoscopy?
Airway obstruction Laryngospasm Bronchospasm Hypoxaemia Arrhythmias Hypotension Vagal Haemorrhage Pneumothorax
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How would you prepare to perform bronchoscopy?
Have indication & consent Monitoring Appropriate sedation/muscle relaxation 100% FiO2 Stop feed/aspirate Position patient and self/equipment Saline flushes etc Post procedure: —Clean/decontaminate/sterilise —document —CXR
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How can you classify the severity of PE?
Using sPESI (simplified Pulmonary Embolism Severity Index) Score for: -Age >80 -Cancer -Chronic heart or lung disease -Systolic BP <100 -HR >110 -SpO2 <90% 0 points = 30 day mortality of 1% >1 point = 30 day mortality of 10%
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How can PE be classified?
Massive PE -haemodynamic instability ->15% PE related mortality -5% of all cases Submassive PE -haemodynamic stability but evidence of RV strain -3-10% PE related mortality -15% of all cases Low risk -stable, no RV strain -75% of all cases
347
What happens to HPA axis in critical illness?
General suppression Cortisol may increase Cortisol may lose diurnal variation
348
What is sick euthyroid syndrome?
Abnormal findings on TFTs that occur in the setting of a non thyroid illness
349
What is a toxidrome? Can you give examples?
A set of clinical signs/symptoms classically due to a group of drugs/toxins Cholinergic: —confusion, salivation, bronchorrhoea, bradycardia, emesis, incontinence, sweating —organophosphates, some mushrooms —give atropine, pralidoxime Anti-cholinergic: —tachycardia, hypotension, confusion, coma, dry skin, fever, flushed, urinary retention —antihistamines/antidepressants/TCAs/anti-parkinsonian/antipsychotics/atropine —supportive care Opioid: —pinpoint pupils, respiratory depression, coma —opioids —naloxone Hypno-sedative: —ataxia, coma, hypothermia, hypotension —Benzos, alcohols —supportive care Serotonin: —autonomic dysfunction, agitation, neuromuscular excitability —serotonin drugs/ecstasy/amphetamines —Benzos, cyproheptadine Sympathomimetic: —delusions, paranoia, tachycardia, hypertension, hyperreflexia —cocaine/amphetamines —Benzos
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What drug is given as an antidote in toxic alcohol ingestion? How does it work?
Fomepizole Alcohol dehydrogenase inhibitor - prevents breakdown into toxic metabolites
351
What is the pathophysiology of hypertensive encephalopathy?
Hypertension overwhelms the autoregulatory mechanisms of the cerebral circulation Resultant hyperaemia causes cerebral oedema
352
What are some causes of hypertension in the ICU?
—‘Normal’ HTN —Pain/agitation —Excessive vasoconstriction —Neurogenic (ICP related) —Drug related - cocaine, ecstasy —Vascular - dissecting aneurysm, vasculitis —Renal - renal failure, renal artery stenosis —Endocrine - phaeochromocytoma, Cushing’s —artefact
353
When might hypertension prompt an ICU referral?
1. Hypertensive crisis/malignant hypertension with end organ failure: -renal dysfunction -cardiac failure -encephalopathy 2. Aortic dissection 3. Pre-eclampsia 4. ICH
354
What are some causes of acute liver failure?
1. Toxins - paracetamol; antibiotics; antiepileptics 2. Vascular - hepatic vein thrombus 3. Viral - Hep B/C; CMV; EBV; HSV 4. Pregnancy - HELLP; AFLP
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What are the clinical manifestations of acute liver failure?
Loss of liver function: 1. Gluconeogenesis = hypoglycaemia 2. Lactate clearance = lactic acidosis 3. Ammonia clearance = hyperammonaemia/encephalopathy 4. Synthetic function = clotting factors
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Define: 1. Inotropy 2. Chronotropy 3. Lusitropy 4. Vasopressor
1. Increase myocardial contractility 2. Increase heart rate 3. Increase relaxation 4. Vasoconstriction leading to increased SVR/PVR; increase vascular tone
357
What factors affect lung compliance?
—Surface tension - surfactant —Lung volume (e.g. at FRC vs at extremes of lung volume) —Lung elasticity (fibrosis, congestion etc) Static: —Lung parenchymal disease - ARDS, pneumonia, fibrosis —Chest wall - kyphoscoliosis, obesity, raised intra-abdominal pressure Dynamic: —Airways resistance
358
What even are respiratory mechanics?
Movement of gas in/out of lungs dependent on: 1. respiratory muscles and actions -diaphragm and accessory resp muscles 2. compliance of chest wall and lungs -lung & thoracic wall 3. gas flow in the airways -types of flow -airway resistance
359
How are hypersensitivity reactions classified?
By type: I - IgE; anaphylaxis II - IgG/IgM; antibody mediated hypersensitivity e.g. rheumatic heart disease, anti-GBM III - IgG & complement; immune complex mediated e.g. rheumatoid arthritis; lupus nephritis IV - T cells; delayed hypersensitivity e.g. chronic transplant rejection, coeliac disease
360
How are air leaks classified?
Any extrusion from a normally gas-filled cavity Continuous Inspiratory Expiratory Forced expiration
361
How is a bronchopleural fistula managed?
Resuscitation initially and diagnose with CXR/CT/bronchoscopy Treat PTX Large bore chest drain -potentially suction on drain Control active infection if the cause Ventilatory measures: -Reduce PEEP -Encourage spontaneous ventilation -2 ventilator ventilation potentially - using DLT Surgery: -bronchoscopic repair -thoracoplasty -stapling ECMO
362
Where is the aorta most likely to be damaged in trauma?
Ligamentum arteriosum - just distal to the L subclavian Aortic root Aortic hiatus Injury can extend partially or completely through aortic wall CT probs best to diagnose
363
Why might a patient be hypotensive?
Inadequate volume -haemorrhage -severe dehydration - burns, diarrhoea, laparotomy Inappropriate vasodilatation -anaphylaxis -sepsis -pregnancy -neurogenic shock Inadequate pump -cardiac failure -obstruction to cardiac output: —PE, tamponade, pneumothorax Iatrogenic -excess treatment for HTN
364
How do calcium channel blockers work?
3 classes - amlodipine/verapamil/diltiazem Act on L-type calcium channels in: -vascular smooth muscle -cardiac muscle (Phase 2 plateau) -pacemaker cell (Phase 0) Actions depend on their selectivity for where the channels are: -relaxation of vascular smooth muscle -decreased cardiac contractility and heart rate
365
What is the management of status epilepticus in children?
1. Benzos (lorazepam 0.1mg/kg or midazolam 0.15mg/kg) 2. Levetiracetam 40mg/kg OR Phenytoin 20mg/kg slowly OR Phenobarbital 20mg/kg 3. I&V - doesn’t matter which you use
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What are some causes of long QT?
Congenital: -Romano Ward -Long QT Acquired: -Electrolyte abnormalities - hypo K/Mg/Ca -Drugs - macrolides, antipsychotics -Hypothermia -SAH -Ischaemia
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What are the BP targets in hypertensive emergencies?
368
Phosphate -Homeostasis -Roles -Causes of imbalances
—Mainly in bone/intracellular PTH/renal at the PCT Calcitonin Vitamin D —Roles: Energy production - ATP Membrane (phospholipid bilayer) 2,3-DPG Buffer —Hyperphosphataemia causes Renal failure (reduced excretion) Rhabdomyolysis (intracellular release) Tumour lysis Haemolysis Raised PTH Rx with Aluminium, Ca, Mg (some sort of binder) —Hypophosphataemia: Renal loss Refeeding Recovery from DKA Insulin Sepsis Adrenaline
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Magnesium: -Homeostasis -Role -Causes of abnormalities
Found in bone/muscle/soft tissues Renal homeostasis & PTH Essential enzyme component DNA/RNA synthesis Calcium antagonist/regulation of calcium flux —Hypermagnesaemia (ECG - prolooongation or PR, QRS; bradycardia) Iatrogenic Rx with calcium —Hypomagnesaemia (ECG - ectopics, VT/torsades/VF): Refeeding Hyperaldosteronism/volume expansion DM D&V Alcohol Hyperparathyroidism; hypercalcaemia
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Calcium: -Homeostasis -Role -Causes of abnormalities
—Mainly in bone PTH Vitamin D Calcitonin — Essential in muscle contraction - skeletal/cardiac Pacemaker cells Coagulation Second messengers Neuronal function —Hypercalcaemia: Malignancy - myeloma, small cell, prostate mets Primary hyper-PTH TB Drugs —Hypocalcaemia: Vit D deficiency Drugs - furosemide Tumour lysis; rhabdomyolysis Pancreatitis Renal failure Hypo-PTH Citrate - massive transfusion, RRT
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Potassium: -Homeostasis -Role -Causes of abnormalities
—Homeostasis: -Aldosterone -Insulin -Osmolality -B-adrenoceptor/adrenaline —Role: -maintains RMP of neuronal tissue -muscle contraction -nerve conduction -regulate acid base —Hyperkalaemia: Impaired excretion - Addison’s, AKI/CKD Altered balance - haemolysis, rhabdo etc, DKA, hyperosmolality, acidosis Increased intake - transfusion —Hypokalaemia: Renal loss - Conn’s, RTA, drugs Balance - alkalosis, refeeding, hypothyroidism, drugs GI loss - D&V, fistula
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Sodium: -Homeostasis -Role -Causes of abnormalities
—Homeostasis: -RAAS -ADH -thirst -PCT reabsorption mainly Exchanged for K -Atrial natriuretic peptide & BNP - increase GFR to cause natriuresis and diuresis; reduce renin/angiotensin II/aldosterone levels Role: -osmolarity key determinant -regulates extra cellular volume Hyponatraemia: -Hypervolaemic: heart failure, liver failure, renal failure -Euvolaemic: SIADH, adrenal insufficiency (Addison’s), hypothyroidism -Hypovolaemic: D&V, diuretics, burns, pancreatitis Hypernatraemia: -HHS -DI
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Which drugs are cleared by RRT?
Low Vd, low protein binding, water soluble MALE VC Methanol Aspirin Lithium Ethylene glycol Valproate Carbemazepine
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Complications of oesophagectomy?
Early: -AF -Pneumonia -Anastamotic leak -Chylothorax Generic: -VTE -Infection -Wound breakdown Later: -Delayed gastric emptying/reflux
375
What body systems are affected in cirrhosis?
1. CVS: Hyper dynamic circulation - decreased SVR, increased CO Cardiomyopathy - blunted response to catecholamines, diastolic dysfunction 2. GI: Alterations in hepatic/splanchnic blood flow - varices; ascites 3. Renal: Hepatorenal syndrome from renal vasoconstriction 4. Pulmonary Hepato-pulmonary - VQ mismatch 5. Haematological 6. Neurological Encephalopathy without raised ICP (in contrast to ALF) 7. Immune Relative immunodeficiency
376
What is the role of albumin in sepsis?
According to 2021 Surviving Sepsis campaign Can be used if using high amounts of crystalloid Useful in liver patients ?
377
How can you grade encephalopathy?
By type: —Type A - due to ALF —Type B - due to porto-systemic bypass e.g. TIPSS —Type C - related to cirrhosis West Haven
378
What happens to haemoglobin in: 1. Sickle cell disease 2. Thalassaemia
1. Beta chain; valine for glutamic acid Autosomal recessive Qualitative problem with Hb 2. Alpha or beta; reduced production Autosomal recessive Quantitative problem with Hb
379
How does citrate toxicity occur?
Due to metabolic effects of excess citrate Citrate normally metabolised to HCO3 with NADH generation via Kreb’s cycle in liver/kidneys/skeletal muscle -increased citrate administration - RRT; massive transfusion -decreased citrate clearance - liver failure; decreased CO/hepatic blood flow -exacerbating factors - hypocalcaemia; hypoalbuminaemia HAGMA -initially alkalosis due to increased HCO3 production from increased SID Suspect if: -acidotic -low ionised calcium (with high total to ionised calcium ratio)
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How do you manage citrate toxicity?
-Give calcium (but caution with rebound hypercalcaemia afterwards) -Decrease citrate dose or decrease blood flow rate -Stop anticoagulation and switch to alternative -Stop dialysis -Improve hepatic blood flow
381
What is in cryoprecipitate?
Fibrinogen (Factor I) Factor VIII Factor XIII Von Willebrand factor
382
What bugs may grow in an empyema?
MRSA Gram -ve Anaerobes Alkaline pH - Proteus
383
What is SHOT?
Serious Hazards of Transfusion Haemovigilance reporting Promote transparency, accountability and improvement in blood transfusion practices
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What is inhalational injury?
Injury either from inhalation of hot gases, from particulate matter or CO/cyanide Divided into: —Supraglottic airway - from thermal transfer —Tracheobronchial - chemical/particulate/fibrin —Alveolar/parenchymal - CO; cyanide Graded on bronchoscopy: I - mild injury II - erythema, deposits of carbon III - inflammation and friable tissues IV - sloughing, necrosis Rx: -BAL -Nebs - NAC/Heparin/Salbutamol Modified Baux score: Mortality from: TBSA burn & presence of inhalational injury & age
385
Summarise the care of the patient donating after brainstem death
386
List some causes of rhabdomyolysis?
Traumatic: —trauma - crush —muscle strain —electric shock Non-traumatic: —drugs - statins, cocaine, MDMA, amphetamines —hyperthermia - MH, NMS, sepsis —infections - nec fasc —autoimmune - dermatomyositis
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What is the mechanism behind rhabdomyolysis?
-ATP depletion from muscle activity -disruption of cellular transport mechanisms and electrolytes -rise in intracellular calcium -hyperactivity of proteases -> produces free radicals which damage cell membrane -cell content leaks
388
What are some different types of diarrhoea?
—Secretory due to infection with e.g. toxin laxative —Osmotic enteral-feed-associated —Inflammatory IBD —Dysmotility Post-ileus recovery
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What are some causes of diarrhoea on ICU?
—Infective: bacterial/viral/fungal/parasitic —Non infective: IBD Drugs - abx, Mg, laxatives Feed Ischaemic bowel Post-ileus Coeliac/lactose/IBS
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How is triage done?
10 second triage pre-hospital (the sieve) - can be non-medic Further triage at hospital (the sort) - usually experienced ED cons
391
How can we do cerebral monitoring?
1. Clinical assessment 2. ICP/CPP monitoring (bolt, EVD, optic nerve, pupillometry) 3. CBF (Doppler) 4. Cerebral oxygenation (NIRS, SjvO2, bran parenchymal oxygen tension) 5. Cerebral metabolism (micro dialysis catheter - glucose, lactate/pyruvate, glutamate, glycerol) 6. Electrophysiological activity (EEG, SSEPs)
392
How do you prescribe RRT?
1. Intermittent vs continuous 2. Dose of effluent i.e. how much filtrate produced ~25-35ml/kg/hr 3. Pre or post-dilution fluid replacement (usually 30:70) 4. Fluid balance target in 24 hours 5. Anticoagulation 6. Blood flow - 250ml/min
393
What happens (physiologically) with brainstem death? How do you care for the donor after confirmation of death by neurological criteria?
Rising BP -> Cushing’s reflex Hyperadrenergic state Once coned, there is loss of sympathetic tone Raised hydrostatic pressure causes pulmonary oedema Pituitary and hypothalamus ischaemia -> DI, hypothermia, hypothyroidism —CVS: -HR 60-120 -BP >100mmHg -MAP 60-80 -CI >2.1 —RS: -recruitment -4-8ml/kg -optimum PEEP 5-10 -PIP <30cmH2O -chest physio —Metabolic: -Methylpred -Warming to 36 —Endocrine: -Insulin infusion -Vasopressin -Rarely thyroid replacement -Sodium control
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How may infection with group A Strep present?
Mild illness: -scarlet fever -impetigo -cellulitis -pharyngitis Severe INVASIVE illness: -necrotising fasciitis -necrotising pneumonia -Strep toxic shock Treatment: -Abx - board spectrum beta lactam +/- clindamycin -IVIg consideration
395
What is the structure of influenza virus?
Orthomyxovirus 2 glycoproteins embedded in cell surface: —Haemagglutinin - binds virus to host respiratory cells —Neuraminidase - releases new virus particles from infected cell
396
How would you classify interstitial lung disease?
1. Idiopathic interstitial pneumonia IPF COP AIP NSIP 2. Known cause/association Connective tissue disease Occupational Drugs 3. Granulomatous disease Sarcoidosis Hypersensitivity Infection 4. Other Lymphangioleiomyomatosis Langerhans cell histiocytosis Or Exposure related Autoimmune related Idiopathic
397
How would you check a temporary pacemaker?
1. Reduce the rate down to see what the intrinsic rate is 2. Check for capture threshold: set the pacing rate ~10 beats above the intrinsic rate, then increase the output (mA) until sustained capture is seen Then double the capture threshold 3. Check the sensitivity threshold: set the pacing rate ~10 beats below intrinsic rate, then reduce the sensitivity (by increasing the voltage/raising the wall) until it stops sensing anything Then increase the sensitivity (lowering the voltage/the wall) until the sensor flashes at the native rate; the value at which this occurs is the sensitivity threshold Set the sensitivity to 30-50% of measured/or at 2mV if no underlying rhythm
398
Why do beta blockers and calcium channel blockers cause cardiogenic shock?
Decreased myocardial cytosolic calcium β-blockers act on beta-receptors through competitive inhibition, indirectly decreasing the production of cAMP and thereby limiting calcium influx through L-type calcium channels with a resulting negative effect on heart rate and cardiac contractility CCBs exert their therapeutic and toxic effects by the direct blockade of L-type calcium channels causing relaxation of the vascular smooth muscle with subsequent vasodilation, and in the case of verapamil and diltiazem, inhibition of the sinoatrial and atrioventricular nodes. Calcium channel blockade concurrently triggers the heart to switch to preferential carbohydrate metabolism as opposed to the free fatty acid oxidation that occurs in the myocardium in the non-stressed state In beta-islet cells of the pancreas, calcium channel antagonism inhibits insulin secretion, producing insulin resistance and hyperglycemia
399
What causes biliary sepsis?
—Usually gallstones —Strictures (PSC) —Malignancy (pancreas)
400
What are some indications for plasma exchange?
—CNS: GBS MG —Renal Anti-GBM ANCAs causing RPGN or diffuse alveolar haemorrhage Microscopic polyangiitis Granulomatosis with polyangiitis —Haem: TTP (note need detergent FFP replacement) Catastrophic anti-phospholipid syndrome
401
Why do we care about micronutrients? What does zinc do? What does selenium do?
Because we may unintentionally malnourish patients (CVVH removes, or inadequate feed requirements) Zinc is needed for normal function of basement membrane —essential in burns, who are trying to re-grow basement membrane Selenium needed in the immune system
402
What do you know about invasive fungal infections?
From FUNDICU (2024 consensus definitions) Can be difficult to detect colonisation vs infection Invasive candidiasis most common; mortality can be >50% -Split into: 1. Candidaemia - grown on blood culture 2. Deep seated candidiasis (usually intra-abdo); can be difficult to diagnose but sample from sterile site Invasive aspergillosis -usually pulmonary Diagnosed on: 1. Detection of Aspergillus in normally sterile site 2. Certain clinical features/bronchoscopic appearances & BAL culture alongside galactomannan Pneumocystis jirovecii - cough/dyspnoea/hypoxia -detection in BAL fluid/sputum
403
How do you treat invasive fungal disease?
Candida (can form biofilm): -Echinocandins (anidulafungin etc) -Fluconazole for Candida albicans Aspergillosis: -Voriconazole PJP: -Co-trimoxazole - +/- steroids if PaO2 <9kPa
404
What complications occur from sickle cell disease?
1. Vaso-occlusive crises (painful; most frequent reason for attendance): -usually in bones/joints -Analgesia, hydration -Antibiotics if infection; O2 if hypoxaemic 1b. Stroke 2. Acute chest syndrome: -pain/fever/infiltrates -may be difficult to distinguish from infection -O2, sometimes ventilation 3. Anaemia - usually have Hb between 50-100 4. Aplastic crisis from parvovirus 5. Sequestration & asplenism
405
What are some treatments for sickle cell disease?
Blood transfusions Hydroxyurea - reduces frequency of attacks Voxeletor - reduces sickling
406
How do anti-virals work?
Whether they act on DNA or RNA viruses ?DNA: Guanosine analogues - acyclovir Neuraminidase inhibitors - oseltamivir RNA (anti-HIV): NRTI - nucleoside reverse transcriptase inhibitor NNRTI Integrase inhibitor Protease inhibitor Fusion inhibitors
407
List some triggers for HLH
—Infection: Viral: HIV, EBV, CMV, HSV Bacterial: mycobacteria Parasitic: malaria Fungal: PJP, candida, aspergillus —Malignancy: Lymphomas Treatments: chemo
408
What is the pathophysiology behind ascites?
Usually in cirrhotic liver disease —increased portal pressure/hypertension —decreased albumin —increased aldosterone (due to RAAS and also decreased hepatic clearance) Chronic splanchnic vasodilatation also worsens effect of RAAS, and causes HRS Other causes of ascites may depend on serum-ascites albumin gradient (transudate vs exudate)
409
What are the causes of ascites?
Transudates vs exudates - SAAG 1.1g/dL Transudates: -cirrhosis -heart failure -nephrotic syndrome Exudates: -peritoneal metastasis -cancer -pancreatitis
410
What are some complications of ascites?
Infection - SBP HRS Malnutrition GORD UGIB (may also have varices) Splinting of diaphragm
411
Where are the IO insertion sites?
Tib tub - 2cm inferomedial Humeral head - 1-2cm above surgical humeral neck on most prominent aspect of greater tubercle Distal femur
412
What is Posterior Reversible Encephalopathy Syndrome?
Sudden rise in BP causing: -headache -confusion -seizures -visual disturbance Often due to: -pre-eclampsia -drugs - ciclosporin -renal disease Diagnosed on MRI with hyperintense lesions in white matter on T2-weighted MRI in parietal and occipital lobes
413
Which patients do we consider for treatment withdrawal?
—Imminently dying - deteriorating despite best therapy —Qualitative reasons - poor functional outcome —Lethal conditions - coexisting severe disease
414
How can you prevent VTE?
(Virchow’s triad (venous stasis, vascular endothelial injury & alterations in coagulation)) Pharmacological: -LMWH (& heparin) -DOACs -Regional anaesthesia -Danaparoid/fondaparinux Non-pharmacological: -TEDS -SCDs -IVC filter -mobilising -hydration -physio
415
How do you decannulate a tracheostomy patient?
416
How do anti-epileptic medications work?
Act on excitatory synapses (inhibits) or inhibitory synapses (enhances): -GABA - benzodiazepines; barbiturates -SV2A - levetiracetam -Sodium channel - phenytoin, carbamazepine, sodium valproate -NMDA receptor - ketamine
417
How would you manage: 1. Hyperthyroid crisis 2. Hypothyroid crisis
1. Most common from Graves, toxic multinodular goitre, thyroid adenoma —Supportive: -O2 -fluids -cooling —Specific: -Propranolol -PTU/carbimazole -Steroids! 2. Iodine deficiency, Hashimoto’s thyroiditis —Supportive: -airway -CVS support -temp control -treat hypoglycaemia/electrolyes —Specific: -liothyronine vs levothyroxine -steroids BEFORE replacing thyroid
418
How can you assess rib fracture severity?
Presence of flail segment, contusions etc Scoring systems: Rib fracture score Chest trauma score RibScore STUMBL scoring system: +1 per 10 years >10 +2 per 5% reduction in SpO2 in air +3 per individual fracture +4 anticoagulant/antiplatelet +5 chronic lung disease >30 = severe
419
Define chronic liver disease
Progressive deterioration in hepatic synthetic & metabolic function over >26 weeks Without encephalopathy Causes: -alcohol -autoimmune -viral -NAFLD Inflammation -> fibrosis -> cirrhosis
420
How does the innate immune system respond to infection
—Pathogen associated molecular patterns (PAMP) bind to pattern recognition receptors (PRR) on the surface of neutrophils/mast cells/dendritic cells/NK cells —Triggers cascade causing activation of: -pro-inflammatory cytokines -iNOS -acute phase proteins - CRP, fibrinogen, ferritin -coagulation factors
421
How does the adaptive immune system respond to infection?
422
What is the pathophysiology of sepsis?
Disruption of glyocalyx resulting in: 1. Vasodilation 2. Loss of endothelial integrity 3. Reduced myocardial contractility 4. Activation of coagulation cascade and fibrinolysis 5. Mitochondrial dysfunction
423
When can we break confidentiality to the police?
Road Traffic Act - they can take whatever they want If serious crime (>5 years jail time) and holding suspect and in need of more info to secure conviction If concern others may come to harm