ICU & FICM Flashcards
What is the MACOCHA score?
Predicts difficult airway in critical ill patients?
What does the MACOCHA score comprise?
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)
What MOCACHA score predicts difficult airway?
A score of >3
Max score of 12
What are the signs of PRIS?
Arrhythmias Rhabdomyolysis - high CK High K Metabolic acidosis Lipidaemia from high triglycerides Enlarged liver/fatty liver Cardiac failure/myocardial collapse
What is the maximum rate of infusion of propofol?
4mg/kg/hr
List risk factors for developing PRIS
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
What might you see on blood tests for PRIS?
Acidaemia Raised lactate Raised CK Myoglobinuria Hyperkalaemia Hypertriglyceridaemia Raised Cr
How do you manage PRIS?
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
Explain why HFNO is so good?
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
What are the contraindications to HFNO?
Unconscious patient Uncooperative/combatant patients Basal skull fracture Epistaxis Facial injury Laser surgery Airway/nasal obstruction T2RF
What is the Parkland formula?
Used for fluid replacement in burn patients:
Weight x % burn BSA x 4ml
First half in 8 hours, second half in 16 hours
What are the criteria for sending a burn to a specialist centre?
>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
Who sets the information about tracheostomies?
National Tracheostomy Safety Project set standards
What % of difficult airways occurred on ICU during NAP 4
25%
List 6 patient related factors that increase the risk of complications during the intubation of critical care patients
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
List some environmental factors that may increase the likelihood of a difficult airway in critical care patients
Not in the theatre environment
Staff not trained as airway assistants
High stress environment
List some indications for tracheostomy in a critical care patient
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
What are the contraindications to tracheostomy?
Absolute: -Unstable C-spine -Infection over site of trache Relative: -High FiO2 >0.6 -High PEEP required >10cmH2O -Difficult anatomy -Previous radiotherapy -Coagulopathy
List some early complications of tracheostomy
Loss of airway Damage to airway Derecruitment Pneumothorax Surgical emphysema Bleeding Damage to RLN
List some late complications of tracheostomy
Displaced tube causing loss of airway Tracheal stenosis Tracheomalacia Erosion into blood vessel - tracheoarterial fistula Infection Scarring/permanent stoma
What are the criteria for diagnosing ARDS?
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
Describe the pathophysiology of ARDS
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
~~~
What are the 3 phases of ARDS?
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
What are the strategies used for management of ARDS?
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
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
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
What is the alveolar gas equation?
PAO2 = PiO2 - PACO2/RQ
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
What are the stages of pulmonary toxicity from excess O2?
- Increase in Reactive Oxygen Species & reduction in anti-inflammatory levels
- Inflammatory stage - destruction of pulmonary lining and migration of inflammatory mediators
- Proliferative phase - cellular hypertrophy & increased secretions from alveolar type II cells
- Fibrotic phase - collagen deposition and interstitial thickening
Irreversible changes
Decreased Vital Capacity is first change in lung function seen
Acute Lung Injury
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
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
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
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
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
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
How would you adjust the APRV if a patient became:
- Hypoxaemic
- Hypercapnoeic
- Increase PHigh +/- THigh
Check TLow = 75% of PEFR (derecruitment if TLow is too long) - Increase alveolar ventilation: increase PHigh +/- THigh
Increase MV: decrease THigh and increase PHigh
How would you wean someone on APRV?
Decrease PHigh while increasing THigh (eventually becomes CPAP)
Once PHigh is ~20 then it is basically CPAP
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”)
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
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
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
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
What are the effects of myasthenia gravis on:
- Depolarising muscle relaxants
- Non-depolarising muscle relaxants?
- Increased resistance to Sux
- Increased sensitivity to NDMR
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)
Which NAP project focused on peri-operative anaphylaxis?
NAP 6
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
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
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
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
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
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
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
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
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
What are the causes of ARDS?
Direct:
- Pneumonia
- Aspiration
- Lung contusion
- Fat embolism
- Drowning
- Inhalational injury
Indirect:
- Pancreatitis
- Sepsis
- Major trauma
- Massive transfusion
- CPB
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
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
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)
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
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
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
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
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
How is ICU acquired weakness diagnosed?
Diagnosis of exclusion
Clinical diagnosis
EMG
Nerve conduction
Nerve biopsy
Muscle biopsy
Imaging: CT/MRI
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
Define the stress response
Physiological and pathophysiological changes occurring in response to stimulus (e.g. of surgery)
- Metabolic response
- Immune response
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
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
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
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
What are the causes of ARDS?
Pulmonary
Extra-pulmonary
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)
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
What are the benefits of prone positioning in ARDS?
—Reduces V/Q mismatch
—Increases FRC
—Allows recruitment of posterior alveoli
Evidence from PROSEVA study
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)
What is RASS?
Agitation/Sedation score used in ICU
From -5 to +4
Aim is for a RASS of -2 to +2
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
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
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
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
What factors are used for prognostication after OOHCA?
—Clinical: corneal blink reflex, pupil response, myoclonus, ongoing seizures
—Radiological: CT, MRI
—EEG
—SSEPs
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:
What spectrum of light is used in a pulse oximeter?
660nm (red) & 940nm (infrared)
Isobestic point - 840nm
What happens in a quinine overdose?
Prolonged QTc
VF resistant to amiodarone
Blindness
Hypoglycaemia
Not removed by CVVh
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
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
What is the management of GvHD?
Steroids
T-cell immunosuppression
Anti-TNF antibodies
MMF
Prophylaxis: calcineurin inhibitors
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
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
What is the management of aortic dissection?
BP control - systolic 100-120mmHg
Beta blockers
Once blocked, SNP/GTN/hydralazine to vasodilate
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
What variables does the Child-Pugh score use?
Bilirubin
Albumin
INR
Ascites
Encephalopathy
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
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
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
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
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
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
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
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
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)
What are the likely organisms in peritonitis in Peritoneal dialysis patients?
Coagulase negative Staph
Staph aureus
Non-Pseudomonas Gram -ves
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
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
What is the management of PJP?
Co-trimoxazole
Prednisolone
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
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
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
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
How are new UK ICUs built?
According to the DoH’s ‘Health Building Note 04-02’ (2013)
What is the minimum bed space area on an ICU?
20m2 or 25m2 for side rooms
One washbasin per 2 beds at least
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
What is the minimum recommended number of side rooms on an ICU?
20% of beds should be side rooms
Ideally with lobby
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
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
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
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
What scoring systems do you know?
Organ/disease specific (e.g. GCS, MELD)
Generic scores (e.g. SOFA, MODS, APACHE)
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
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(?)
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
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
What is ICNARC?
Intensive Care National Audit and Research Centre
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
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
What is the post-intensive care syndrome?
Up to 50% of ICU survivors will experience cognitive, psychological and physical changes following discharge
What is Cardiac Output?
SV x HR
Normal value = 4.5-8L/min
What is Cardiac Index?
CO/BSA
Normal value = 2.7-4L/min/m2
What is stroke volume?
(CO/HR) x 1000
60-130ml/beat
What is Systemic Vascular Resistance?
80 x (MAP-CVP)/CO
Normal value = 770-1500dynes/s/cm5
What is Pulmonary Vascular Resistance?
80 x (PAP - PCWP)/CO
Normal value = 100-250dynes/sec/cm5
What is Ejection Fraction?
(EDV-ESV)/EDV
Normally >0.6
What is Mean Arterial Pressure?
MAP = CO x SVR
Normal = 80-90mmHg
What is the normal value for Flow Time corrected (FTc) on oesophageal Doppler?
330-360ms
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
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
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
What are your ICP targets in TBI?
ICP <20mmHg
CPP >60mmHg
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
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
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
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
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
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)
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
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
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
What BP are you aiming for with an unsecured aneurysm that has caused SAH?
<140mmHg
Use beta blockers
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
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
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
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
What is the definition of pulmonary hypertension?
2022 definition:
Mean PASP >20mmHg at rest
PVR >2 Wood units
PAWP <15mmHg
What is the initial test for pulmonary hypertension?
TTE
Tricuspid regurgitation velocity is used to estimate the PASP
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
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
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
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
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)
How do you manage a failing RV?
- Optimise RV preload - closely monitored fluid/diuretic/RRT
- Augment the RV - milrinone strengthens RV contraction and reduces PVR; (also dobutamine, adrenaline, levosimendan)
- Reduce RV afterload - optimise HPV factors; inhaled NO, milrinone, prostacyclin
- Maintain systemic BP/coronary perfusion - noradrenaline/vasopressin (may cause pulm vasodilatation too and improve PVR/SVR ratio)
What are the clinical signs of alcoholic hepatitis?
Jaundice
Pyrexia
Tender hepatomegaly
What are the lab findings in alcoholic hepatitis?
Moderate AST & ALT rise with AST:ALT ratio >2
Bilirubin and GGR raised
Leukocytosis with neutrophils
What drugs might you give in alcoholic hepatitis?
Steroids if Maddrey discriminate function score >32
Pentoxifylline (?)
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
- Increased response
- Increased response
- Normal response
- Normal response
- Decreased response
- No response
- No response
- No response
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
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 (?)
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
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
What is prothrombin complex?
Concentrated factors II, IX and X at significantly higher levels than FFP
What are the causes of thrombocytopaenia?
- Dilution
—massive transfusion/fluid administration - Sequestration
—hypersplenism; extreme hypothermia - 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 - Increased destruction
—Drugs: Heparin
—Autoimmune: TTP, HUS, ITP, MAHA, Anti-phospholipid, SLE
—Haem: DIC, HELLP
—Machinery - CPB, IABP, RRT
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
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
Define:
1. Inotropy
2. Chronotropy
3. Lusitropy
4. Vasopressor
- Increase myocardial contractility
- Increase heart rate
- Increase relaxation
- Vasoconstriction leading to increased SVR/PVR; increase vascular tone
What are the BP targets in hypertensive emergencies?
Summarise the care of the patient donating after brainstem death
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
How can we do cerebral monitoring?
- Clinical assessment
- ICP/CPP monitoring (bolt, EVD, optic nerve, pupillometry)
- CBF (Doppler)
- Cerebral oxygenation (NIRS, SjvO2, bran parenchymal oxygen tension)
- Cerebral metabolism (micro dialysis catheter - glucose, lactate/pyruvate, glutamate, glycerol)
- Electrophysiological activity (EEG, SSEPs)
What causes biliary sepsis?
—Usually gallstones
—Strictures (PSC)
—Malignancy (pancreas)
How do you decannulate a tracheostomy patient?
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
How does the adaptive immune system respond to infection?
What is the pathophysiology of sepsis?
Disruption of glyocalyx resulting in:
- Vasodilation
- Loss of endothelial integrity
- Reduced myocardial contractility
- Activation of coagulation cascade and fibrinolysis
- Mitochondrial dysfunction
