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.
Vasopressin evidence
VASST - add vasopressin to noradrenaline, no difference in mortality.
Activated protein C
PROWESS - improved mortality
concern re bleeding events
PROWESS-SHOCK - no improvement.
withdrawn
Evidence against in sepsis
starches
terlipressin
vitamin C
- CITRIS-ALI - no difference
- LOVIT - increased mortality
Multi-organ dysfunction syndrome
2 or more organ systems altered function during acute illness such that homeostasis cannot be maintained
genetics, comorbidity, iatrogenesis, inflammation
severity depends on nature of insult, pre-existing organ reserve, therapies
PRIS
Condition associated with propofol use
acute bradycardia plus
- metabolic acidosis (86%)
- rhabdomyolysis (45%)
- lipaemia (15%)
- enlarged fatty liver
PRIS ECG
Brugada like changes coved STE V1-3
Arrhythmias
Bradycardia –> systole
PRIS pathophysiology
imbalance of energy demand and utilisation
oxidative phosphorylation and FFA utilisation are impaired leading to lactic acidosis and muscle necrosis
propofol contributes to lipid load and negative chronotropy
risk factors PRIS
high sedation requirements - TBI, sepsis
high endogenous catecholamine, glucocorticoids
low carb-lipid ratio
children have lower glycogen stores and high dependence on fat metabolism
management of PRIS
stop propofol
pacing / chronotropy
adequate carbohydrate load
RRT
prevention
- propofol < 4mg/kg/hr
- sedation holds
- monitor CK and triglycerides
delirium
acute, fluctuating, reversible disturbance in cognition and consciousness characterised by disorientation and inattention
29% on ICU
increased LOS, mortality, hospital acquired complications
delirium types
hyperactive - heightened arousal, restless, agitatied
hypoactive - somnolescent, withdrawn, quiet
mixed - alternating between two
other features
- inattention
- delusions, hallucinations
- sleep wake cycle disturbance
risk factors
patient
- age > 65
- alcohol
- pre-existing cognitive dysfunction
- sensory impairment
illness
- severity
- infection / sepsis
- hypoxia, hypotension
- constipation
- pain
management
- drugs e.g. benzodiazepines, opioids, steroids
environment
- lack of sleep
- lack of day-night routine
diagnosis of delirium
4-AT
AMTS
CAM-ICU
- altered mental state or any fluctuation
- inattention - squeeze letter A CASABLANCA
- Altered level of consciousness RASS other than 0
- Disorgenised thinking - questions / commands
1 + 2 + 3/4
management of delirium
prevention
- regular assessment
- sleep - wake - sleep hygiene, avoiding medications, eye masks, ear plugs
- avoid constipation
- minimise sedation
- analgesia
- avoid hypotension, hypoxia
- avoid causative medications
conservative
- re-orientation
- family present
- early mobilisation
- removal of lines
pharmacolgical
- management of agitation or psychosis
- antipsychotics
- clonidine
- Benzes if alcohol
ICU-AW
Secondary muscle weakness occurring after critical illness
symmetrical, generalised, proximal weakness with low tone affecting limbs, respiratory muscles and sparing facial and oral muscles
- polyneuropathy
- polyneuromyopathy
- myopathy
pathophysiology ICU-AW
muscle atrophy - immobilisation, disuse, unloading, denervation
muscle dysfunction - microcirculatory, structural alteration
neuropathy - oedema, microvascular dysfunction
risk factors icu-aw
patient
- older, frailer, obese
disease state
- duration, severity, mechanical ventialtion, sepsis, MOF
- hyperglycaemia
Medications
- steroids, NMB, sedation
diagnosis
clinical - MRC < 48/60, hand dynamoterey, 6mwt
electrophysiological - CMAP / SNAP
muscle biopsy
respiratory weakness
- max insp.exp pressure
lagophthalmos
incomplete closure of eyes
- exposure keratopathy
- corneal abrasion
eye infections
systemic fungal infection - affect eye and lead to visual loss
conjunctivitis - red and sticky eye, bacterial, viral. chloramphenicol eye ointment
microbial keratitis - HSV, bacteria - red watery sticky
endogenous endophthalmitis - red eye in septic patient, haematogenous spread
Non-infective eye issues
ischemic optic neuropathy - hypotension, CRAO
acute glaucoma
chemises
Poisoning presentatoions
accidental
intentional
recreational
suspect in undifferentiated
- altered consciousness
- respiratory depression
- cardiovascular instability
- vomiting
- seizures
Cholinergic toxidrome
Pupils: miotic
Neuro: Sedation, seizures
Vitals: hypotension, bradycardia
Other: diaphoresis, SLUDGE
Causes: nerve agents, neostigmine, organophosphate
Anti-cholinergic toxidrome
Pupils: myriatic
Neuro: agitation or sedation, seizures, clonus
Vitals: tachycardia, hypretension, hyperthermia
Other: urinary retention
Causes: antihistamines, TCA, hyoscine, parkinsons medications
Sedative toxidrome
Pupils: Miotic
Neuto: sedation
Vitals: hypoventilation, hypotension, hypothermia, bradycardia
Other: constipation
Causes: opioids, alcohol, Benzes, barbiturates, GHB
Stimulant toxidrome
Pupils: mydriatic
Neuro: agitation, seizures, tremor
Vitals: tachycardia, hypertension, hyperthermia, hyperventilation
Causes: cocaine, amphetamine, theophylline
reduce effect of poisons
reduce absorption
- activated charcoal
- decontamination - emesis, lavage, whole bowel
- lipid sink - LAST
- skin decontamination
enhance elimination
- IV fluid
- extracorporeal
- urinary alkalisation
neutralise
- antidotes
Extracorporeal removal of toxins
low protein binding, low Vd, low molecular weight
< 10kda dialysis < 25kda filtration
drugs cleared by RRT
Haemodialysis (most)
- salicylates
- lithium
- carbamazepine
- metformin
- valproate
- alcohols
- aminoglycosides
- theophyllines
Haemofiltration
- lithium
- opioids
- sympathomimetics
Specific antidotes
Opioids - naloxone
Benzos - flumazenil
Beta blocker - glucagon
cyanide - hydroxycobalamin
toxic alcohols - fomepizole / ethanol
Serotonin - cyproheptadine
Paracetamol - NAC
Digoxin - Digibind
TCA Overdose
Anticholinergic toxidrome
Dysrhythmias (Na channel blockade)
Hypotension
Seizures
Delirium
ECG in TCA overdose
- Prolonged QRS (> 100 - seizure risk > 160 VT)
- Prolonged QT
- Sinus tachycardia
- Right axis deviation
Management priorities in TCA OD
General
- Toxbase
- Airway protection - seizures, loss of airway reflexes
- High flow O2
- CVS support - IV access, fluid, cardiac monitoring, vasopressors
- Seizure tx - benzodiazepines
Specific
- Na Bicarb - QRS > 100, seizure, hypotension
Antipsychotic OD
Management principles
- Benzodiazepines for agitation
- supportive care - intubation
- delirium on emergence
Typical Antipsychotics (haloperidol) - fluctuant mental state, CNS depression, hypertension, tachycardia, anticholinergic
Atypical antipsychotics (olanzepine, risperidone) - respiratory depression, CNS depression, hypotension
Lithium
- Neuro - fine tremor, ataxia, nystagmus, myoclonus, seizure, coma
- GI - N, V, D
- CVS - bradycardia, hypotension, long QT
Mx lithium toxicity
narrow therapeutic index - may be precipitated by polypharmacy, altered physiology
- lithium levels, renal function
fluid repletion
dialysis - level > 4-5 acutely, 2-3 chronically
- neuro decompensation
- renal dysfunction
challenges of illicit drug use
common - 10% 16-60yr olds
presentation - covert, secondary. lethality of overdose, contamination of substances
pharmacological - unpredictable dynamics, infections with prescribed, evolving chemical substances
others
- behavioural -aggression, intoxication
- capacity issues
- concomitant psychiatric conditions
- social issues
- complications of long term use - vascular access, abscess, manutirition
drug of abuse classification
by desirable effect
- narcotics - heroin
- sedatives - alcohol, benzodiazepines, barbiturates, GHB
- stimulant - cocaine, MDMA
- hallucinogenic - mushrooms, acid, ketamine
- anabolic - steroids
recreational, therapeutic, physical or psychological dependencea
approach to agitated intoxicated patient
pragmatic approach, unclear diagnosis
maintain safety - security
assessment of capacity / compliance with mx
de-escalation strategies
extreme agitation (threat to self or others)
- rapid tranquillisation
- GA e.g. facilitate CT
manage underlying cause of agitation
- urinary retention
- cocaine / MDMA - benzos
manage complications
- serotonin syndrome
unconscious intoxicated patient
conscious state, pupils, reflexes, airway protection
intubation - risk of aspiration, failure of gas exchange, MODS
thiamine if risk of wernickes encephalopathy
causes
- ethanol, toxic alcohols
- opioid
- other overdose
Rule out DDX - meningoencephalitis, sepsis, myxoedema, ICH
Alcohol intoxicaion
disinhibition, stupor, coma
complications - dehydration, hypoglycaemia, ketoacidosis, lactic acidosis, hypokalaemia, dysrthyhmias
toxic alcohols
can be screened for, or treated if clinical signs and symptoms
Ethylene glycol toxicity
- antifreeze, detergents
- alcohol dehydrogenase –> glycoaldehyde –> oxalic acid
- toxic metabolites cause effects - calcium oxalate precipitates in kidney and brain
stage 1 - 30mins - 2hrs - similar to ethanol toxicity + coma, seizures
stage 2 12-24hr - myocardial dysfunction, MODS
stage 3 24-72hr - AKI
stage 4 72hr + - cranial nerve defects
methanol toxicity
- antifreeze, wiper fluid, paint remover
- home distillation
- alcohol dehydrogenase to formaldehyde –> formic acid
0-6hr- similar to ethanol
6-30hr - latent phase
6-72hr - visual symptoms (blurring, snowstorm, blindness) seizures, coma, cerebral oedema
isopropyl alcohol
hand sanitisers, antiseptic
metabolised by alcohol dehydrogenase to acetone
isopropanol - direct toxic effects from GABA agonism
profound intoxication - haemorrhage gastritis, cerebellar signs, coma
toxic alcohol treatment
bicarb - pH 7.35-45 (alkalisation of urine, enhances elimination)
cofactors - pyridoxine, thiamine
fomepiazole
- competitive antagonist of alcohol dehydrogenase
- 15mg/kg
- serum concentration > 20mg/dl or
- osmolar gap > 10, pH < 7.3, HcO3 > 20
haemodialysis
- concentration > 50
- pH < 7.25
- visual disturbance, AKI, refractor electrolyte abnoramlity
osmolar gap = difference between calculated (2xNa + urea + glucose) and measured osmolarity.
GHB
Gamma hydroxybutyrate
euphoria, CNA and respiratory depression, rapidly eliminated
features in common with toxic alcohol poisonings
high anion gap
high osmolar gap
rapid absorption
metabolites and unchanged drug cleared by kidneys
all cause inebriation
Serotonin syndrome
altered mental state
autonomic instability
neuromuscular excitability
serotonin produced from metabolism of tryptophan - neurotransmitter, then reupatke and inactivated by MAO
thermoreception, behaviour, attention, platelet aggregation
mechanisms
- excessive formation of precursors (LDOPA)
- increased released - cocaine, MDMA
- receptor stimulations - TCA, pethidine, fentanyl
- decreased reuptake _SSRI, tramadol
- decreased metabolism - MAOI
serotonin syndrome presentation
benign –> life threatening
Altered mental status - confusion, agitation, delirium
Neuromuscular excitability - clonus, Hyperreflexia, hypertonia, tremor, rigidity
Autonomic - Labile BP, flushing, diaphoresis, hyperthermia
high index of suspicion - hunter serotonin toxicity criteria - 1 feature + history of serotniergic agent
DDX serotonin syndrome
- thyrotoxicosis
- MH
- heat stroke
- NMS
- sedative withdrawal
Neuroleptic malignant syndrome
systemic deficit in dopamine
idiosyncratic reaction to neuroleptics or withdrawal of dopamine agonists
tetrad
- altered mental state
- rigidity
- autonomic instability
- hyperthermia
compared to serotonin syndrome - more rigidity, Hyperreflexia are. catatonia, encephalopathy, coma. insidious onset. rhabdo and MODS
supportive mx, benzos, dantrolene
calcium channel blocker OD
elongating preparations, concomitant CVS disease
can lead to refractory hypotension as well as bradycardia, heart block, multi-organ hypo perfusion
- vasoactive agents - catecholamines
- calcium chloride
- vasopressors - metaraminol
- hyperinsulinaemic euglycaemic therapy (HIET)
- high dose glucagon
general - echo (pump failure vs vasodilation), early intubation, decontamination if modified release
HIET
useful in myocardial dysfunction
intracellular transport of substrate and oxygen
might help weaning of high dose catecholamine infusions
- bolus 1unit/kg insulin following 1unit/kg/hr, titrated up to 10unit/kg/hr
- 50% dextrose 50-100ml concurrently followed by 1ml/kg/hr
- close monitoring glucose with moderately high target. titrate to BP > 90 HR > 60
maye also be used in severe beta blocker OD
Beta blocker OD
Glucagon and milrinone - indirect sympathomimetic effects (not reliant on beta receptors)
increased myocardial cAMP
positive iontrotopr and chronotyopu
bradycardia and myocardial suppression more likely to respond than vasodilation
salicylate toxicity
respiratory alkalosis before HAGMA
nausea vomiting tinnitus
seizures, hypotension, low GCS. hyperthermia
urinary alkalisation with bicarbonate
500mg/l mod 750mg/l severe
haemodialysis
- failure of urinary alkalinsation
- end organ impairment
- > 1000mg/l
digoxin toxicity
- narrow therapeutic index
GI symptoms then CNS (chronic - progressive CNS)
GI - N/V/D/pain
CVS - bradycardia, AV block, AF, junctional, bigeminy
neuro - visual disturbance, delirium, sieuzres
digoxin specific Ab
LAST
early - dysphoria, tinnitus, perineal numbness, metallic taste
CNS - agitation, LOC, seizures
CVS - heart block, bradycardia, systole, VT
Mechanisms of LAST
systemic absorption / IV injection
affected by agent, dose, patient
interference of conduction in heart and brain
risk factors
- long acting
- more vasoactive agents - bupivacaine vs levobupivacaine
- proximal block
- use of adjuncts
- bilateral blocks
Reducing risk of LAST
pre-procedure - assessment, dose calculation
procedure - USS, aspiration, serial injection
post-procedure - labelling of catheters, NRFiit
institutional - availability of lips emulsion
Mx LAST
- stop infusion
- ABC
- lipid emulsion
- hyperventilation
- seizure managagement - benzo, porropofol
- antiarrhythmics as usual
- e-cpr
Intralipid 20% dose
1.5ml/kg bolus
15ml/kg/hr infusion
repeat bolus 3x
max dose 12ml/kg
corrosive ingestion
acid / alkali
readily available
airway compromise, GI perforation, strictures
decontamination, airway intervention, endoscopy
acute heavy metal ingestion
GI irritation - N/V/D, fluid loss, electrolytes and dose related systemic toxicity
iron - ALF, cirrhosis
Lead - encephalopathy
arsenic - hypersalivation, encephalopathy, peripheral neuropathy
pro kinetics, endoscopy
iron - chelation with dexferrioamine
arsenic - chelation with succimer
chemical weapons
nerve agents - organophsphares irreversibly bind to anticholinesterase - cholinergic toxidrome
managed with anticholinergic infusion, cholinesterase reactivator - pralidoxime
cyanidses - impair aerobic respiration, severe refractory lactic acidosis. supportive oxygenations, hydroxycobalamin
acute radiation syndrome
whole body irradiation
significant history and lymphopenia
dose dependent
- large dose, external, penetrating, delivered over short time
prodrome, latent, manifest illness, death or recovery
manifestations
- bone marrow destruction
- GI destruction
- CVS . CNS syndrome
management - supportive, treat contamination, lymphocyte count expectant management and palliative care
mental health and critical care
common admission
repeat admissions
evolving medications
complex polypharmacy
ECT
dilirium and withdrawal symptoms
refusal of medical interventions
need psychiatric follow up
may need detention under mental health act
