General ICU stuff Flashcards
Protective effects of hypothermia
- reduced CMR
- Reduced cerebral O2 demand
- decreased production of neurotraminssters
- reduced free radical exposure and oxidative stress from reperfusion
Therapeutic hypothermia
Cooling patient to subnormal temperature for specific indication
previously used in OOHCA, TBI
now neonatal hypoxic brain injury and deep hypothermic circulatory arrest in aortic surgery
Targeted temperature management
constant targeted temperature maintained
unconscious cardiac arrest patient
- OHCA initial shockable rhythm (previous recommendation)
- OHCA initial non-shockable (previous suggestion)
CI to < 33 C include severe systemic infection and coagulopathy
TTM fallen out of favour
now avoidance of hyperthermia and maintenance of low normal temperature
TTM trial 33 vs 36 degrees OOHCA no difference in mortality or disability
TTM 48 33 degrees for 24 or 48 hours. no difference, sig more adverse events
TTM 2 33 vs 37.5 no difference
TTM methods
devices - feedback loop with monitoring and delivery - heat exchange water circulating cooling pads in arctic sun
simple ice packs
intravascular head exchanger
sedation with NMB due to shivering
rewarming risks of rebound hyperthermia, vasodilatory hypotension, reperfusion injury
How would you manage temperature following cardiac arrest
- temperature control
- actively preventing fever > 37.7
- use cooling device to target temperature of 37.5 if antipyretics, exposure etc unscuccesful
How would you manage temperature following TBI
Normothermia aiming 36-37
challenges of nutritional assessment in ICU
patient
- extremes of prior health
- frailty
- varied population
illness
- acute gut injury
- sepsis
- major trauma
- organ failure
treatment
- ventilation
- RRT
- sedation
MUST score
- BMI
- % change
- acute disease effects
add scores for overall risk
0 = low 2 or more = high
nutritional assessment on icu
ESPEN
- all patients > 48hr on icu risk of malnutrition
- pre icu weight loss, pre icu decline in physical performance
- muscle mass, body composition, strength
BMR
energy expended per unit time during rest.
40cal/m2/hr
energy expenditure is sum of internal heat produced and external work. internal heat = BMR + thermic effectst of food
critical illness - catabolic and significant energy deficit
measuring energy expenditure
- indirect calorimetry - need VO2 / VCO2
- feeding equations - Harris - Benedict, Schofield based on gender, age, sizue
respiratory quotient
CO2 : O2 during respiration
carb = 1.0 protein 0.8 lipid 0.7
body weight terms
actual / total = measured weight
LBW - excludes fat
IBW - based on height
ABW - use in obese patients
Daily nutritional requirements in critical illness
energy - 25-35kcal/kg
carb - 2g/kg
protein 0.8-1.5g/kg
lipid 1-1.5g/kg
water 30ml/kg
Na K Cl 1mmol/kg
PO4 0.4mmol/kg
Mg and Ca 0.1mmol/kg
Nutritional support
oral supplements, EN, PN
- increased risk of malnutrition
- little or no diet for 5 days, continuing another 5 days
- poor absorption
- high nutritional loss
- high demand
ESPEN - EN via NG within 48hrs once stable
50% of estimated target, increase to 70% after 48hrs
contraindications to EN
- gut - anastatmotic leak, necrosis, ischaemia
- maintaining oral inake
- peritonitis
- uncontrolled severe shock
relative - > 500ml gastric aspirate/6 hrs
- abode compartment syndrome
- < 5 days fasting
- localised peritonitis, abscess
EN disadvantages
- needs healthy gut
- tube discomfort
- tube misplacement
- diarrhoea
trophic feeding
minimal administration of EN <20% requirements to preserve gut integrity rather than nutrition
- preserves epithelium
- prevents translocation
- enhance immune function
permissive underfeeding is deliberately administering < 70% of target calories.
Parental nutrition
IV administered sterile nutrients
central access due to risk of thrombophlebitis and infection
lipid triglycerides 40% non protein calories
carbohydrates mainly glucose 60%
all essential amino acids
electrolytes
trace elements and vitamins separately
late day 8 plus probably better than early
protein increased supplementation in burns, trauma, neck fas
decreased in hepatic encephalopathy
stress ulceration
stress mediated mucosal injury can be caused by critical illness, maybe due to hypoxia, hypo perfusion, coagulopathy
deep ulcers may cause haemorrhage or perforation
compared to PUD - usually affects gastric fungus and is painless
GI bleeding in critical care
highest risk
- mechanical ventilation without EN
- CLD
High risk
- coagulpathy
Mod risk
- mechanical ventilation with EN
- AKI
- Sepsis
- shock
Low risk
- steroids
- anticoagulants
stress ulcer prophylaxis
- enteral feeding
- pharamcoglocial prophylaxis (PPI / H2)
- if high or highest risk
- avoid f low risk of bleeding - increase bacterial overgrowth and HAP (potentially also CDI)
- cautious vasopressors
- optimised fluid status
Plasmaphoresis vs PLEX
- Aphoresis - removal of component of patients blood using extracorporeal circuit
- plasmapheresis - type of aphorises removing plasma
- plasma exchange - plasmapheresis and replacement with substitute - removing high molveculr weight substances causing pathology. 100-150% of plasma exchanged, often 5 exchanges. 5% HAS replacement
other therapeutic aphorises
- leucopheresis
- thrombocytaphoresis
- erythrocytaphersis (severe malaria, sickle cell crisis, polycythaemia ruby vera)
- rheaphoresis - separate high molecular weights
how does plasmaphoresis work?
two methods
- centrifugation - blood spins to separate components by density. used in donation
- filtration - blood passes through specialised filter to separate components - similar set up to RRT, can be adapted for PLEX with replacement fluid given back to bloodstream
Indications for PLEX
Category 1
- Neuro - GBS, acute MG, NMDA encephalitis
- Renal - ANCA-vasculitis, anti-GBM, GPA
- Haem - TTP, catastrophic APLS
- Post transplant - desensitisation in ABO incompatibility
Category 2
- Neuro - ADEM, LEMS, MS, VGKC disease, chronic MG
- Renal - amyloidosis
- Haem - AIHA
- Transplant - antibody mediated rejection
- Other - thyroid storm, SLE severe complications
Category IV (ineffective / harmful) PLEX
- ALS
- Rheumatoid arthritis
- schizophrenia
Complications of PLEX
- dilution coagulopathy
- complications of access
- transfusion reaction
- fluid imbalance / hypovolaemia
- complications of anticoagulation
- drug dose alterations
post-intensive care syndrome
constellation of physical and psychological syndromes affecting patients following intensive care stay
- physical - weakness, pain, reduced mobility, breathlessness
- mental health - PTSD, anxiety, depression
- cognitive - memory loss, difficulty concentrating
Sequelae of critical care admission
RESP - laryngeal injuries, voice changes, stenosis. Pulmonary hypetension, embolism, fibrosis, long term trachesotomy
CVS - LV / RV dysfunction
RENAL - AKI, CKD, RRT dependence
NEURO - seizures, HII, focal deficit, cognitive deficit
NUTRITIONAL - appetite loss, dysphagia
PHYSICAL - ICUAW, joint pain, pressure sores
COMMUNICATION - difficulties
PSYCHOLOGICAL
FATIGUE
CHRONIC PAIN
Identifying rehab needs
prevention e.g. minimises IPPV
Screening - within 4 days, prior to discharge, on the ward. PICCUPS tool / Chelsea critical care assessment tool
Considerations when assessing critical care related morbidity
- LOS
- Severity of illness
- Severity of longterm injury e.g. neurology
- premorbid respiratory and physical function
- nutritional issues
- psychiatric e.g. recurrent nightmares, intrusive thoughts, hallucinations
Rehab goals
short, medium, long term
achievable and can change
regular assessment and MDT
e.g. goal of early mobilisation
early - sit on edge of bed with support
medium - stand aided
long - march on spot
Handover from critical care
Summary of stay including management and diagnosis
monitoring and investigation plan
plan for ongoing treatment
individualised rehab programme
Discharge from hospital
Discussion about
- physical and cognitive recovery
- psychological and emotional recovery
- diet
- continuing treatment
follow up of critical care patients
- more than 4 day admission should be followed up at 2-3 months
- assessment of new physical and non-physical problems
- rate of recovery
- social care / equipment
- arranging support
Sepsis 3 definitions
Sepsis = life threatening organ dysfunction caused by deregulated host response to infection
septic shock = vasopressors needed to maintain MAP > 65 and lactate > 2. 40% mortality
SOFA score
6 organs 0-4
0 - 24
2 + = organ dysfunction = 10% mortality
Resp = P/f
CVS = MAP, vasopressors
Neuro = GCS
Renal - creatinine, UO
Coag = platelets
Liver = Bili
correlates with mortality
e.g. initial score 4-5 = 20% > 12 = 95%
Glycocalyx
layer of proteoglycans and glycoproteins semi bound to capillary wall. semi-permeable layer, allows passage of anions and small molecules. manages mediators such as NO
injury –> permeability alteration in starling forces and pro-inflammatory pathways.
Pathophysiology of sepsis
Cascade of vicious cycles
initially PAMPs on microbe activate immune system via TLRs
transcription of pro inflammatory cytokines TNF, IL-1B
adhesion molecules, acute phase proteins, pro-oxidants pro-coagulant released
systemic injury when threshold exceeded by inflammatory response
- ROS - damage cells and DNA
- Complement
Surviving sepsis campaign 1 hr bundle
- measure lactate
- take cultures
- give abx
- administer 30ml/kg fluid if hypotensive or lactate > 4
- vasopressors if remains hypotensive
Timing of abx
- immediately if definite or probable sepsis or possible sepsis with shock
- possible sepsis without shock - 3 hours
circulatory failure in sepsis
30ml/kg fluid < 3 hrs if hypo perfusion or shock
NA MAP > 65, peripheral if no cvc
consider VP if > 0.3mcg/kg/min
if cardiac dysfunction consider dobutamine
add steroid if ongoing requirements > 4 hrs
Early goal directed fluid therapy evidence
rivers 2001 - target MAP, CVP, ScVO2. significant improved mortality
Process, arise, promise - no difference
Rivers protocol
- 1st 6 hrs
- supplemental O2
- CVP 8-12
- MAP 65-90
- SCVO2 > 70%
- If < 70% - red cell transfusion if Hb < 100 or dobutamine
MAP targets evidence
SEPSISPAM - MAP 65-70 vs 80-85. no difference in mortality. less AKI in higher group with chronic hypertension
65 - ‘permissive hypotension’ MAP 60-65 in over 65s vs usual care. mean 66.7 vs 72.6. no difference in mortality. Chronic hypertensives faired better with lower MAP.
