Icu Flashcards
Indications for artificial ventilation in adult at rest
VC 10ml/kg
RR >35
AA gradient over 300mmhg
Types of ventilator associated lung injury
Volutrauma Barotrauma Atelectatrauma Biotrauma (inflam) Sheer stress
Ventailator associated lung injury can appear like ARDS
True both can present bilateral infiltrates on CXR
How to set PEEP in VALI
Set PEEP at the lower inflection point (I.e the point that alveolar recruitment happens in inflation)
Note peep improves oxygenation but not mortality
Indications for artificial ventilation in gbs
VC <15ml/kg
Reducing trend
Clinical features of tricyclics antidepressant overdose
Tachycardia Hypotension Flushed Raised temperature Dry mouth Dry skin Dilated pupils Seizures Agitation Reduced conscious level Urinary retention
ECG features of tricyclics antidepressants
Sinus tachycardia Short pr interval Wide qrs Long QT AV block
What is proposed mechanism for intralipid I’m drug toxicity ieLAST and TCA
Intralipid acts as lipid sink. Binds to free lipid soluble drug and reduces the free plasma concentration. Drug then redistributes from the tissues and is excreted as normal
Specific changes to ALS protocol in poisoning secondary to TCA or LAST
Administer hco3
Prolonged resuscitation
Use intralipid
Initial approach to poisoning
ABCDE approach 100% o2 PPE Secure airway if GCS <8 IV access and bloods for Fox inc paracetamol salicylate alcohol Toxbase Identify agent or toxidrome Specific antidote if available
Scoring tool by trauma audit and research network to measure overall severity of injury
Injury severity score
Out of 75
If any area gets a score of 6 (unsurvivable) they are automatically given score of 75
Injury severity score more than 15 is major trauma
3 core principles of damage control resuscitation
Permissive hypotension (first clot is best) Haemostatic resuscitation with early use of blood Damage control surgery
Aims of damage control surgery
Control haemorrhage Prevent triad of death Restore physiology Prevent contamination Return to theatre at later date to restore anatomy
What is triad of death in trauma
Coagulopathy
Hypothermia
Metabolic acidosis
Mechanism of action of TXA
Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin
Therefore prevents plasmin induced fibrinolysis
Stabilises the clot
Dose of TXA
1 gram immediately (less than 3 hours)
1 gram over 6-8 hours
What evidence supports use of TXA
CRASH 2
Benefit if transexamic used less than one hour
Poor outcome more than 3 hours
Mortality reduced
Indications for tracheostomy (grouped)
Indications for trache grouped into
- requirement for prolonged mechanical ventilation
- provision of pulmonary toilet
- protection of airway
- management of upper airway obstruction
- as part of a surgical procedure
Considerations choosing tracheostomy tube
Type and size (appropriate internal diameter remembering That inner tube may significantly reduce the diameter )
Subglottic suction required
Longer or extended tube size (obesity or anatomy may result in needing adjustable flange)
Checking position of trache on insertion
Capnography
Endoscope
Neutral head position
Leak test to 20-30cm h2o
NAP 4 most common reason for trache critical incident
Displaced trache
Project that audits and teaches re tracheostomy
National tracheostomy safety project
National tracheostomy safety project algorithm patent upper airway
- Call for help, look listen feel mouth and tracheostomy, mapleson c may help if available and capnography
- If breathing - high flow o2 to mouth and stoma
(If not breathing cpr)
3. Assess tracheostomy patency Remove speaking valve Remove inner tube Try pass suction catheter If unable to pass deflate cuff Look listen and feel/map c/ capnography Is patient improving.
- If not improving remove trache tube
Look listen feel/map c - Is patient breathing
No call resuscitation team, cpr if no pulse - Primary emergency oxygenation
Oral airway manoeuvres and cover stoma
Or tracheostomy stoma ventilation
7, secondary Emergency oxygenation.
Oral intubation prepared for difficult intubation
Intubation of stoma
Complications of tracheostomy
Early
Haemorrhage
Pneumothorax
Failed
Short term Blockages Tube displacement Surgical emphysema Tracheal necrosis Tracheal arterial fistula
Long term
Tracheomalacua
Tracheal stenosis
Decannulation issues
Bedside signs in tracheostomy
Size When was inserted (Tracheostomy vs laryngectomy) Why Inserted How ie surgical vs percuatneous Any sutures in place Any issues with airway and how was managed
Bedside equipment tracheostomy
Spare tube and inner cannula
Suction
Stitch cutters
Emergency bell
Fibreoptic scope nearby
Bleeding trache
Causes abberant vessels…. rarely Inominate artery fistula
Suction
External compression surgical clips or cautery
Gauze soaked in adrenaline or tranexamic acid around bleeding site
Consider hyperinflating cuff to tamponade
Surgical exploration and repair
Types of RRT
Peritoneal dialysis
IHD
CVVHF CVVHD CVVHDF
SLED (sustained low efficiency dialysis)SCUF (slow continous ultrafiltration)
Aims of RRT
Solute and water removal
Correction electrolyte abnormalities
Normalisation a die base
Basics how RRT works
Diffusion (hd)or convection (hf)
Extracorpeal curcuit filled with blood
Roller lumps control speeds of flow towards memebrane
Por size of membrane effects what can pass through
Middle molecules are preferentially cleared by convective measures
Small molecules better cleared by diffusion
Describe haemofiltration in terms of CVVHF
Haemofiltration is a comvective process where a hydrostatic pressure gradient is used to filter plasma, water and solute across a membrane
Solute drag where appropriately sized molecules are pulled along with mass movement of solute
Convective transport is independent of solute concentration but determined by magnitude or transmembrane pressure
Ie higher flow rate equals increased UF
Measures that increase negative pressure across membrane including pump in effluent line can have marked effect - high volumes effluent discarded and circulating volume of patient replaced with balanced crystalloid buffer
Describe haemodilaysis as in CVVHD
Hamodilaysis solute clearance is achieved by diffusion across the membrane
Space outside the blood containing fibres within the filter is filled with dialysate which is pumped counter current to flow.
Diialysate is reconstituted to include a buffer and essential electrolytes
Diffusion occurs down a concentration gradient to equilibrium - countercurrent maintains a waste solute gradient
Types of RRT membrane
Cellulose
Synthetic
Types of filter fluid in RRT
Lactate based (lactate accumulation in hepatic dysfunction) Hco3 based
Can be added before filter (reduces risk of filter clotting) or mixed with blood in venous drip chamber ( increases clearance solutes)
Positives of continuous RRT in icu
Enhanced haemodynamic stability
Superior management of fluid balance
Enhanced clearance of inflammatory mediators
Better preservation cerebral perfusion
No difference in survival benefit
Kdigo favours CRRT for haemodynamic instability
Classical indications for initiating RRT
Refractory hyper Kalaemia over 6.5 Refractory fluid overload Refractory metabolic acidosis Certain drug and alcohol intoxication’s Signs of uraemia ie pericarditis or encephalopathy Temperature control
Risks of RRT
Cannula insertion Biocompatibility Fluid shifts Altered drug metabolism Nursing workload Cost
Discontinuation RRT
When kidney function improving
Ie UOP
Creatinine clearance
Dosing RRT
Continuous technieques dosing is sum of effluent in ml per kg per hour
Initial high rates used but now dosing 20-25ml/kg/hr
Vascular access choices RRT kdigo
1) Right IJ
2) Femoral
3) Left IJ
4) Subclavian
In order.
Anticoagulation in RRT
Systemic or regional anticoagulation
Systemic heparin most common cheap but risk of haemorrhage and heparin resistance and HIT
Systemic with heparnoids ie danaparoid especially if HIT
Regional anticoagulation with citrate but as chelates calcium (inhibiting platelet aggregation) require calcium infusions, and potential metabolic complications (alkalosis and acidosis hypocalc and hypomagnesia)
Regional prostacyclin
What percentage those with aki and RRT never regain full renal function
40
Classifications of renal failure
RIFLE (risk injury failure loss esrf)
AKIN (aki network)
Based in serum creatinine and urine output
Causes of non specific aki
Sepsis Critical Illness Circulatory shock Burns Trauma Cardiac surgery Nephrotixic drugs Radiocontrast agents
Susceptibilties to aki
Dehydration Age Female Black CKD DIABETES cancer Anaemia
Traumatic and non traumatic causes Rhabdo
Traumatic causes
Crush injury
Burns esp electrocution
Compartment syndrome
Non traumatic Injection MH Serotonin syndrome Drug related Exertional Status Metabolic ie DKA
Clinical findings traumatic rhabdo
Signs of compartment syndrome ie Swelling tense Pallor Pain Myalgia
Tests for rhabdo
Urine for myoglobin
Lactic acidosis
CK over 5000
Principles of managing a patient with rhabdo
Aggressive fluid rehydration aiming for UOP more than 3ml/kg/hour
Early surgical fixation cause
Treat hyperk
Alkalise urine
Renal replacement therapy
Early enteral nutrition
MDT involvement
Electrolytes values for brain stem death
Na 115-160
K more than 2
Phosphate and mag 0.5-3
Glucose 3-20
Brain stem tests and CN
Pupillary light II III Corneal V and VII Ocvestibular reflex VIII and III,IV,VI Painful stimuli V VII Gag IX X Cough XX
Apnoea test
Increase fio2 to 1
ABG to calibrate ETCO2
Reduce minute volume until ETCO2 is 6 and ph 7.4 (sats 95%)
Disconnect and apneoic ventilation 5 mins either with oxygen or CPAP
Confirm increase paco2 more than 0.5kpa
Drugs used prior to organ donation
Vasopressin
Methylprednisolone 15mg/kg
T3
Absolute contraindications to donation
Cjd HIV disease Metastatic cancer Melanoma unless sumo,e Untreated TB Ages over 85
Vasopressin functions physiologically
Reabsorb water at collecting duct (plasma osmolality) Maintains circulating volume ACTH release Thermoregulation Circadian rhythm
Vasopressin receptors
V2 kidney at CD
V1 sm arteriolar (vasoconstriction)
Oxytocin like receptors in myometrium (vasoconstriction)
ACTH receptors pituitary (increase acth)
Pharm agents derived from vasopressin
Desmopressin DI VWD
Terlipressin varicella bleeding
Argipressin hypotensive or septic shock
Delirium
Delirium is acute syndrome
Deficits in attention and cognitive function
Hyper or hypo psychomotor activity
Disordered sleep wake cycle
Features of hyperactive delirium
Agitation
Delirium
Can’t follow commands
Hallucinations
How many types delirium
Hyper
Hypo
Mixed
Screening tools delerium
Cams ICU
4 AT
Delerium detection score
Patient factors predisposing to delerium
Increased age Dementia Depression Alcohol or drug withdrawal Visual impairment
Critical illness factors predisposing to dementia
Acidosis Hypothermia Sepsis Anaemia Metabolic disturbances
Apart from pharmacological management what other management of delerium
Orientation ie clocks Sleep hygiene Maintain physiological homeostasis Management of withdrawal phenomenon Medications review
Types of critical illness weakness
Polyneurpathy
Myopathy
Neuromyopathy
Things to rule out before diagnosis of CIW
GBS CNS infection Anterior spinal artery stroke MG LEMS Porphyria Drug induced weakness
Patient factors contributing to CIW
Age Female Multiple comorbidities Infection Mof iPpv Hyperglycemia Low albumin
Pharm factors contributing to CIW
Neuromuscular blockade
Long term steroids
Aminoglycosides
RRT
Motor findings in CIW
Symmetrical weakness
Reduced reflexes
Facial sparing
Mrc scale out of 60- 48 suggests a diagnosis
Investigations of weakness in icu
LP for csf
Nerve conduction
MRI
Muscle biopsy
Symptoms PE
Sob
Cp
Collapse
Signs of pe
Cyanosis
Tachycardia
Lous s2
Investigations in pe and what would be looking for
ECG sinus tachycardia Rv strain
Echo rv dikation , tricuspid regurgitation
Ctpa filling defect
Vq mismatch
Management massive PE
Fluid resuscitation Consider intubation and ventilation Thrombolysis is hypotension and RVF Dobutamine MDT input ie cardiology Therapeutic anticoagulati’n Thrombectomy
Point of care ultrasound in icu
Airway and vascular use pre tracheostomy Diagnostic lung ultrasound Poc echo Placement of drains Oesophageal Doppler Trasncranial doppler
Indications for tracheostomy
Airway obstruction Airway protection Pulmonary toilet Long respiratory wean Laryngectomy
Benefits of percutaneous tracheostomy technique
Avoid transfer
Reduced wound infection
Reduced early complications
Things to check or do pre tracheostomy
Who checklist Check coagulation NG stopped 6 hours US neck Check airway equipment Check laryngoscopy view
Complications of tracheostomy early & management to help
Bleeding - use la with adrenaline
Airway loss - 2 person procedure
Pneumothorax - under direct vision
Misplacement - under direct vision
What is nec fasc
Nec fasc is a subcutaneous infection through fasciae layers rapidly spreading leading to potential life threatening emergency
Risk factors nec fasc
Diabetes IVDU Malignancy Renal disease Obesity Peripheral vascular disease
Classification nec fasc
Anatomical
Type 1 poly microbial
Type 2 monomicrobial
Type 3 grams negative
Type 4 fungal
Diagnosis nec fasc
Clinical - pain more than expected, crepitus, bullae
Investigations raised inflammatory markers raised CK low calcium
CT air in fascia layers
Treatment nec fasc
Early diagnosis
Broad spectrum antibiotics including clindamycin for endotoxins
Debridement
Hyperbaric oxygen
Immunoglobulin (strep and staph)
Organ support fluid resus and vasopressors
Benefits early nutrition
Reduced mortality Reduced length of stay Improved muscle function Reduced duration weaning Psychosocial Reduced wound breakdown Reduced infection
Energy requirements per kg by artificial nutrition
Energy 25kal per kg
Carb 2 gram per kg Protein 1 Fat 1 Sodium 1-2 mol kg day Potassium 1 mol kg day Calcium and magnesium 0.1 Phosphate 0.4
Micronutrients ie zinc
Immune modulators
Positives enteral nutrition
Cheap
Reduced risk ileus
Reduced risk gastric ulcers Reduced infection
Negatives enteral nutrition
Micro aspiration
Displacement
Peg if more than 4 weeks
Define acute liver failure
Specific liver condition that evolves rapids,h into life threatening illness
Hallmarks are coagulopathy
Hepatic encephalopathy
Hyper acute vs acute vs subacute liver failure
Hyperacute less than 7 days is rapidly evolving but also offset faster
Acute 7-28 days
Subacute 28 days to 12 weeks - more insidious BUT prognosis often poor by time diagnosed
Grades encephalopathy
Grade 1 mild
Grade 2 disorientated
Grade 3 incoherent, somnolence
Grade 4 coma
Tests in acute liver failure
Intrahepatic tests ie LFTs, coagulation, ammonia
Extra hepatic ie u&e, Fbc
For cause Viral screen Autoantibodies ie ana for aih or anti mitochorndrial psc Paracetamol levels Pregnancy test
Management ALF
Early intubation and ventilation
Lung protective strategies but need to be balanced with cerebral protection
Fluids and vasopressors. Avoid terlioressin in acute use norad
Early renal replacement therapy if aki continous proffered
Treat intracranial hypertension and seizur3s
Coagulation abnormalities use TEG
Sepsis most common cause death so prophylactic antibiotics especially if on urgent transplant ,list
Treat hyperglycemia
Early enteral feeding as protein catabolism
Specific treatments
Refer to specialist centre early
NAC for paracetamol ( cysteine precursor of gluthione which neutralises NAPQI)
Steroids for autoimmune
Hep b lamivudine
Wilson’s penicillamine
? Plasma exchange
? Mechanical assist
Liver transplant definitive
Kings college criteria for paracetamol overdose liver transplant
Ph less than 7.25
Create more than 300
Inr more than 6.5 or PT more than 100
Grade 3 or 4 encephalopathy
Kings college non paracetamol guidelines
Inr more than 6.5 PT more than 100
Biki over 300
Jaundice to encephalopathy more than 7 days
Seronegative
