General ICM Flashcards
If a patient doesn’t respond to a fluid challenge, what does this mean?
- The patient is intravascularly full and another cause of shock should be sought
or - The patient is so hypovolaemic that not enough fluid has been given to result in a response
How can you assess whether a patient might be fluid responsive?
- Clinically - tachypnoea, tachycardia, hypotension, cool peripheries, end organ dysfunction - oliguria, confusion, arterial line swing
- Fluid challenge - 250mls fluid over 5 mins
- Straight leg raise
- CO monitoring
- ECHO - kissing ventricles, RV volume statu, IVC collapsibility/distensibility
What are the different methods of CO monitoring?
Non-invasive - ECHO, thransthoracic impedance
Minimally invasive - PICCO, LIDCO, flotrac, oesophageal doppler, TOE
Invasive - PAFC
Describe the PAFC
8 French calibre
110cm in length
Distal lumen used to measure PCWP and for sampling mixed venous blood
Proximal lumen at 30cm from tip that’s used to monitor CVP and to inject cold to measure CO by thermodilution
Thermistor 3.7cm proximal to tip
10cm long thermal filament which allows CO calculation without cold saline bolus
1.5ml balloon located at the tip
What is normal right atrium pressure?
3-8mmHg
What is normal RV pressure?
25/0-10 mmHg
What is the normal pressure in the pulmonary artery?
25/10-20 mmHg
What is the PCWP?
Trace from a branch of the PA
Similar to the CVP
4-12mmHg
Reflects left atrial pressure
What information is measured by the PAFC?
CO CVP RAP RVP PAP PCWP SvO2 Core temp
Which variables are derived from the PAFC?
CI SV SVI SVR SVRI PVR PVRI
What are mixed venous sats?
The oxygen sats of venous blood in the pulmonary arterial tree, after mixing with anatomical and physiological shunt
Exceeds the ScvO2 in healthy people as it samples from the SVC and the brain has a higher oxygen extraction ratio
In which situations might ScvO2 exceed SvO2?
- Anaesthesia
- TBI
- Shock
What are the complications associated with use of the PAFC?
CVC-related: Bleeding/haematoma, air embolism, vascular injury, arterial puncture, pneumothorax, tamponade
Floating catheter: arrythmias, tamponade, valvular trauma, misplacement, knotting
PAC in situ: VTE, pulmonary infarct, pulmonary arterial rupture
What is the evidence for PAFCs?
The PAC-man trial (2005) was an RCT that showed no difference in in-hospital mortality, ICU or 28-day mortality, or ICU of hospital LOS.
10% complication rate
No clear evidence of benefit or of harm
The authors concluded that they were most useful in undifferentiated shock, RVF and pulmonary HTN although the study was under powered for this
What is the doppler effect?
When a sound wave reflects off a moving object, the frequency shift is proportional to the velocity of the object - the basis for oesophageal doppler monitoring
How does oesophageal doppler work?
The US probe emits US waves that are reflected off RBCs travelling in the descending aorta, producing a velocity-time curve of blood flow
The stoke distance (the distance travelled by the blood in one heart beat) is then calculated
The aortic cross-sectional area is then determined from a normogram based on height and weight, and multiplied by the stroke distance to give stroke volume
Describe an oesophageal doppler probe
90cm long
Markers at 35, 40 and 45 cm to aid placement
The descending aortic doppler trace is normally obtained between 35-40cm
The probe must be directed posteriorly
What assumptions are made when using the oesophageal doppler?
- The angle of the probe to the direction of blood flow is constant
- The aortic CSA is constant throughout the cardiac cycle
- There is laminar flow within the aorta
- 70% of the cardiac output enters the descending aorta
In ODM what is the flow time corrected?
The time in milliseconds that the heart spends in systole, corrected for heart rate
A low value indicated high afterload and a low value indicates low afterload
In ODM, what is the stroke distance?
The distance that a column of blood moves along the aorta with each contraction of the LV - it’s the area under the velocity time curve - multiply by aortic CSA to get SV
In ODM, what is the mean acceleration?
The angle of the upslope
Used as a marker of LV contractility.
When should ODM be used?
Recommended by NICE perioperatively to guide fluid therapy
Studies show decreased complication rate and shorter LOS in hospital
What is delirium?
An acute change in consciousness and awareness that fluctuate with time?
What are the typical features of delirium?
- Disordered thinking
- Reduced attention
- Abnormal sleep/wake cycle
- Abnormal psychomotor activity
- Abnormal perceptions
- Abnormal emotional behaviour
What are the 4 diagnostic criterion for delirium according to the DSM IV?
a) disturbance in consciousness
b) change in cognition
c) acute
d) caused by the direct physiological consequences of a general medical condition, or drug/withdrawal induced
What is the ICD-10 definition of delirium?
a) clouding of consciousness
b) disturbance of cognition
c) psychomotor disturbances
- unpredicatble shifts from hypo to hyper activity
- increased reaction time
- increased or decreased speech
- enhanced startle reaction
d) sleep/wake disturbance
e) acute
f) underlying illness is responsible
What is the pathophysiology of delirium?
Neurotransmitter imbalance, with reduced acetylcholine and increased dopamine resulting in neuronal excitability
There may also be cerebral microvascular dysfunction following exposure to inflammatory mediators, or global failure of oxidative metabolism resulting in cerebral insufficiency
How common is delirium?
Very
70-80% of mechanically ventilated patients are affected
What are the subtypes of delirium?
- Hyeractive - confused, agitated, combative, aggressive, paranoid - 1%
- Hypoactive delirium - inattentive, stuporous, withdrawn, often mistaken for depression - 35%
- Mixed - 64%
What are the risk factors for the development of delirium?
- Patient factors
- age, comorbidities, baseline cognitive impairment, psychiatric history, alcohol or substance abuse - Illness related
- high APACHE II score, sepsis, hypoxaemia, metabolic derrangement, surgery esp CPB - Iatrogenic
- disturbed sleep/wake cycle, sedatives esp benzos, anticholinergic medication
What are the adverse consequences of delirium?
- Increased risk of short-term complications e.g. accidental extubation/line removal
- Medium term complications - increased LOS, increased duration MV, increased mortality (independent risk-factor for a 3-fold increase in mortality at 90 days)
- Long-term complications - risk of PTSD, risk of long-term cognitive impairments
How is delirium diagnosed on the ICU?
The 2 most widely used bedside scoring systems are
- Confusion assessment method (CAM) - ICU
- Intensive Care Delirium Screening Checklist (ICDSC)
Describe CAM-ICU
- Is the patient different from their baseline mental status? or has the patient had any fluctuaiton in mental status in the past 24 hours?
- Test of inattention - hand squeezing on the letter A >2 = positive
- Is the RASS score anything other than 0
- Disorganised thinking - e.g. will a stone float on water
Feature 1 plus 2 and either 3 or 4 present = CAM-ICU positive
What can be done to reduce the risk of delirium?
The ABCDE bundle (Vasilevskis et al 2010)
Awake and Breathing (daily sedation breaks and SBTs)
Choice of sedation - minimise medications that can provoke delirium e.g. benzos
Delirium monitoring
Early mobilisation
Plus, sleep hygiene, removal of invasive lines when no longer needed
What is the pharmacological management of delirium?
- Antipsychotics are the drug of choice for those posing risk to themselves e.g. haloperidol, olanzipine
- Use of dexmedetomadine as a sedation agent
What trials support use of dexmedetomidine for management of delirium?
- DahLIA trial (JAMA 2016) - double blind MC RCT. Showed a statistically significant reduction in median ventilator-free hours at day 7 and a significant decrease in antipsychotic use. Non-significant decrease in ICU LOS.
- Midex-Prodex trial (JAMA 2012) - DB MC parallel design that showed the non-inferiority of dexdor when compared to midaz or propofol. Duration of sedaiton was significantly shorter with dexdor. There was a non-significant decrease in ICU LOS.
What is drowning?
Primary respiratory impairment following submersion or immersion in a liquid medium, whatever the outcome.
The term near drowning is no longer used.
How id drowning classified?
According to the findings at the scene
- No evidence of aspiration
- Evidence of aspiration but with adequate ventilation
- Evidence of aspiration with inadequate ventilation.
- Absent ventilation and drowning
What cardiovascular pathophysiological changes occur as a result of drowning?
- The diving reflex. Stimulated by cold water to the face. Mediated via CN V1. Results in apnoea, bradycardia and vasoconstriction
- A massive cathecholamine surge during the diving reflex causing profound vasoconstriction, arrhythmias, pumonary oedem.
- Progressive hypoxaemia and hypothermia leading to bradycardia, pulmonary hypertension and cardiac failure
What neurological pathophysiological changes occur as a result of drowning?
Hypoxic brain injury
- starts within 5 minutes
- hypothermia not usually protective because its onset is unlikely to occur before the hypoxia starts
What are the metabolic consequences of drowning?
Hypothermia
No clinically significant differences in volume status, electrolytes or lung function in those who drown in fresh compared with salt water
What are the infective consequences of drowning?
Aspiration of contaminated fluid results in infection in up to 50%
Aerobic gram positive organisms (strep/staph) may be aspirated from the oropharynx
Aerobic Gram-negative organisms (e.g. Pseudomonas, Aeromonas, Burkholderia pseudomallei, Leptospira) may contaminate fresh water
Fungal infections including delayed CNS infections due to Aspergillus and Pseudallescheria boydii are a risk, esp in immunocompromised patients.
Describe the pathophysiology of drowning
Immersion or submersion results in panic, breath-holding, laryngospam, aspiration and swallowing of water. These lead to hypoxia, which eventually results in relaxation of laryngeal muscles. Hypercapnia and acidosis result in respiratory stimulation which result in aspiration. This results in direct alveolar toxicity - resulting in pulmonary oedema, surfactant washout and dysfunction resulting in atelectasis and bronchospasm.These all result in V/Q mismatch (shunt), reduced compliance and ARDS.
What are the risk factors for drowning?
- Age - 0-4 year olds may drown in the bath tub, or swimming pools e.g where fencing is inadequate. Adolescence when risk taking behaviour may occur.
- Male gender
- Intoxication
- Occupation/hobbies - scuba diving, farming, fishing
- Medical conditions - IHD, cardiomyopathies, arrhythmias, epilepsy, diabetes, depression
- Conditions increasing the risk of drowning - currents, rip tides, waves, cold water.
What is the immediate management of a drowning victim at scene?
- Remove from the water
- Consider whether spinal precautions are needed
- 5 rescue breaths
- Start chest compressions if there’s no response
- Compression only CPR is not appropriate in drowning
- Consider the effects of hypothermia
What is the immediate management of a drowning victim on arrival to hospital?
- ATLS approach - secure airway is needed, treat any life-threatening injuries
- Optimize oxygenation - lung protective ventilation, bronchoscopy may help to remove the aspirated debris
- Optimize cardiac output - fluid resus as likely to be hypovolaemic, may need vasopressors/inotropes
- Neuroprotective measures
- Temperature control
Is there any evidence for the use of ECMO in drowning?
A retrospective review published in Resuscitation 2016 (Burke et al) revealed 247 patients who received ECLS following drowning between 1986 and 2015. Cardiac arrest with ROSC prior to ECLS occurred in 34.8%, ECLS was initiated during cardiac arrest in 31.2% and 34% did not arrest prior to ECLS. Overall survival was 51.4%, with al increase in survival across all 3 categories. Veno-venous ECLS was associated with a better survival that veno-arterial ECLS in patients with cardiopulmonary failure. The presence of AKI and need for CPR during ECLS were associated with increased mortality.
What are the indicators for a poor prognosis in drowning victims?
- Submersion > 5-10 minutes
- Resuscitation not attempted for > 10 minutes after resuce
- > 25 minutes of resuscitation
- GCS < 5 or unreactive pupils on arrival to hospital
- Pulseless and apnoeic on arrival to hospital
- pH < 7.10 on initial blood gas
What determines stroke volume?
- Preload
- Afterload and SVR
- Myocardial contractility
What does preload depend on?
Ventricular end-diastolic volume (EDV), which is governed by the volume and pressure of blood returning to the heart.
Haemorrhage, sepsis, anaphylaxis and raised intra-thoracic pressure are all common causes of inadequate preload.
What increased afterload?
Valve stenosis, hypertension, high SVR, low intrathoracic pressures and ventricular dilatation
What are the two types of failure of myocardial contractility?
- Systolic dysfunction
2. Diastolic dysfunction
Describe systolic dysfunction
- Inadequate systolic ejection which is a result of reduced contractility (e.g. ischaemia, cardiomyopathy) or increased impedence (e.g. hypertension, aortic stenosis). Increasing EDV will maintain SV provided myocardial reserve is adequate, otherwise SV and CO will fall and inotropes will be required.
Describe diastolic dysfunction
Characterised by reduced ventricular compliance with impaired diastolic filling (i.e. stiff ventricle). It may be caused by mechanical factors e.g. restrictive cardiomyopathy, or impaired relaxation due to myocardial ischaemia or severe sepsis.
- The resulting increase in end-diastolic pressure and associate venous congestion can cause characteristic ‘flash’ pulmonary oedema
Why are diabetics at increased risk of diastolic dysfucntion?
Endomyocardial ischaemia caused by small vessel arteriopathy
Why are renal failure patients at increased risk of diastolic dysfunction?
Hypertension - blood flow from the epicardium to endomyocardium is impeded by ventricular wall hypertrophy and the resulting ischaemia impairs ventricular relaxation
What are the ethical principles that govern management of donation after cardiac death prior to withdrawal of life-sustaining support?
- No treatment aimed at organ donation should be started prior to the decision to withdraw being made.
- Maintenance of life-sustaining treatment can be considered in the best interests of patients who wanted to be donors if this facilitates donation and doesn’t cause harm or distress.
- Agents can be used to maintain arterial pressure
- It’s not appropriate to initiate treatment against the wishes of the family
What is the process of OD after circulatory death?
- Withdrawal of life-sustaining treatment one retrieval team and family are ready.
- Following cessation of cardio-resp function there is a 5 minute window to confirm monitored asystole prior to certification
- The relatives have 5 minutes to spend with the patient prior to transfer to the OT
- For lung donation reintubation is required and lungs are recruited with a single breath and CPAP maintained with 100% O2. Ventilation is reinstated once the chest has been opened and the aorta clamped.
What is functional warm ischaemia?
Starts when the SBP falls below 50mmHg of sats < 100%. Stand-down times from the onset of FWI vary by organ and by receiving centre. Approx times are:
- Liver 30 mins
- Pancreas 30 mins
- Lungs 60 mins from FWI to reinflation
- Kidney 120 mins
What is the Maastricht classification of donation after cardiac death
There are 2 principle types of DCD - controlled and uncontrolled
1 - uncontrolled - dead on arrival
2 - uncontrolled - unsuccessful resus
3 - controlled - cardiac arrest following planned withdrawal
4 - either - cardiac arrest in a patient who is drain dead
5 - uncontrolled - cardiac arrest in hospital inpatient
What are the absolute contra-indications to organ donation?
Absolute:
vCJD
HIV disease
Unlikley to be accepted:
- Active invasive cancer in the past 3 years excl non-melanoma skin cancer and primary brain tumour
- Primary intracerebral lymphoma
- All secondary intracerebral tumours
- Haematological malignancy
- Melanoma
- Untreated systemic infection
- Active and untreated TB
- West Nile virus
- History of Ebola infection
There is no upper or lower age limit
What are the main disorders of consciousness?
- Coma
- Vegative state
- Minimally conscious state
What is a coma?
- A state of absent wakefulness and absent awareness
- Unrousable unresponsiveness lasting > 6 hours
- Can’t be awakened
- Fails to respond to pain, light and sound
- Lacks normal sleep-wake cycle and
- Does not initiate voluntary actions
What is a vegatative state?
- Wakefulness with absent awareness
- Severe cortical damage with preservation of some brainstem activity
- Preserved capacity for spontaneous or stimulus-induced arousal, evidenced by sleep-wake cycles and a range of reflexive and spontaneous behaviours
- Complete absence of environmental awareness or awareness of self
What is a minimally conscious state?
- Wakefulness with minimal awareness
- A state of severely altered consciousness in which minimal but clearly discernible behavioural evidence of self or environmental awareness is demonstrated.
- Inconsistent by reproducible responses above the level of spontaneous or reflexive behaviour.
What are the causes of disordered consciousness?
- TBI
- Vascular event - ICH, SAH, CVA
- Toxic/metabolic - alcohol, drugs/poisons, anaesthetics, benzos, hypoglycaemia, hyper or hypo-osmolar states
- Infection - encephalitis, abscess, vasculitis, sepsis
- Hypoxia
- Systemic illness - liver failure, renal failure, endocrine
How would you manage a patient presenting with disordered consciousness?
ABCDE approach
Intubation to protect the airway if GCS < 9
Indentify cause - BM, u+es, LFTs, ammonia, FBC, TFTs, ABG, culture, CT/MRI, consider LP
Maintain normal physiology - o2, BP, correct hypoglycaemia, correct hypo/hyperthermia, correct electrolyte abnormlities
Review meds
EEG
Detailed neurological assessment
ICP management if needed
How can you prognosticate in hypoxic brain injury following cardiac arrest?
- Should start 72 hours after ROSC
- Exclude confounders
- If M1-2 and no pupil or corneal reflexes or bilateral absent SSEPs ->poor outcome very likely (FPR < 5%, 95% CI)
- If these criteria aren’t met them two or more of the following also suggest likely poor outcome
- status myoclonus < 48 hours after ROSC; High NSE level, Unreactive birst-suppression or status on EEG, diffuse anoxic brain injury on CT.
What EEG features suggest poor outcome following cardiac arrest?
- Absence of EEG reactivity to external stimuli
- Presence of burst suppression
- Status epilepticus
What is locked in syndrome?
Results from brain stem pathology that disrupts voluntary control of movement
Wakefulness and Awareness are both still preserved
Able to communicate by blinking
What is sepsis?
A life-threatening organ dysfunction caused by a disregulated host response to infection
(SEPSIS-3 definition, published in JAMA 2016)
What is septic shock?
A subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality that with sepsis alone
- Identified clinically by vasopressor requirement, or lactate > 2
- The combination is associated with an in-hospital mortality of > 40%
What is the qSOFA score?
Used as a quick bed-side guide to diagnosing those with poor outcomes due to sepsis, if they have 2 or more of the following
- RR > 21
- SBP < 100
- GCS < 15
What is the pathophysiology of sepsis?
- Vasoldilatation (iNOS causes endothelial NO production)
- Loss of endothelial integrity due to inflammatory mediator-related disruption of the tight junctions
- Reduced cardiac contractility
- Activation of the coagulation cascade and fibrinolysis due to IL-1,6 and TNF-a
- Mitochondrial dysfucntion - results in reduced O2 utilisation
What are exotoxins?
Peptides secreted by Gram +ve bacteria
What are endotoxins?
Located within the Gram -ve bacterial cell walls
How should sepsis be manages?
- Measure lactate, Obtain cultures, administer broad-spectrum antibotics
- 30mls/kg IV fluid for hypotension/ lactate > 4
- if hypotension persists then vasopressors to maintain MAP > 65 and reassess fluid status e.g. CVP, ScvO2, ECHO, SLR, LiDCO
What is brain death?
A complete and irreversible loss of brain and brainstem function as a result of neurological injury. The heart is still beating but respuratory function is dependent on a ventilator.
The Academy of the Medical Royal Colleges Uk outlines 3 essential components
-1. Fulfilment of essential preconditions
-2. Exclusion of potentially reversible causes of coma
-3. Formal demonstration of coma and apnoea.
What are the preconditions for brainstem testing?
- Pt should be deeply unconscious, apneoic and mechanically ventilated
- Irreversible brain damage of known aetiology
What are the exclusion criteria for brainstem testing?
Ensure that coma is not secondary to reversible factors such as CNS depressant drugs, biochemical/metabolic abnormalities or hypothermia.
What approaches are there that can help exclude drug intoxication being the cause of a coma?
- A period of observation 2-3 times the elimination half-life of the drug in question
- Administration of specific antagonists
- Plasma analysis
- Confirmatory test to confirm absence of cerebral flow/perfusion
What are the potentially reversible causes for coma?
- Circulatory - ensure MAP > 60
- Respiratory - ensure normal pH, PCO2< 6, PO2 > 10
- Metabolic - ensure temp > 34
- Biochemical - ensure Na 115-160, K > 2, Mg 0.5-3, Po4 > 0.5, gluc 3-20
Which agents can you carry out a plasma analysis on to ensure that they are not the cause of a coma?
- Midazolam - brainstem testing should not take place if levels > 10 micrograms/litre
- Thiopentone - brainstem testing should not be done if levels > 5 mg/l
Who can perform brainstem death testing?
2 competent clinicians who have held GMC registration for > 5 years, one of whom must be a consultant
What does brainstem testing test for?
- It assesses the integrity of the sensory and motor pathways of the cranial nerves reflexes
- An apnoea test.
Describe the assessment of the cranial nerves in brainstem testing
- Pupillary reflex (afferent II, efferent III) - check for direct and consensual reflexes
- Corneal reflex (afferent V, efferent VII) - the cornea os brushed lightly with a swab
- Response to painful stimuli (Afferent V, efferent VII) - a painful stimulus is applied to the supraorbital ridge
- Vestibulo-ocular reflex (afferent VIII, Efferent III, IV, VI)- visualise the TM prior to beginning the test. Instil 50mls ice cold saline into each external auditory meatus in tuen, looking for eye movements/nystagmus
- Gag reflex (afferent IX, efferent, X) - the pharynx is stimulated with a spatula/similar
- Cough reflex (afferent X, efferent X) - a bronchial catheter is passed down the ET tube to stimulate the carina
How do you carry out the apnoea test for brainstem testing?
- Increase FiO2 to 1.0
- Perform ABG to confirm measured PaCO2 and SaO2 correlate with monitored values
- decrease the MV until ETCO2 > 6. Check PaCO2 > 6 and pH < 7.4 on ABD
- Maintain apnoeic oxygenation by either instilling 5L O2 per minute via suction catheter of by using CPAP
- Five minute observation to look for the presence of spontaneous resp activity
- Perform final ABG to confirm an increase in PaCO2 of > 0.5kPa
Following the test the ventilator should be recorrected and any acid-base abnormality corrected prior to carrying out the second set of tests. There is no defined time period between the 2 sets.
When is legal time of death?
The time at which the first set of tests was completed
In which circumstances might you not be able to confirm brainstem death via clinical tests alone?
- Inability to exclude the influence of sedatives
- High cervical cord injury
- severe maxillofacial injury
What auxiliary tests can be carried out to establish brainstem death where clinical testing alone cannot be used?
- Measure brain electrical activity
- EEG - little value in hypothermia or drug intoxication as these factors suppress neuronal activity
- SSEPS - peripheral stimulus to median nerve looking for response at the contralateral primary sensory cortex - Flow studies
- cerebral angiography - reveals absence of intracerebral filling beyond the entry of the carotid and vertebral arteries into the skull
- transcranial doppler - useful only if a reliable waveform is found - complete absence of flow may not be reliable if inadequate windows exist
Why might patients with haematological malignancy require critical care admission?
- Neutropenia and sepsis
- Resp failure - infection, pulmonary oedema/haemorrhage/infiltration by underlying disease
- Tumour lysis syndrome
- Graft vs host disease
- Complications of chemotherapy and stem cell transplant
- CNS dysfunction and seizures - hyperviscosity syndrome/intracerebral bleed or thrombosis, underlying malignancy, electrolyte imbalance
- GI dysfunction including neutropenic enterocolitis (typhlitis)
- Acute renal failure - nephrotoxic drugs/sepsis/underlying disease
How does NICE define neutropenia?
Neutrophil count < 0.5 x 10(9)/l
How does NICE define neutropenic sepsis?
Neutropenia and clinical signs of infection OR temp > 37.9
What precautions should be taken when looking after a neutropenic patient to reduce risk of sepsis?
- Reverse barrier nursing
- Positive pressure side room isolation
- Avoid invasive procedures where possible
- Avoid rectal exam/rectal temp probe insertion
- Meticulous oral hygiene
What are the principles of management for a patient with neutropenic sepsis?
ABCDE aproach
- History and exam - including pets/exposure/hobbies/travel/occupation/invasive lines. Examine for infection ensuring you check oropharynx, skin and perirectal areas.
- Follow surviving sepsis guidelines - cultures, antibiotics, lactate, bloods, fluid and vasopressors as needed
- Imaging - CXR and any abdo imaging as necessary
What should an antibiotic regime for neutropenic sepsis include?
- IV anti-pseudomonal B-lactam e.g. piperacillin-tazobactam or meropenem
- Additional antibiotics (e.g. aminoglycoside) if Gram-negative or resistant organisms suspectd, or if hypotensive or potential respiratory infection
For those anaphylactic to penicillin alternatives include ciprofloxacin and clindamycin, or vancomycin and aztreonam
What is tumour lysis syndrome?
Metabolic derangement that occurs when large volume tumour cells are lysed, usually following chemotherapy. Typically a/w acute leukaemia and high-grade lymphomas
Metabolic derangement include hyperkalaemia, metabolic acidosis and renal failure, severe hypocalcaemia and hyperphosphataemia can occur and increased serum and urinary urate levels are seen
What is the treatment of tumour lysis syndrome?
ABCDE approach
- Aggressive fluid resuscitation
- Treat hyperkalaemia
- Rasburicase (a recombinant urate oxidase enzyme which reduces plasma uric acid concentration)
What complications of a stem cell transplant may result in ICU admission?
Early (< 100days)
-infection, haemorrhage, acute GvHD, interstitial pneumonitis, aplastic anaemia secondary to graft failure
Late complications
-chronic GvHD, chronic pulmonary disease, infections, autoimmune disorders
What is host vs graft disease?
An immune-mediated disease following allogenic haematopoietic cell transplant (and transplant of solid organs containing lymphoid tissue) that results from a complex interaction between donor and recipient adaptive immunity (APCs of the recipient interact with the mature T-cells of the donor). It can occur even when the donor is perfectly matched
How does acute host vs graft disease present
Typically with enteritis, hepatitis and dermatitis
Diagnosis can be histological (skin, liver, rectal) or by using a clinical diagnosis and staging system
How does chronic GvHD present?
Diverse syndrome with varying clinical features resembling autoimmune disease e.g. sclerodermia, primary biliary cirrhosis, bronchiolitis obliterans and chronic immunodeficiency.
What are the treatment options for GvHD?
- High dose steroids
- Immunosuppressant e.g. ciclosporin
- Parenteral nutrition may be required to facilitate gut rest
What is typhlitis?
Neutropenic enterocolitis
Life-threatening complication of chemotherapy
Symptoms include nausea, abdo pain and distension, fever and chills
Poor prognosis and successful treatment depends on an early diagnosis achieved with a high index of suspicion and use of CT imaging. Elective right hemicolectomy may be required to prevent recurrence.
What are the aims of fluid resuscitation?
- Replace normal fluid and electrolyte losses
- Maintain BP, cardiac output and tissue perfusion to satisfy metabolic needs, aid temperature regulation and facilitate waste removal
- Replenish substantial defects or ongoing losses
- Avoid excessive tissue oedema
What is compartmental distribution of water dependent on?
- Osmotic pressure exerted by small diffusible ions e.g. Na
- Osmotic pressure reflects ion concentration gradients between compartments created by cellular ion pumps, e.g. Na and Cl that are mainly extracellular and K and PO4 that are intracellular
e. g. saline increased extracellular Na and Cl, raising ECF osmotic pressure and attracting water out of the intracellular compartments in to the ECF
What does intravascular volume depend on?
- Plasma oncotic pressure - which is the ability of large plasma proteins to bind and retain water in the circulation. POP is normally ~ 3.4kPa with 75% of the effect due to albumin, 20% Hb and 5% globulins. 1g albumin ‘binds’ about 18mls water, thus intravascular albumin binds ~ 2.25L of plasma water
- Vascular permeability - normal albumin leakage across capillary membranes is limited to 4-5% per hour by its high MW and negative charge. Thus all of the normal intravascular albumin leaks into the ISF each day. It returns via the lymph and thoracic ducts at the same rate. Inflammation increases vascular permeability and albumin leakage by up to 300%. Acute illness also decreases production of albumin by 15g/day. Low albumin reduces intravascular volume, and increases in ISF albumin causes oedema
- Circulatory hydrostatic pressure - increases leakage of intravascular water, whilst plasma oncotic pressure draws water into and maintains plasma volume
What is the normal daily water requirement?
1.5-2.5L /day
What is the normal Na requirement /day?
~70-100mmol
1-1.5mmol/kg/day
What are the normal K requirements/day?
40-70mmol/day
0.5-1mmol/kg/day
What is normal urine osmolality?
620-740 mosmol/dau
What is the compartmental breakdown of fluid?
60% of body weight
~42L in a 70kg man
~25L = IC and 15-17L = EC
The ECF comprises ISF 11-13L and intravascular plasma 3-4L
What is HUS?
Haemolytic uraemic sydrome It's a triad of 1. Microangiopathic haemolytic anaemia 2. Thrombocytopenia 3. Renal failure
What causes HUS?
There are 2 causes - epidemic and atypical. The epidemic form is a/w a prodromal illness and bloody diarrhoea following infection with verotoxin-producing enterococci (E.coli 0157) or Shigella
Atypical is much rarer and has a poorer prognosis. It may occur following
-step pneumoniae, CMV or HIV infection
-bone marrow transplant/solid organ transplantation
-drug exposure e.g. quinine, heroin, ciclosporin
-malignancy
-pregnancy
What is the pathophysiology of HUS?
Following ingestion of the toxin bloody diarrhoea occurs as a result of haemorrhagic colitis. AKI develops as a result of direct injury to the renal vascular endothelium secondary to toxin production. This leads to excessive platelet aggregation, platelet microvascular thrombin and ultimately AKI. Subsequent HTN and fluid overload are common
-In atypical HUS there is often dysregulation of the complement system
What investigations would you carry out in someone suspected of having HUS?
- Bloods
- FBC and film: looking for reticulocytes, evidence of haemolysis and thrombocytopenia
- Direct Comb’s test: differentiate between immune and non-immune mediated
- Lactate dehydrogenase (LDH, raised in haemolysis)
- U+Es (AKI)
- LFTs: including split bilirubin
- Clotting- incl fibrinogen and d dimers
- HIV and hepatitis serology
- Full renal screen: autoimmune and vasculitis screen - Stool MC+S
- Urinalysis
- Consider renal imaging to rule out other causes of AKI
How would you manage a patient with HUS?
ABCDE aproach Specific: 1. O2 2. Fluid and electrolyte balance 3. CV support/BP control 4. Renal and haematology input early 5. Treat the cause - cipro for e.coli and shigella 6. Plasma exchange - PEx is often used as HUS can be difficult to distinguish from thrombotic thrombocytopenia purpura initially, recommended in atypical HUS. In epidemic HUS PEx, IVIg, steroids and anti platelets have not proved beneficial
What is the prognosis in HUS?
Mortality rate is 3-5%
70-85% with epidemic HUS recover normal renal function
Atypical HUS has poorer prognosis with an initial mortality of ~25%, and up to 50% progressing to ESRD.
How does HUS differ clinically from TTP?
They are considered a spectrum of the same disease process
TTP is a malignant condition with a mortality of >90% if untreated
It’s a clinical diagnosis characterised by:
1. Thrombocytopenia
2. MAHA (microangiopathic haemolytic anaemia)
3. Fluctuating neurological signs (due to endothelial injury in the cerebral circulation)
4. Renal impairment
5. Fever
Clotting is usually normal - DIC is a late, ominous sign.
What is the underlying pathology in TTP?
The hallmark in TTP is deficiency of von Willebrand factor-cleaving protease, which may be genetic or acquired.
vWF is a large glycoprotein present in the plasma whose functions include binding factor VIII, and activating and binding platelets in response to endothelial injury. It is produced in the endothelium as ultra-large multimers that are inactivated when cleaved by the vWF-CP. In TTP, these multimers are not cleaved and there is uncontrolled platelet activation. Fibrin is deposited and thrombus propogated creating ischaemia distally, and red cells are shredded as they pass the fibrin/platelet mesh (i.e MAHA)
How is TTP managed?
Specific interventions are recommended by the British Committee for Standards in Haematology
- PEx using Octaplas, this should continue daily for at least 2 days after platelet counts recover. This removes the autoantibodies from the circulation and replaces their plasma with plasma containing normal levels of vWF-CP
- Adjuvant high-dose pulsed methylprednisolone can be considered. Has been shown to improve outcome but not RCT of PEx and steroids vs Pex alone
- Rituximab - used in life-threatening TTP and in patients with refractory or relapsing disease
- Low dose aspirin when plts > 50
- Supportive measures - RBC and folate supplementation during active haemolysis, plt transfusions are contraindicated unless life-threatening haemorrhage, routine thromboprophylaxis once plts > 50.
What is normal serum sodium?
135-145 mmol/l
What is total body sodium?
60mmol/kg
Where is Na absorbed?
Small intestine
In the kidney, what influences sodium reabsorption?
- Renin-angiotensin-aldosterone system
- ADH
- Thirst
- B-adrenoreceptor stimulation at the PCT
In the kidney which parts reabsorb which %s of sodium?
70% PCT
20% thick ascending loop of Henle
5% DCT
3% collecting duct
How do you classify hyponatraemia?
Typically classified according to the tonicity of the extracellular fluid/plasma osmolality and the patients volume status - specifically hyper-, eu- and hypovolaemia
What is true hyponatraemia?
Low sodium level in the presence of hypoosmolality
Hyponatraemia occurring without hypoosmolality is referred to as pseudohyponatraemia (occurs secondary to elevated levels of lipids or proteins)
Describe hypovolaemic hyponatraemia
TBW and total body sodium are low, but there is a disproportionate loss of sodium compared to water. e.g. increased ADH secretion in hypovolvaemic states (vomiting, diarrhoea, xs sweating).
Urinary sodium differentiates renal vs extra-renal losses: urinary sodium < 20 suggests an extra renal cause
Describe euvolaemic hyponatraemia
The most common category of low sodium in hospital patients. Causes include:
SIADH, glucocorticoid deficiency, hypothyroidism, low solute intake (e.g. beer potomania), psychogenic polydipsia.
describe hypervolaemic hyponatraemia
Essentially due to dilutional hyponatraemia. Oedema is seen as a result of impairment of the kidneys ability to excrete water maximally. There is paradoxical increase in total body sodium, but a simultaneous and proportionally larger increase in total body water.
Causes include:
Nephrotic syndrome, CCF, cirrhotic liver disease
What is the pathophysiology of the neurological signs seem in hyponatraemia?
Result from changes in the osmotic gradient that develops between the intracellular and extracellular fluid compartments producing tissue oedema. The effects of this tissue swelling are clinically most pronounced in the brain, where the non-compliant skull combined with lack of adaptive mechanisms means raised ICP can be rapidly devastating. This is particularly important in patients with severe hyponatraemia that has occurred over hours, when convulsions, coma and death secondary to cerebral herniation can result.
If you have low sodium and a plasma osmolality that is high (>295) what are the potential causes?
Due to shifts of water out of cells due to osmotic gradient
e.g. due to:
Hyperglycaemia
Mannitol
If you have a normal osmolality but low sodium what is the cause?
Pseudohyponatraemia - increase in the non-water component of plasma results in a falsely low reading e.g. hyperlipidaemia, hyperproteinaemia
If you have a low serum osmolality (<285), are hypovolaemic and have a low urinary sodium (<20) what are the possible causes of hyponatraemia?
Vomiting, diarrhoea, sweating, burns, pancreatitis
If you have a low serum osmolality (<285), are hypovolaemic and have a high urinary sodium (>20) what are the possible causes of hyponatraemia?
Diuretics
If you have a low serum osmolality (<285), are euvolaemic and have a low urinary sodium (<20) what are the possible causes of hyponatraemia?
Low solute intake
Polydipsia
If you have a low serum osmolality (<285), are euvolaemic and have a high urinary sodium (>20) what are the possible causes of hyponatraemia?
Hypothyroidism
Adrenal insufficiency
SIADH
If you have a low serum osmolality (<285), are hypervolaemic and have a low urinary sodium (<20) what are the possible causes of hyponatraemia?
CCF
Nephrotic syndrome
Cirrhosis
If you have a low serum osmolality (<285), are hypervolaemic and have a high urinary sodium (<20) what are the possible causes of hyponatraemia?
Renal failure
How would you manage a severely hyponatraemic patient presenting with seizures?
ABCDE approach
3% hypertonic saline until symptoms subside
The aim is to address the cerebral oedema but not to normalise sodium. Increasing the Na by 4-6 mmol/l or a level of about 120 is normally sufficient to reverse the most severe manifestations of acute hyponatraemia.
It is possible to calculate the expected change in sodium concentration on the basis of the volume of and rate at which the hypertonic saline is infused
Admit to critical care and monitor sodium levels 1-2 hourly.
The rate of increase shouldn’t exceed 8-10 mmol/l in a 24hour period.
What is central pontine myelinolysis?
Rare neurological disorder characterised by symmetrical midline demyelination of the central pons. Extrapontine lesions can occur in the basal ganglia, internal capsule, lateral geniculate body and cortex. Symptoms include motor dysfunction, respiratory paralysis, mental state changes and coma.
Osmotic demyelination is the major risk associated with excessively rapid sodium correction.
Who is at high risk of central pontine myelinolysis?
Malnourished Alcoholics Burns victims Hypokalaemia Na change > 12 mmol/24 hours.
What is SIADH?
Failure to suppress ADH production in lowered osmolality states
This results in disproportionate water retention compared with sodium.
What are the causes of SIADH?
Drugs: hypoglycaemic agents, antipsychotics, antidepressants, chemo esp vincristine and cyclophosphamide
Malignancy: Lung (esp small cell), brain, neck, duodemun, pancreas
CNS disorders: Infection, trauma, ischaemia, haemorrhage
Pulmonary disorders: Pneumonia, acute respiratory failure
Pain: Can mediate an increase in ADH secretion post-op
How do you treat SIADH?
- Fluid restrict aiming for slow rise in Na of 1-1.5 mmol/l/day
- If symptomatic - hypertonic saline 1.8%
- Demeclocycline 600-1200mg/day to inhibit the renal response to ADH (i.e it induces nephrogenic DI)
- ADH receptor antagonists are available e.g. conivaptan
Define ICU-acquired weakness
Clinically detectable weakness in critically ill patients in whom there is no plausible aetiology other than critical weakness
The underlying pathology may be myopathy, neuropathy or a mixture of both. The clinical presentations of each are indistinguishable
What are the risk factors for ICU-acquired weakness?
- Severe sepsis and MOF
- Prolonged MV
- Excessive sedation
- Muscle immobilisation
- Use of corticosteroids
- Neuromuscular blockade
- Hyperglycaemia
How is muscle weakness assessed?
Symmetrical, flaccid tetraparesis with sparing of the facial muscles
Motor weakness can be assessed using the MRC sumscore. Three muscles in both upper and both lower limbs are assessed and each graded from 0-5. A sum-scors of < 48 suggests polyneuromyopathy.
Which movements are tested in the MRC sum-score for ICUAW?
Arm abduction Flexion at elbow Wrist extension Hip flexion Extension at the knee Foot dorsiflexion
What is the differential diagnosis of ICU-acquired weakness?
- Guillain-Barre syndrome
- Myasthenia gravis
- Lambert-Eaton syndrome
- Motor neurone disease
- Spinal cord injury
- Rhabdomyolysis
- Drug-induced weakness
- Myopathy/myositis
- Infective causes, including botulism
How is ICUAW investigated?
- Lab tests: infl markers, ESR, electrolytes, CK, auto-antibodies, B12 level; LP
- Imaging - MRI brainstem and spine
- Neurophysiological investigations - Nerve conduction studies. CIM: normal; CIPN decreased compound muscle action potential and sensory action potentials with noraml conduction velocity. Electromyography: pts need to be fully compliant. Typical patterns of myopathic EMGs are motor unit potentials with small amplitudes and short duration.
- Muscle biopsy - only indicated where there is diagnositic uncertainty. Excludes other diagnoses. Allows subclassification into the 3 morphological subtypes 1. unspecific and uncomplicated CIM; 2 thick filament myopathy; 3 acute necrotising myopathy
How is ICUAW managed?
MDT supportive approach
Focus on prevention and avoidance of risk factors
Early mobilisation, sedation weaning protocols, daily physical and occupaitonal therapy
Optimise nutrition, correct electrolytes
Minimise steroids and neuromuscular blockade
Strict glycaemic control is the only strategy that has been shown to reduce the incidence of critical illness polyneuropathy - although this is in conflict with the conclusions drawn from the NICE-SUGAR trial.
What is HIV?
A cytopathic retrovirus that preferentially infects CD4-receptor positive (CD4+) T helper cells
This results in reduced immune surveillance and increased susceptibility to opportunistic infections and malignancy
What is AIDS?
Acquired immunodeficiency syndrome (now call HIV-related disease) is defined as a CD4 count < 200cells/mm3 in a person infected with HIV, or the presence of an AIDS defining illness
How is HIV classified?
According to the CDC:
Group 1 - acute seroconversion illness - occurs soon after infection, although most patients are asymptomatic. There is a high viral load, but there is a 3 months period where anti-HIV IgG antibodies are not detectable in the blood
Group 2- Asymptomatic infection - most people with HIV remain asymptomatic, the virus reproduces at a slow rate. Approx 10% will develop AIDS within the first 3 years, the remainder progress with a median of 10 years
Group 3- persistent generalised lymphadenopthy
Group 4 - Symptomatic HIV infection. Untreated patients with AIDS typically survive 3 years.
How do patients with HIV present to critical care?
- Resp failure - Pneumocystis jirovecii penumonia (PCP); exacerbations of chronic lung disease; bacterial pneumonia
- TB
- Cardiovascular disease - IHD is common - which may be attributable to HAART; endocarditis and myocarditis esp in IVDUs
- Liver failure - often due to coninfection with hep b or c. NrTIs and NNRTIs may cause hepatotoxicity
- Gastro - CMV colitis and cryptosporidial diarrhoea; GI bleeding secondary to ulcer,lymphoma or kaposis sarcoma; AIDs cholangiopathy; pancretitis
- Renal failure - HIV-associated nephropathy; diabetes and hypertension are common
- Neuro - meningoencephalitis, SOL incl toxoplasmosis, aspergillomas, abscesses or lymphoma; progressive multifocal leucoencephalopathy
What is the prognosis of patients with HIV admitted to ICU?
A poor prognosis is a/w
- high apache 2 score
- organ failure
- AIDS - defining illness
- sepsis
What is PCP?
Pneumocystis pneumonia is caused by the yeast-like fungus Pneumocystis jirovecci
It has a slow and indolent course
Presents with SOB, fever and dry cough
CXR may reveal diffuse granular opacities resembling ARDS, penumoatoceles or pneumothoraces
Definitive diagnosis is based on presence of organism in samples of induced suptum or from BAL or lung biopsy
How is PCP treated?
IV co-trimoxazole for 2-3 weeks +/- IV pentamidine
Second line is primaquine +clindamycin; atovaquone; trimethoprim +dapsone
Steroids given within 48-72 hours of diagnosis reduce the risk of respiratory failure, meachanical ventilation and death and are indicated if:
PaO2 < 9; A:a > 5
How is HIV treated?
Normally involves 3 antiretrovirals (ARV) - most commonly 2 NRTIs plus a protease inhibitor
describe necleoside reverse transcriptase inhibitors (NRTIs)
ARV drig
e.g. Lamivudine and zidovudine
Act as a false nucleotide and functions as a competitive inhibitor
s/es lactic acidosis, hepatic steatosis, rhabo
Describe non-nucleoside reverse transcriptase inhibitors (NNRTIs)
ARV drug
e.g. nevirapine
binds to reverse trascriptase and inhibits enzyme activity
s/es - hepatotoxicity
Describe protease inhibitors
ARV drug
e.g. saquinavir
Prevents processing of viral proteins
s/e/ SJS, dyslipidaemias
Describe fusion inhibitors
ARV drug
e.g. enfurviratide
Blocks fusion of HIV virus with host cell membranes
s/e/ GI side-effects
What are the challenges of HIV treatment on the ICU?
Continue pre-admission HAART
Input from ID/HIV pharmacist
1. Drug delivery - only zidovudine has an IV preparation. Others are tablets/capslues that can be crushed and used NG
2. Absorption may be affects by pathology. NG feed has to be interrupted to give certain ARVs. Gastric alkalinsation is CI’d with some ARVs
3. Dosing - changes in hepatic insufficiency and renal impairment
4. Interactions - benzos should be used with causiton with NNRTIs. NRTIs interact with numerous agents incl benzos, amiodarone, PPIs and H2RAs
5. Toxicity - can result in severe and life-threatening side-effects incl SJS, heoatic necrosis, pancreatitis and lactic acidosis
6. Immune reconstitution inflammatory syndorme (IRIS)
When should HAART be initiated in the HIV patient on ICU?
- AIDS-defining illness
- CD4 < 200cells/mm3
- Anticipated prolonged stay
- Deterioration despite optimal ICU management
Which patients can we test for HIV?
If knowledge of HIV status will make a difference to the treatment of a patient without capacity then it should be done
What is immune reconstitution syndrome?
There is a risk of precipitating IRIS on initiation HAART
Immune function begins to recover and then responds to the previously acquired opportunistic infection with an overwhelming inflammatory response
Treatment should be initiated against the offending organism. Supportive care is used and steroids are given in severe cases.
What are the AIDS - defining illnesses?
Candidiasis of the esophagus, bronchi, trachea, or lungs (but NOT the mouth) Cervical cancer Coccidioidomycosis Cryptococcosis, Cryptosporidiosis, Cytomegalovirus disease (other than liver, spleen, or nodes) Cytomegalovirus retinitis (with loss of vision) Encephalopathy, HIV related Herpes simplex: chronic ulcer Histoplasmosis Kaposi sarcoma Lymphoma, Burkitt's (or equivalent term) Lymphoma Mycobacterium avium Mycobacterium tuberculosis Mycobacterium, other species Pneumocystis jiroveci pneumonia Pneumonia, recurrent Progressive multifocal leukoencephalopathy Salmonella septicemia Toxoplasmosis of brain Wasting syndrome due to HIV
What is the definition of ARDS?
2012 Berlin definition:
-ARDS is an acute diffused, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight and loss of aerated lung tissue with hypoxaemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.
What is the oxygenation criteria for mild ARDS?
PaO2/FiO2 200-300mmHg (26.7-40kPa) + PEEP > 5
What is the mortality for mild ARDS?
27%
What is the oxygenation criteria for moderate ARDS?
PaO2/FiO2 ratio 100-200mmHg (13.3-26.7kPa) + PEEP > 5
What is the oxygenation criteria for severe ARDS?
PaO2/FiO2 ratio <100mmHg (< 13.3kPa)
What is the mortality of moderate ARDS?
32%
What is the mortality of severe ARDS?
45%
What are the essential criteria required to diagnose ARDS?
- Development within one week of insult/worsening resp symptoms - i.e. acute
- Bilateral opacities on CXR not explained by effusions, collapse or nodules
- Respiratory failure not explained by LVF or fluid overload
- Oxygenation criteria
- Patient has to be ventilated for a diagnosis of ARDS to be considered
What are the causes of ARDS?
Direct - pneumonia, pulmonary contusion, aspiration pneumonitis, inhalational injury, pulmonary vasculitis, submersion.drowning
Indirect - sepsis, burns, major trauma, TRALI, severe acute pancreatitis, cardiopulmonary bypass
What is the pathophysiology of ARDS?
- Exudative phase (days 2-4): inflammatory insult to epithelium, leakage of protein-rich fluid and inflammatory cells into alveoli and intersititium; destruction of the pulmonary vascular bed; dysregulation of coag and fibrinolysis leading to microthrombus formation; results in V/Q mismatch, leading to hypoxic hypoxia and a reduction in lung compliance, causing increased WoB.
- Proliferative stage (days 4-7): proliferation of type II pneumocytes and fibroblasts, with alveolar fibrin deposition; organisation of exudate leading to scar formation
- Fibrotic stage (days 7-14): fibrosis of lung tissue and global damage to underlying lung structure.
How does ARDS present?
Patient presents with increasing respiratory distress, hypoxia and tachycardia
Presentation will vary according to the underlying aetiology
Patients often have a level of multi-organ failure which is their usual cause of death
How would you investigate patients with ARDS?
Blood tests incl infl markers, serum amylase/cultures, ABG
CXR or CT chest
ECHO - if there are no known risk factors for ARDS
What are the ventilatory strategies for ARDS?
ARDSnet protocol
- Low tidal volumes - 5-7 ml/kg IBW with a high RR (< 35) to minimise volutrauma
- Aim sats 88-95% - consider increasing I:E ratio or using inverse ratios if oxygenation a problem
- Use PEEP to minimise atelectrauma - aim to find the optimum PEEP, there is evidence for mortality benefit to using high PEEP in severe ARDS
- Maintain plateau pressures (< 30) to minimise barotrauma
Which mechanisms result in ventilator-induced injury (VILI)?
- Volutrauma (overdistension of healthy aveoli)
- Barotrauma (high pressure injury to aveoli)
- Atelectrauma (shearing forces due to repeated collapse and expansion alveoli)
- Biotrauma (release of inflammatory mediators in response to high-volume ventilation)
What is the Murray score?
Severity scoring for patients with ARDS
What are the parameters of the Murray score?
0 1 2 3 4
PaO2/FiO2 ratio >40 <13
PEEP <5 >15
Compliance (ml/cmH2O) >80 <19
CXR (quads infiltrated) 0 4
At what Murray score should consideration for ECMO referral be made?
more than or equal to 3
Describe the basic principles of the aortic balloon pump
Inflates in diastole (after aortic valve closure, corresponds to dichrotic notch) and deflates in early systole (immediately prior to the aortic valve opening - just prior to to the upstroke)
Inflation causes volume displacement in both directions - leading to a potential increase in coronary blood flow and systemic blood flow
What are the physiological effects of the IABP?
Balloon inflates in diastole - increasing diastolic pressure and deflates in systole decreasing LV afterload
Increased myocardial o2 supply
Decreases myocardial oxygen demand
Renal perfusion should increase
What are the indications for IABP?
Acute MI Cardiogenic shock Acute MR and VSD Refractory unstable angina Weaning from bypass Refractory LVF Refractory ventricular arrythmias Sepsis
What are the contraindications for IABP?
Absolute: - aortic regurg - aortic dissection - chronic end-stage heart disease with no - chance of recovery - aortic stents Relative: -uncontrolled sepsis -AAA -tachyarrythmias -severe PVD -major arterial reconstructive surgery
What are the complications associated with IABP?
Limb ischaemia Thromboembolism Compartment syndrome Aortic dissection Local vascular injury - false aneurysm, bleeding, haematoma Infection Balloon rupture +/- gas embolism Thrombocytopenia and haemolysis Malposition causing cerebral or renal compromise Cardiac tamponade
What is VA ECMO?
Blood is pumped from the venous to the arterial circulation
Facilitates gas exchange and provides haemodynamic support
What is VV ECMO?
Blood is removed from and returned to the venous circulation
Facilitates gas exchange
Doesn’t provide any haemodynamic support
What is ECCO2R?
Extracorporeal CO2 removal
What are the main components of an ECMO circuit?
- Cannulae
- Tubing (heparin bonded) - systemic heprain is used but is not essential in the bleeding patient
- Pump - blood movement is facilitated by an external pump with a centrifugal or roller mechanism of action
- Membrane oxygenator and heat exchanger
- Gas blender
What are the absolute contraindications to ECMO?
Irreversible organ damage Multi-organ failure Those who are not candidates for transplant Advanced malignancy Chronic severe pulmonary hypertension
What are the relative indications for ECMO?
- Age > 75
- Polytrauma with multiple bleeding sites
- CRP > 60 mins
- MOF
- CNS injury
What are the contra-indications specific to VA ECMO?
Severe aortic regurgitation
Aortic dissection
What are the specific contraindications to VV ECMO?
Unsupportable cardiac failure
Severe pulmonary hypertension
Cardiac arrest
What are the complications of ECMO?
- Cannulation - pneumothorax, vascular disruption, infection, emboli, bleeding
- Systemic anticoagulation - haemorrhage incl intracranial and GI bleeding
- Equipment - exsanguination from circuit disruption, oxygenator failure, pump failure
What does 0.9% saline contain/whats its pH and osmolality?
9gNaCl/L h20 Na 154 mmol/L Cl 154 mmolL Osmolarity 300mosmol/L pH 5-6.5
Describe Hartmanns solution
Contains Na 131 mmol/L Cl 111 mmol/L K 5 mmol/L Ca 2 mmol/L HCO3 as lactate 29 mmol/L Osmolarity: 278 mosm/L pH 6.8
What does 0.18% NaCl + 4% glucose contain?
1.8g NaCl and 40g glucose/L
Na 31 mmol/L
Cl 31 mmol/L
Osmolarity 271 mosm/kg H2O
Describe 5% glucose
50g glucose /L
205 calories/L
Osmolarity 278mosm/L
What is capacity?
The ability to make your own decisions
What legislation surrounds capacity?
The mental capacity act 2005
- it protects vulnerable adults and empowers them to make their own decisions
- applicable to those over 16
What are the principles of the mental capacity act?
- A person is assumed to have capacity until proven otherwise
- A person is not to be treated as unable to make a decision unless all practicable steps to help him/her to do so have been taken without success
- A person is not to be treated as unable to make a decision merely because they make an unwise decision.
- An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his/her best interests
- Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is least restrictive of the persons rights and freedom of action.
How do you assess capacity?
Stage 1: Is there a disorder or disability of the brain or mind?
Stage 2: Can the patient
-understand the information given to them
-retain this information long enough to make a decision
-weight the information in the decision making process
-communicate their decision
What do you do if a patient lacks capacity?
Apply the principles of best interest. This involves:
- Ascertain the patients past and present wishes, including advanced decisions/directives
- Ascertaining the beliefs and values of the patient that may influence their decision
- Discussion with the next of kin or an IMCA (a doctor is not obliged to adhere to the opinion of an IMCA but should document clearly why not)
What is a deprivation of liberty safeguard?
The Mental Capacity Act was amended in 2009 to include deprivation of liberty. Article 5 of the human rights act 1998 requires that no one should be deprived of their liberty except in certain, pre-defined, circumstances.
There must also be an appropriate, legally based, procedure in place to protect the individuals rights
What is the purpose of DOLs?
- To protect vulnerable adults who lack capacity against arbitrary detention that is not in their best interests
- Gives the person a right to challenge their confinement
Who does a DOLs order apply to?
Anyone who lacks the capacity to consent to detention imputable to the state (ie in a public sector facility) that is determined by an independent review to be in their best interests e.g. pts with delirium, those requiring restraint, long stays and those with red flags (trying to leave/family conflicts etc)
What constitutes deprivation of liberty?
As determined by the Cheshire West case in 2014
- The patient lacks the capacity to consent to their care/treatment arrangements
- The patient is under continuous supervision and control
- The patient is not free to leave (wants to but is being prevented from)
Does DOL apply to critically ill patients?
Any DOL resulting from the administration of life-saving treatment falls outside of article 5 as long as it is unavoidable as a result of circumstances beyond the control of the authorities and necessary to avert a real risk of serious injury or damage and is kept to a minimum for that purpose.
When is a DOLs order not necessary?
- Those who have previously consented to the accommodation e.g. as part of pre-op assessment
- Pts who are deeply unconscious
- Pts who are expected to regain capacity within 7 days
- Pts who are expected to die
Why might it be appropriate to deprive a patient of their liberty?
Justifiable where a person lacks capacity to consent to this:
- If it is in their best interests to protect them from harm
- It is a proportional response compared to the harm faced by the person
- If there is no less restrictive alternative
How do you apply for DOLs authorisation?
Application is made to the trust (if urgent) or the local authority (if not urgent).
Urgent authorisations can only be made where a standard authorisation has been applied for but is not yet granted
An independent assessment is then carried out - usually by a psychiatrist
It’s not transferable between institutions.
What are the goals of sedation on ICU?
To prevent pain To relieve anxiety To relieve dyspnoea To permit mechanical ventilation To facilitate nursing care To decrease oxygen consumption To treat delirium
What are the risks of under-sedation?
Severe anxiety and agitation
Acute cardiopulmonary instability (hypertension, tachycardia, tachypnoea)
Ventilator dysynchrony
Hypoxaemia
Inadvertent removal of devices and catheters
Unplanned extubations
What are the risks of over sedation?
Drug-induced coma
Undetected intrathoracic or intracranial catastrophes
Unnecessary investigations (e.g. CT brain)
Cardiovascular instability (hypotension, bradycardia)
Drug accumulation
Prolonged mechanical ventilation
Prolonged ICU length of stay
How is level of sedation assessed?
there are 3 scoring systems:
- Ramsay sedation scaler
- Riker Sedation-Agitation Scale
- Richmond Agitation-sedation scale
+4 Combative: Overtly combative, violent, immediate danger to staff
+3 Very agitated: Pulls or removes tubes or catheters; aggressive
+2 Agitated: Frequent non-purposeful movement, fights ventilator
+1 Restless: Anxious, but movements not aggressive or vigorous
0 Alert and calm
-1 Drowsy: Not fully alert, but has sustained awakening (eye-opening/eye contact) to voice (>10 s)
-2 Light sedation: Briefly awakens with eye-contact to voice (<10 s)
-3 Moderate sedation: Movement or eye-opening to voice, (but no eye-contact
-4 Deep sedation: No response to voice , but movement or eye-opening to physical stimulation
-5 Unrousable: No response to voice or physical stimulation
What are the potential advantages of a daily sedation break?
Fewer days on mechanical ventilation
Fewer days on ICU
Fewer diagnostic studies to investigate alterations in mental status
More patient days spent awake and able to follow commands
Enhanced physician/patient communication and improved physical examination
Allows focused downward titration of infusion rates over time
Facilitates spontaneous breathing trials
What are the potential disadvantages of a daily sedation break?
Abrupt awakening and agitation
Risk of self-extubation
Cardiopulmonary instability and stress response
What non-pharmacological factors may precipitate delirium?
Sleep deficit Nosocomial infection Hypoxia Substance withdrawal Congestive cardiac failure Metabolic disturbance Electrolyte imbalance Dehydration Hyperthermia Prolonged immobility
What pharmacological factors may precipitate delirium?
Sedatives Midazolam Fentanyl Morphine Propofol Anticholinergics Steroids
Which patients are most at risk of delirium?
Advanced age Dementia Depression Hypertension Smoking Alcoholism
What factors influence antibiotic choice in critically ill patients?
- Likely site of infection
- Likely causative organism
- Likelihood of resistance
- recent abx, LOS in hospital/ICU, institution, recent travel, occupation, results from screening swabs, local resistance - Severity of infection
- Risk of side effects
- Potential drug interactions
- Pharmacokinetic consideration eg cross BBB
Broadly speaking how do antibiotics work?
They may be
- Bacteriostatic - limit bacterial growth allowing the immune system to get rid of the bacteria
- Bactericidal- cause cell death
Which antibiotics are bactericidal and which are bacteriostatic?
Bactericidal - penicillins, cephalosporins, aminoglycosides, glycopeptides, quinolone, nitroimidazoles, rifampicin, nitrofurantoin
Bacteriostatic-macrolides, tetracyclines, lincosamides, sulphonamides, trimethoprim
What mechanisms are involved in antibiotic activity?
- Inhibition of cell wall synthesis- prevent cross linking within the call walls
- Inhibition of DNA synthesis or function
- Inhibition of tetrahydrofolate synthesis
- Inhibition of protein synthesis
What is time dependent killing with respect to antibiotics?
Refers to agents whose activity depends on the amount of time the serum concentration is above the minimum inhibitory concentration
These include beta-lactams, erythromycin, clindamycin, linezolid, vancomycin
They are therefore doses regularly to keep the serum levels above MIC as long as possible
What is concentration dependent killing with respect to antibiotics?
Refers to agents whose activity correlated with peak serum concentration. Eg aminoglycosides and quinolones.
Higher doses are used with lower frequency of administration. However this may impact toxicity. Eg gent toxicity correlates to tissue accumulation (ie trough levels) rather than peak serum concentration and works best at 10-12 times MIC
What are the gram positive bacilli
Actinomyces Bacillus Clostridia Diphtheria Listeria
What is the Stanford system of classifying aortic dissection?
Type A: Involves the ascending aorta
Type B: Involves the descending aorta only, distal to the origin of the left subclavian artery
What in the DeBakey classification of aortic dissection?
Type I: Originates in the ascending aorta and propogates at least to the aortic arch
Type II: Involves the ascending aorta only
Type III: Originates in the descending aorta and has 2 subtypes
- type IIIa: limited to the thoracic arch
- type IIIb: extends below the diaphragm
What are the risk factors for aortic dissection?
Hypertension Advanced age Male gender Smoking Family history Pregnancy Trauma (deceleration injury) Congential disorders e.g. Marfans, Ehlers-Danlos, aortic corarctation, Turners, congential aortic stenosis, bicuspid valve
What are the presenting features of aortic dissection?
- Pain - type A = sudden onset, severe anterior chest pain with extension into the back. Type B - back pain
- Differential or absent pulses in the extremities
- Aortic regurg (early diastolic murmur best heard between the scapulae in expiration)
- Syncope - resulting from impairment of cerebral blood flow, stroke and other neuro manifestations may also be present.
What are the complications of aortic dissection?
CVS - acute aortic regurg, MI or ischaemia, cardiac tamponade, HTN, hypotension or shock (secondary to tamponade, dissection or coronaries, acute AR, blood loss, intra-abdo catastrophe), limb ischaemia.
Neuro - Ischaemic stroke, acute paraplegia secondary to spinal cord hypoperfusion
Pulmonary - pleural effusions - usually left
Renal - AKI
Haematological - major transfusion requirment, coagulopathy
GI - mesenteric ischaemia
What are the CXR features of aortic dissection?
Widened mediastinum
Cardiomegaly secondary to effusion
Blunting of the costophrenic angles as a result of haemothorax
Possibly be able to see separation of calcified intima at the aortic knuckle
What findings might with find on TTE in someone with aortic dissection?
May be able to see intimal flap
Aortic regurg
What findings might you fine on TOE in someone with aortic dissection?
true and false lumens may be identified
Which investigations can be used to confirm diagnosis of aortic dissection?
CT
MRUI
Aortography - used to be gold standardbut now rarely performed
What are the principles of management of a patient with aortic dissection?
ABCDE approach
- Initial investigation and management
- o2, large bore cannulae, bloods, BP monitoring, catheter, 12-lead ECG, analgesia - Manage hypotension - judicious volume resuscitation aiming BO 100-120mmHg; search for underlying aeitology
- Manage hypertension - it’s important to reduce shear force around the origin of the dissection by avoiding tachycardia, therefore adequate beta-blocker should be establish prior to vasodilator (GTN or sodium nitroprusside)
- Imaging and ongoing care, transfer to regional cardiothoracic centre as appropriate.
How does the management of Stanford type A and B aortic dissection differ?
Type A are surgical emergencies and are usually surigcally fixed via and median sternotomy
Complicated type B will usually require a left lateral thoracotomy
Uncomplicated type B are normally managed with beta-blockers and anti-hypertensives.
There is a developing role for endovascular intervention for some type B dissections.
What is a patient safety incident?
Any healthcare event that is: Unexpected Unintended Undesired Associated with actual or potential harm
Why are critically ill patients at particular risk of a patient safety incident?
Pts are:
- undergoing highly invasive treatments with concomitant complications
- Receiving frequent parenteral drugs/fluids
- Undergoing invasive interventions
- Lacking capacity
- Lacking physiological reserve
- More likely to be sedated and unable to communicate concerns
What are the stages involved in patients receiving medications and at which stage do most errors occur?
- prescribing
- transcription
- preparation
- dispensing
- administration - the majority occur here
What are medication errors vs adverse drug events?
Medications errors are any mistakes in the prescription/preparation/administration of a drug. Doesn’t necessarily result in harm.
Adverse drug events are medication errors where harm occurs
Why are medication errors more common on the ICU?
Patient factors - severity of illness, extremes of age, prolonged hospitalisation, sedation, lack of capacity, altered pharmocodynamics
Environmental and human factors - high turnover of patients and staff, difficult work conditions, high stress, emergency admissions, knowledge and performance deficits, communication problems, inadequate information technology
Medication specific - number of medications (risk of interactions), types of medications - use of infusions and boluses, pump programming, use of estimated weight
Are there any measures that have been shown to reduce medication errors in the ICU?
- Eliminate environmental and situational risk factors - avoid excessive working hours, minimise interruptions, trainee supervision
- Optimise the medication process - computer systems, IV infusion devices, medication standardisation
- Prevention of oversights - adequate staffing, pharmacist involvement, education and quality assurance
What is a never event?
Serious incidents that are wholly preventable, as guidance or safety recommendations that provide strong systemic protective barriers are available at a national level and should have been implemented by all healthcare providers
Which never events are relevant to ICU?
Surgical - wrong site, retained foreign object post-procedure
Medication - mis-selection of a strong potassium-containing solution, insulin ODs due to abbreviations or wrong device, wrong route of administration of medication, mis-selection of high strength midazolam for conscious sedation
General - misplaced NGT, transfusion of ABO-incompatible blood products
What is the correct procedure for confirming the position of a NGT?
- Nothing should be introduced down an NGT until its position is confirmed
- 1st line testing - pH 1-5.5 is the safe range.
- 2nd line: CXR. Documentation should include who authorised the CXR, who confirmed the position, confimration that the x-ray was the most current one for the correct patient, the rationale for confirmation of the position
- Checking the external markings for displacement remains vital.
What processed are in place to help minimise the occurrence of never events?
- two person checking drugs/blood
- barcode scanners
- checklists
- debriefs
- standardisation of processes
- team training in communication and awareness of human factors
- mandatory learning modules and competency based training for staff.
- growing culture of open communication to enable learning from mistakes
What would you do if you were ever involved in a never event?
Immediate steps should be taken to ensure patient safety systems and procedures are reviewed
- Patient safety is paramount - ensure they’re stable and treat any complications
- Inform the consultant responsible for care asap.
- Inform the patient/family/carer asap
- complete an incident report
- never events must be highlighted to the commissioner within 2 working days as per the serious incidents framework
- they must be investigated in line with the serious incidents framework (e.g. root cause analysis)
What is cardiogenic shock?
Evidence of tissue hypoperfusion secondary to primary cardiac failure after correction of preload
What are the characteristics of cardiogenic shock?
SBP < 90
Hr > 60
oliguria
with or without evidence of organ congestion
What is the pathophysiology of cardiogenic shock?
- Impaired LV systolic function leads to decreased CO and SV. Results in hypotension, decreased coronary perfusion and ischaemia. Decreased systemic perfusion results in compensatory vasoconstriction and fluid retention. These lead to progressive myocardial dysfunction.
- Impaired LV diastolic function results in increased LVEDP, pulmonary congestion, hypoxemia, ischaemia and also results in progressive myocardial dysfuction.
What are the causes of cardiogenic shock?
The most common cause is acute decompensation of established cardiac failure, which can be triggered by non-compliance with meds, ishaemia, arrythmia, hypertensive crisis, brain injury, sepsis, drug abuse or volume overload. Can also present de novo in a patient with previously normal cardiac function.
- Arrythmias
- Valvular pathology - acute or decompensation of a chronic state
- Viral myocarditis - e.g. coxsackie and adenovirus
- Tamponade - trauma/dissection/pericarditis
- High output cardiac failure - thyroid storm/severe anaemia
- Decompensation of chronic cardiac failure
What are the causes of chronic cardiac failure?
- Hypertensive heart disease i.e. diastolic heart failure
- Dilated cardiomyopathy - alcohol, toxins e.g. heavy metals, drugs e.g. doxorubicin, MDMA, cocaine, peripartum
- Restrictive cardiomyopathy - infiltrative e.g. sarcoid, amyloid, haemochromatosis, CT disorders, and radiation.
- Congenital - hypertrophic cardiomyopathy
How does cardiogenic shock present?
CV - cool peripheries with prolonged crt, tachy or brady, arrythmias, BP may be high due to high SVR or low is decompensated, myocardial ischaemia, signs of RHF incl peripheral oedema, raised JVP and hepatomegaly with RUQ tenderness
Resp - tachypnoea with pulm oedema, hypoxia
Neuro - low GCS, confused/altered mental state
Renal - oliguria
How do you manage patients with cardiogenic shock?
ABCDE approach
- O2, may need NIV or I+V
- IV access - bloods for FBC/U+E/LFTs/cardiac enzymes/BNP/clotting/viral serology if indicated
- ECG/CXR/ECHO
- Cautious fluid bolus ideally with cardiac output monitoring
- Low threshold for inotropic support and consider vasodilators to reduce preload and afterload and reduce myocardial work. May need a vasopressor.
- Mechanical support e.g. IABP, ventricular assist device as a bridge to recovery or transplant
Which inotropes are available?
- Adrenaline - low dose: b1 and b2 (tachycardiac, positive inotropy, vasodilation); high dose: a1 effects (vasoconstriction)
- Dobutamine - predominantely b1 effects, some b2
Which vasodilators are available?
- Milrinone/enoxiomone - phosphodiesterase 3 inhibitor (increases cyclic AMP). Reduces PVR and SVR, positive inotropy and lusitropy. Useful in diastolic heart failure.
- GTN - nitric oxide donor - predominantly causes venodilatation.
What is levosimendan?
- Sensitises troponin C to calcium (positive inotropy)
- Opens ATP-dependent potassium channels (increased coronary perfusion, reduced preload, reduced afterload)
- Overall effect: increased contractility without increasing myocardial oxygen consumption
- Evidence that it improves short and long term survival in patients with cardiac failure
How can you reduce myocardial oxygen demand?
- Reduce hr - ensure adequate preload, beta-blockade if diastolic dysfunction, sedation
- Reduce afterload - vasodilators, diuretics if volume overloaded, sedation
How can you improve myocardial oxygen delivery?
- Increase myocardial perfusion - vasodilators, inotropes
2. Increase oxygen carrying capacity - increase fio2, consider blood transfusion
How does IABP work?
Inserted via femoral artery, and lies within the descending aorta just distal to the origin of the left SCV.
Balloon is inflated with helium during diastole to augment DBP, which improves coronary perfusion.
Balloon is deflated in systole to reduce afterload.
The overall effect is improved myocardial oxygen delivery and reduce myocardial oxygen demand.
Where on a ECG does the IABP inflate and deflate?
- Inflate in the middle of the T wave (dicrotic notch)
- Deflate at the peak of the R wave (just before the systolic upstroke)
What are the contra-indications to IABP insertion?
Absolute:
- aortic regurg
- aortic dissection/aneurysm
- severe PVD
Relative:
- arterial turtuosity
- LVOT obstruction
- Sepsis
- CI to anti-coagulation
What are the complications of IABP placement?
Vascular
- bleeding
- haematoma
- pensudoaneurysm
- dissection
- perforation
Balloon-related
- mesenteric/renal ischaemia
- left upper limb/cerebral ischaemia
- helium embolus
- haemolysis
- thrombocytopenia
What is a ventricular assist device?
A surgically placed mechanical device that can support the left (LVAD) or right (RVAD) or both ventricles (BiVAD).
BiVAD implantation is uncommon as RV failure often results from pulmonary hypertension secondary to LV failure and will improve with LVAD insertion
They reduce myocardial work, allowing the ventricles to rest whilst ensuring forward flow and organ perfusion
They can be used as a bridge to recovery instead of VA ECMO in acute heart failure or as a bridge to transplantation in chronic cardiac failure
What are the complications of ventricular assist devices?
- Bleeding
- Tamponade
- Haemodynamic distrubance - if the pt is hypovolaemic the IV septum is entrained towards the inflow cannula
- RV failure
- Fluid overload - may occur as fluid is mobilised as a result of the higher CO.
- Infection
- Intra-cardiac thrombosis
What is diabetic ketoacidosis?
A potentially life-threatening metabolic complication of diabetes defined by a triad of ketonaemia, hyperglycaemia and acidaemia.
What is the pathophysiology of DKA?
Usually occurs as a result of relative insulin deficiency which, when combined with increases in glucagon, catecholoamines and cortisol stimulates lipolysis, free fatty acid production and ketogensis.
Accumulation of ketoacids (3-B-hydroxybutyrate, acetone, and acetoacetate) then results in a metabolic acidosis.
Hyperglycaemia results from increased hepatic gluconeogenesis and glycolysis in addition to reduced glucose uptake peripherally due to insulin deficiency
What processes result in fluid depletion in DKA?
- Osmotic diuresis secondary to hyperglycaemia
- Vomiting
- Reduced oral intake secondary to reduced consciousness
What are the clinical features of DKA?
Thirst Polyuria N+V Abdo pain Dehydration Ketotic breath Kussmaul breathing Confusion Coma
What are the diagnositic criteria for DKA?
As stated by the Joint British Diabetes Societies
- Cap blood glucose > 11
- Ketonaemia > 3mmol/l or urinary ketones > 2+
- Venous bicarb < 15 or pH < 7.3
What are the indications for consideration of admission to ICU?
- Bloods ketones > 6
- Bicarb < 5
- pH < 7.1
- hypokalaemia on admission < 3.5
- GCS < 12
- SpO2 < 92%
- SBP < 90
- hr < 60 or > 100
- Anion gap > 16
How do you calculate anion gap?
(Na + K) - (Cl + HCO3)
How is DKA treated?
Most hospitals have clear guidelines ABCDE approach Main principles: 1. Fluid and electrolyte replacement 2. Insulin therapy 3. Treatment of underlying cause 4. Other supportive treatment - thromboprophylaxis, stress ulcer prophylaxis
Describe fluid management in DKA
- 0.9% saline is fluid of choice (still debated)
- aim to restore circulating volume, clear ketones and correct electrolyte imbalances
- if SBP < 90 then 500mls bolus
- normally 1L in the first hour then one over 2 and then a further over 4
- rate needs to be modified in the young and elderly and those with renal and heart failure (increased risk of cerebral oedema)
- normally 3-5 mmol/kg of potassium debt. Each bag of saline should have potassium replacement when K < 5.5.
Describe insulin therapy in DKA
- Suppresses ketogenesis, decreased blood sugar and corrects electrolyte disturbances
- fixed insulin infusion should be started at 0.1unuts/kg/hr
- continue long acting insulin
- aim to decrease ketones by 0.5mmol/l/hr; increase bicarb by 3/hr/decrease BVM by 3/hr/maintain K 4-5.5
- increase infusion if targets not met
- add in 10% glucose once blood glucose falls to allow insulin to continue
What is the commonest cause of death in DKA?
Cerebral oedema
How does the management of DKA differ in children?
Increased cerebral oedema in paeds - necessitates judicious use of fluid
- 10ml/kg bolus only if shocked
- fluid requirement = deficit + maintenance - volume used in resuscitation. Tis volume is given over 48 hours.
- insulin therapy is delayed by 1 hour
What is hyperglycaemic hyperosmolar state?
Severe hyperglycaemia and fluid depletion with no or mild ketosis. It’s usually seen in elderly patients with uncontrolled type 2 diabetes and often other significant co-morbidities.
What is the mortality associated with HHS?
15-30 % (higher than DKA)
What are the clinical features of HHS?
- Hypovolaemia - estimated between 100-220ml/kg
- Marked hyperglycaemia (>30) without significant hyperketonaemia (<3) and no significant acidosis.
- serum hyperosmolarity (> 320)
Symptoms are vague and include anorexia, malaise, weakness, severe dehydration, renal impairment and coma.
Tends to develop over days and consequently metabolic derangement and dehydration may be very severe.
What are the goals of treatment of HHS?
ABCDE
- Treat underlying cause
- Normalise osmolality
- Replace fluid and electrolyte losses - normally with 0.9% saline +/- K
- Reduce Na by <10mmol/24 hours
- Reduce glucose by < 5mmol/hr - only stsrt low dose insulin (0.005 units/kg/hr) once glucose stops falling with fluids alone. Otherwise risks precipitous drop in glucose.
- Prevent complication - thrombotic events in particular.
In HHS what are the indications for potential admission to ICU?
- Osmolality > 350
- Na > 160
- pH < 7.1
- K < 3.5 or K > 6
- GCS < 12
- SpO2 < 92%
- SBP < 90
- Hr < 60 > 100
- U/o < 0.5mlk/kg/hr
- Cr > 200
- Hypothermia
- MI, stroke or other serious comorbidity
How is osmolality calculated?
2NA + glucose + urea
What is a colloid?
A fluid containing large molecules that exert an oncotic pressure at the capillary membrane
What colloids are there?
Natural - bloods and its constituents, albumin
Synthetic - gelatins, hydroxyethyl starch
Describe gelatins
- Modified bovine collagen suspensions.
- Ave molecular weight 35kDa
- Long shelf-life
- Rapidly excreted by the kidneys - effect lasts about 1.5 hours
- May cause anaphylaxis
Describe hydroxyethyl starches
- Corn/potato starch suspensions
- Large ethylated, polymerised amylopectin molecules
- Available in several different molecular weights
- Longer plasma half-life than other synthetic colloids (>6 hours)
- The higher MW solutions impair factor VIII and vWF causing coagulopathy. Increased incidence of renal failure and mortality in critically ill
What is albumin?
A globular single polypeptide with a MW 69kDA
Highly negatively charged and is repelled by the negatively charged glycocalyx of the endothelium which extends its intravascular half life to 5-10 days when given as a volume expander (assuming intact capillary endothelium)
What is HAS?
A solution containing protein derived from plasma, serum and normal placentas.
Available in 2 concentrations in the UK: isotonic 4.5% and concentrated 20%.
Its made from thousands of pooled donations and therefore carried a theoretical risk of new variant CJD
Where is albumin produced?
In the liver
Rate of 0.2g/kg/day
Under the influence of the neuroendocrine systems and the plasma oncotic pressure
Accounts for about 50% of the plasma proteins
It’s a negative acute phase protein, with its production being suppressed in physiological stress
What are the functions of native albumin?
- Transport molecule - cations, hormones e.g. T4, steroids, unconjugated bilirubin, bile salts, acidic drugs e.g. NSAIDS, warfarin
- Maintenance of oncotic pressure - it accounts for ~80% of colloid oncotic pressure in healthy people
- Acid-base balance (acts as a buffer)
When do we use albumin?
- Fluid resuscitation
- Prophylaxis and management of HRS
- Facilitate large volume paracentesis in cirrhosis
- As a replacement fluid in plasmaphoresis
Describe the SAFE trial
NEJM 2004
Double-blind multi-centre Australian RCT
Compared 4% HAS to 0.9% saline for fluid resus in ICU patients
Equivalent mortality in the 2 groups
Non-significant trend favouring 0.9% saline in trauma and albumin in sepsis.
Sub-group analysis showed increased mortality in pts with TBI who received albumin
Describe the ALBIOS trial
NEJM 2014
Non-blinded multi-centre Italian RCT
Compared 20% HAS (to maintain albumin > 30) with crystalloid in adults with severe sepsis and septic shock
No difference in mortality between the 2 groups
What are the disadvantages to using HAS?
- Worsens TBI 28 day mortality and long-term outcomes when used as a resus fluid
- More expensive
- May worsen third space loss in patients with endothelial dysfunction (protein molecules leak into the interstitial space, drawing water with them)
- There is a theoretical risk of new variant CJD transmission
Describe the VISEP trial
Efficacy of volume substitution and insulin therapy in severe sepsis, NEJM 2008.
German multi-centre RCT focussing on the safety and efficacy of HES versus Hartmanns in pts with severe sepsis/septic shock
-It was stopped early for safety reasons
-HES increases risk of AKI and need for RRT
- However high doses were used and may not reflect usual practice
-They also looked at intensive glycaemic control which found an increased rate of adverse events associated with hypos
What is the 6S trial?
NEJM 2012
Scandinavian double-blinded multi-centre RCT
Compared HES with Ringers lactate
No difference in 28 day mortality but a significant increase in 90-day mortality and use of RRT in the intervention group
Pts in the HES group were more likely to receive blood products, with a trend towards more bleeding.
What was the CHEST trial?
NEJM 2012
Double-blind multicentred Antipodean RCT
Compared 6% HES with 0.9% saline for fluid resus in critically ill pts
No difference in 90-day mortality
Use of RRT was greater and received more blood products in the HES group.
What is COPD?
A progressive inflammatory condition affecting peripheral and central airways, lung parenchyma and pulmonary vasculature
Defined as “a common, preventable and treatable disease characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by exposure to noxious particles and gases”
What are the risk factors for COPD?
- Smoking
- air pollution
- occupational exposure
- alpha1- antitrypsin deficiency
Hos is COPD diagnoses?
- Symptoms - exertional breathlessness, chronic cough, regular sputum production and frequent winter bronchitis or wheeze
- Spirometry - demonstrable airway obstruction with a post-bronchodilator FEV1/FVC < 0.7
What is the modified MRC dyspnoea scale?
Grade 1: Strenuous exercise
2: SOB when hurrying on the level or walking up a slight hill
3: Walks slower than most on the flat, stops after 15mins of walking.
4: Stops after 100yrds or a few minutes
5: Too SOB to leave the house or breathless on dressing/undressing
What is the GOLD classification of airflow limitation severity in COPD?
1: Mild - FEV1>80% predicted
2: Moderate - FEV1 50-79% predicted
3. Severe - 30-49% predicted
4: Very severe - < 30% predicted
Describe the key features of the pathophysiology of COPD
- Airflow limitation and gas trapping
- Gas exchange abnormalities
- Mucous hypersecretion
- Pulmonary hypertension
- Exacerbations
- Systemic features - muscle wasting and cachexia
Describe gas trapping in COPD
Peripheral airway limitation traps gas during expiration, resulting in hyperinflation
Static hyperinflation reduced inspiratory capacity and is commonly a/w dynamic hyperinflation during exercise leading to increased SOB and limitation of exercise capacity
Describe gas exchange abnormalities in COPD
Worsens as disease progresses
Reduced ventilatory drive and increased dead space lead to reduced ventilation, which leads to CO2 retention
Abnormalities in alveolar ventilaiton and reduced pulmonary capillary bed further worsen V/Q abnormalities
Describe mucous hypersecretion in COPD
Results in a chronic cough and is due to chronic airway irritation by cigarette smoke and other noxious agents. Leads to increased number of goblet cells and enlarged submucosal glands
Describe the pulmonary hypertension associated with COPD
Hypoxic vasoconstriction of the small pulmonary arteries results in structural changes including intimal and smooth muscle hyperplasia, causing pulmonary hypertension. This usually occurs late in the course.
What are the indications for intensive care admissions in patients with COPD?
- Persistent or worsening hypoxaemia and/or resp acidosis (pH < 7.25) despite supplemental oxygen and NIV
- Need for ventilation
- Need for vasopressors/inotropes
- Changes in mental state/consciousness
- Severe dyspnoea responding poorly to initial treatment
How is an exacerbation of COPD managed?
ABCDE approach
- Investigations: bloods, sputum, ABG, CXR, consider TTE
- Pharmacological therapies: B2-agonists, anti-cholinergics, steroids, antibiotics, oral mucolytics, aminophylline isn’t recommended due to its side effect profile
- Resp support: target sats 88-92%, controlled oxygen delivery, NIV, I+V
- Prevent further exacerbaitons - optimise bronchodilators and mucolytics, pneumococcal and flu vaccines, assess need for LTOT
What are the indications for NIV in COPD patients?
- Persistent or worsening resp acidosis despite optimal medical therapy
- Severe acidosis (pH < 7.25) - these pts have a higher risk of treatment failure and should be managed on ICU
- As ceiling of treatment for pts who are not candidates for invasive ventilation.
Aside from NIV what other interventions have been shown to be of benefit in pts with COPD?
- Smoking cessation
2. LTOT - confers a survival benefit and improves pulmonary haemodynamics.
When does the BTS recommend LTOT in COPD pts?
- Stable, chronic COPD and a resting PaO2 < 7.3
2. Resting PaO2 < 8 and evidence of peripheral oedema, polycythaemia (hct > 55%) or pulmonary hypertension
What are the indications for I+V in AECOPD?
- Imminent resp arrest
- Severe respiratory distress
- Failure of or contra-indications to NIV
- Persisting pH < 7.15 or deterioration despite NIV
- GCS < 8
What are the principles of invasive ventilation for a patient with COPD?
- Reduced resp rate or I:E ratio - produces prolonged exp time, reducing the risk of breath-stacking; reduced minute volume will consequently lead to hypercapnia, acidosis, increased PVR and potential haemodynamic instability
- Application of extrinsic PEEP - keeps small airways open during expiration, if values are kept below iPEEP there should be no significant increase in alveolar pressure and no worsening of CV effects
- Treatment of bronchospasm to optimise gas flow
What are the physiological principles of intrinsic PEEP?
- Decreased venous return and consequent hypotension
- Increased PVR and right heart strain
- Pulmonary barotrauma, volutrauma, hypercapnia and acidosis.
What is the in-hospital mortality of pts with severe COPD that get intubated
25%
What are the causes of ascites?
Hepatic - cirrhosis, Budd-Chiari, Portal vein thormosis
Nephrogenic
Cardiogenic - CCF, constrictive pericarditis
Malignant - Gynae/GI/peritnoeal carcinomatosis
Infectious - SBP, TB, fungal infections, parasites, chalamydia
Miscellaneous - pancreatitis, chylous ascites, protein losing enteropathy, SLE, sarcoidosis, ovarian disease
What are the classes of ascites as per the International Club of Ascites?
Simple - not infected or a/w development of hepatorenal syndrome. Sub-class 1 (detetable by US only to 3 - marked abdo distension) Refractory - ascites that cannot be mobilised or early recurrence that cannot be prevented by medical therapy - diuretic resistant and diuretic intractable (can't effectively diurese due to complications a/w the diuretic)
What are the indications for abdominal paracenteis?
Diagnostic - aetiology/presence of infection
Therapeutic - to relieve the pain of peritoneal stretch or resp compromise due to diaphragmatic splinting
What are the contra-indications to abdominal paracentesis?
Absolute: DIC, pt refusal
Relative: pregnancy, bowel obstruction, infection of the abdominal wall.
Normally ok if plts > 20.
What is the optimal insertion site for needle paracentesis?
2-4 cm medial and cephalad of the ASIS. Left lower quadrant may be better than the right.
What is the serum ascites albumin gradient?
SAAG
serum albumin - ascitic albumin
If > 11 then= acites is a/w the presence of portal hypertension
Which causes of ascites are associated with the presence of portal hypertension?
Cirrhosis
Cardiac failure
Hepatic malignancy
What are the indications for a trache on ICU?
Prolonged ventilation Aids weaning Tracheal toilet Reduce sedation Prevent aspiration Upper airway obstruction
What are the contra-indications for a perc trache?
Abnormal/difficult anatomy - short neck, obesity, congential abnormalities
Unstable C-spine (difficult not to move neck with the force required)
Unstable patients - FiO2 < 60 and PEEP < 10 should be ok
Coagulopathy
What are the complications of a perc trache insertion?
Bleeding
Barotrauma
Lobar collapse (loss of recruitment during the procedure)
Damage to the posterior tracheal wall resulting in tracheo-oeophageal fistula (rare)
Nerve damage - rare
What are the main roles of calcium?
Bone mineralisation Neuronal function Coagulation Co-factor for many enzymes and proteins Essential in endocrine, exocrine and neurocrine functions Second messengers in signal transduction Mediates muscle contraction
In what forms does calcium exist in the plasma?
- free ions
- ions bound to plasma proteins - primarily albumin, reduced by metabolic acidosis, increased in resp alkalosis
- diffusible complexes
What is the role of parathyroid hormone in calcium homeostasis?
- It ensures tight plasma control of ionised calcium by
1. Release of calcium from bones (increased osteoclast activity)
2. Increased reabsorption from distal convoluted tubule
3. Reduced phosphate reabsorption, leading to increased ionised calcium levels (less phosphate available to complex with calcium)
4. Vitamin D3 conversion to 1,25-dihydroxy-vitamin D3, which causes GI calcium absorption.
What is the role of calcitonin in calcium homeostasis?
It’s released from C-cells of the thyroid in response to hypercalcaemia and opposes the action of PTH
- Inhibits calcium absorption from the GIT
- Inhibits osteoclast activity
- Stimulates osteoblast activity
- Inhibits tubular reabsorption leading to increased excretion - but it does also inhibit reabsorption of phosphate in the DCT.
What is hypercalcaemia?
Serium calcium > 2.6mmol/l
What are the clinical features of high calcium?
Groans - constipation, vomiting, anorexia, nausea, pancreatitis, peptic ulcer.
Bones - bony pain (osteolysis, fractures)
Moans - psychosis, hallucinations, confusion
Stones - kidney stones
Cardiac arrhythmias with ECG abnormalities incl short QTc and broad T waves, prolonged PR interval, Cardiac arrest due to AV block may occur if calcium > 3.75
What are the causes of hypercalcaemia?
Malignancy - bony mets, myeloma, ectopic PTH and 1,25-(OH)D
Endocrine - primary hyperparathyroidism, hyperthyroidism, familial hypocalcuric hypercalcaemia, tertiary hyperparathyroidism
Granulomatous disease - sarcoid, TB
Drugs - thiazides, lithium, aminophylline, vit D
Misc - rhabdo, milk-alkali syndrome, renal failure
How do you treat hypercalcaemia?
ABCDE approach
Treat underlying cause
- IV hydration with 0.9% saline - this forces diuresis
- Bisphosphonate therapy - pamidronate 60-90mg over 2-4 hours
- Diuretics - furosemide, although this promotes bony uptake of calcium
- stop any contributing meds
- Calcitonin, mobilisation, RRT
At what level is hypocalcaemia considered severe?
Ca < 1.9mmol/l
What causes hypocalcaemia?
Endocrine - primary hypoparathyroidism, congenital deficiency (DiGeorge syndrome), psuedohypoparathyroidism, vit D deficiency
Malnutiriotn - decreased intake, intestinal malabsorption, rickets, osteomalacia
Drugs - furosemide, calcitonin, bisphosphonates, phenytoin, aminoglycosides, amphotericin B
Misc - acute hyperphosphataemia, tumour lysis syndrome, rhabdomyolysis, acute renal failure, acute pancreatitits
What ECG changes occur in a pt with low calcium?
QTC prolongation, which may progress to polymorphic VT
How do you treat low calcium?
Oral or parenteral calcium supplementation
Calcium chloride contains 6.8mmol calcium vs 2.2mmol in calcium gluconate
What are the signs and symptoms of low calcium?
Mental status changes
Neuromuscular excitability - tetany, Chvostek sign (contracture of the facial muscles produced by tapping on the facial nerve), Trousseaus sign (carpopedal spasm with contraction of fingers elicited by BP cuff inflation)
Seizures
What systems are used to classify kidney injury?
RIFLE (risk injury failure loss end-stage renal disease)
KIDGO (kidney disease:improving global outcomes)
AKIN (acute kidney injury network)
What is contrast-induced acute kidney injury?
The development of AKI within 48 hours of a contrast load
What mechanisms may contribute to contrast induced AKI?
- direct nephrotoxicity of reactive oxygen species
- imbalance of vasoconstriction vs vasodilatation
- increased oxygen consumption
- contrast-induced diuresis
- increased viscosity of urine
What are the risk factors for contrast-induced AKI?
- > 75 yrs
- Underlying renal impairment - eGFER < 60
- pre-renal: hypovolaemia, hypoxaemia
- renal: diabetes, hypertension, renl artery stenosis
- post-renal: renal calculi, other obstruction
- Nephrotoxic drugs
- IV contrast > oral contrast; risk proportional to the load.
Describe the KIDGO classification of AKI
- Cr 1.5-2 fold increase in baseline. > 26.5 increase. urine output < 0.5ml/kg/hr for 6-12 hours
- 2-3 fold increase in baseline creatinine. u/o < 0.5ml/kg/hr for > 12 hours
- > 3 fold increase in baseline Cr, Cr > 354, need for RRT. U/o < 0.3 ml/kg/hr for > 24 hours or anuric for >12 hours.
What strategies help prevent contrast-induced nephropathy?
- Avoid contrast in high risk patients - consider other imaging modalities. If contrast is necessary - use the lowest possible dose, avoid repeat dosing.
- Stop other nephrotoxics
- IV hydration
- IV sodium bicarb - it’s postulated that alkalinisation of renal tubular fluid reduces production of ROSin addition to volume expansion.
- RRT - removes contrast but there’s no evidence that it works prophylactically.
- NAC - given for 2 days prior to contrast - no definitive evidence for any benefit.
How is contrast- induced nephropathy diagnosed?
A rise in serum creatinine > 44 or an increase in cr by 25% from baseline within 48 hours of contrast (KDIGO)
How should you manage a patient with AKI?
ABCDE approach
The London AKI network have producerd a STOP-AKI acronym
S - sepsis and hypoperfusion - treat sepsis, ensure euvolaemia, optimise cardiac output
T - toxins - remove nephrotoxics
O - Obstruction - rule this out with renal trast US +/-0 catheterisation
P - primary renal - screen for intrinsic renal disease, urine dip +/- immunological/viral screen
What are the indications for RRT on the ICU?
- Metabolic acidosis
- Hyperkalaemia
- Symptomatic uraemia
- Fluid overload unresponsive to medical therapy
- treatment of overdose with dialysable toxins e.g lithium and salicylates
Describe CVVHF
Continuous veno-venous haemofiltration
- utilises the principle of v=convection
- there is bulk flow of solute and water down a hydrostatic pressure gradient, across a semi-permeable membrane
- rate of fluid removal is proportional to blood flow rate, hydrostatic pressure gradient and membrane surface area.
Describe CVVHD
Continuous veno-venous haemodialysis
- utilises the principle of diffusion (not widely used in the UK)
- There is a countercurrent of flow of blood and dialysate, with diffusion of solutes down a concentration gradient, across a SPM
- The higher the dialysate and blood flow rates the better maintained the concentration gradient and the more effective the solute removal.
Describe CVVHDF
Combines convective and diffusive clearance of solutes
What is SCUF
Slow continuous ultrafiltration
Ultrafiltration only - i.e. solely fluid removal
What is SLEDD?
Sustained low-efficiency daily dialysis
Can be performed for 8-10 hours per day, usually overnight
benefits from being intermittent but with less haemodynamic and osmotic disturbance that intermittent haemodialysis
Are there any studies looking at the effluent dose in RRT?
Generally it’s initially started at 35ml/kg/hr
- The RENAL trial (NEJM 2009) showed no mortaloty benefit when doses in excess of 25 were used
- the IVOIRE study (ICM 2013) failed to show any benefit with ultra-high flow rates (70)
How quickly should you reduced urea in patients who are uraemic that you’re starting on RRT?
By 30% or less in the first 24 hours
Otherwise you risk disequilibrium syndrome
Describe the pros and cons of pre- and post filter fluid replacement
- If you replace fluid pre-filter you reduce the bloods viscosity and reduce the risk of clotting inside the filter, however it also reduces solute clearance
- if you replace it post then this is better for solute clearance, however my compromise the lifespan of the filter.
Typically a compromise is made e.g. pre:post ratio 30:70.
What are the pros and cons of using citrate as an anticoagulant?
Advantages - goo regional anticoagulation, decreased risk of bleeding, premixed solutions with established protocols to follow.
Disadvantages - large sodium load with trisodium citrate, metabolic alkalosis (citrate metabolised to lactate in the liver), special dialysate required, contra-indicated in liver failure (citrate is acidic, so causes a metabolic acidosis in liver failure)
What is the pathophysiology of major burns?
- Burn -> SIRS -> activation of inflammatory cascade (can lead to ARDS)-> increased vascular permeability -> generalised oedema
- Inhalational injury -> ARDS or airway obstruction
- Hypermetabolic state -> increased protein catabolism, increased gluconeogenesis, decreased protein synthesis -> decreased wound healing, immunosuppression, increased infective complications.
How is burn severity assessed?
- Burn area
2. Burn depth
How do you assess burn area?
- Lund-Browder charts - age specific
- Rule of nines (head =9%, back =18%, arm = 9%, leg = 18%, perineum = 1%)
- Patients palm and adducted fingers also estimate 1%
How do you assess burn depth?
- Superficial - involves the epidermis only, erythematous, painful and dry with no blistering
- Partial thickness - erythematous, painful and oedematous with blistering
- Full-thickness - painless and white
What are the management priorities in a patient presenting with major burns?
ATLS approach
- Airway
- IV access and fluid resuscitation
- Analgesia - opioid +/- ketamine
- Avoid hypothermia
- Early surgical management - urgent escharotomy. Debridement of deep burns allows controls of the SIRS response and reduces metabolic rate - improves M+M.
What features of major burns would suggest the need for intubation?
- Features suggestive of potential inhalational injury - facial burns, carbonaceous sputum, singeing of nasal hair, oropharyngeal oedema, stridor, hoarse voice
- Other features e.g. neck burns, resp failure, reduced conscious level, to facilitate intervention/humanitarian
How to do calculate fluid requirements in burns patients?
Parkland formula calculates the volume required for the first 24 hours
= 4mls x kg x %BSA
Half is given in the first 8 hours and the other half over 16.
What is inhalational injury?
Caused by prolonged smoke exposure in a confined space particular in the presence of neurological impairment. It includes:
- Upper thermal injury
- may cause significant airway oedema
- consider early intubation with an uncut tube
- Chemical irritation throughout the respiratory tract
- caused by direct injury to the respiratory epithelium and capillary endothelium by acidic or alkaline compounds released from burning material
- results in severe tracheobronchitits, impaired mucociliary clearance and loss of surfactant causing atelectasis
- early inflammatory and capillary leak followed later by exudate formation produce an ARDS-type picture
How is inhalation injury managed?
- Early bronchoscopy - confirms diagnosis and assesses severity
- BAL/aggressive pulmonary toilet
- Triple nebuliser therapy - bronchodilators, heparin (to reduces fibrin deposition), NAC (mucolytic)
- Lung protective ventilation
What is ‘burn shock’?
A term used to describe the combination of hypovolaemic, distributive and cardiogenic shock seen in patients with major burns, which is refractory to massive fluid resuscitation
When should infection be suspected in burns patients?
Regular microbiological surveillance should be carried out
Three criteria from the American burn association should be present in addition to a documented infection before sepsis can be diagnosed
1. Temp < 36.5 or >39
2. Resp rate > 25, or MV > 12
3. Hr > 110
4. Glucose >12.8 in a non-diabetic pt
5. Intolerance of enteral feed for > 24 hours
6. Plt count < 100 (> 3 days after resuscitation phase)
What is the pathophysiology of carbon monoxide poisoning?
CO has an affinity for Hb 250 times that of oxygen. There is impaired oxygen delivery to the tissues due to reduced oxygen carrying capacity and reduced dissociation once bound - left shift in the oxygen dissociation curve
Additionally there is inhibition of cytochrome oxidase, resulting in impaired oxygen utilisation at the mitochondrial level
How does CO poisoning present?
N+V Headache Hypotension Confusion, coma, seizures Cherry-red skin discolouration in rarely seen
How is CO poisoning investigated?
HbCO level on ABG
How is CO poisoning managed?
100% oxygen, which reduces the half-life of CO from 4 hours to 1
I+V if HbCO > 25%
Hyperbaric oxygen at 3atm reduces half-life to 15-20 mins, which might be indicated in pregnancy if > 15%, if > 40% or pt is in a coma
What is the pathophysiology of cyanide poisoning?
Cyanide inhibits mitochondrial cytochrome oxidase, blocking oxidative phosphorlylation and resulting in anaerobic metabolism.
How does cyanide poisoning present?
SOB hypotension Dizzy Vomiting Psychomotor agitation LOC Unexplained metabolic acidosis and high central venous saturation
How is cyanide poisoning managed?
Supportive therapy aimed at maximising oxygen delivery Antidotes: 1. Hydroxycobalamin 2. Dicobalt edetate 3. Sodium thiosulphate
What is the prognosis in CO poisoning?
Poor correlation between HbCO level, symptoms and long-term outcome
HbCO > 60% is likely to be fatal
What is the prognosis in cyanide poisoning?
Good for patients with moderate symptoms and rapid treatment
Poor in those who suffer cardiac arrest
Those who survive are at risk of neurological sequelae including delayed manifestations such as movement disorders and neuropsychiatric disturbance.
What are the criteria for referral to a burns centre?
- age < 5 or > 60
- Presence of significant co-morbidities e.g. DM, pregnancy, cardioresp disease, immunosuppression, cirrhosis.
- Site - hands, face, perineum, any flexure, circumferential full or partial thickness.
- Inhalational injury
- Mechanism - chemical injruy, ionising radiation, high pressure steam, high tension electrical injury, cold injury, hydrofluoric acid, suspicious of NAI
- Dermal or full thickness burns > 5% in under 16s or > 10% over 16.
What are the risks of over-resuscitating a burns patient?
Generalised oedema
Abdo/limb compartment syndrome
Pulmonary oedema
Need for prolonged ventilation
What are the possible respiratory complications in major burns patients?
Airway obstruction
ARDS
What are the possible cardiovascular complications in burns patients?
Arrythmias
Ischaemia
Cardiac failure
Vasoplegia
What are the possible neurological complications in burns patients?
Pain
Opioid tolerance
What are the possible renal complications in a burns patients?
AKI - secondary to under resuscitation, abdo compartment syndrome or rhabdo
What are the possible GI complications in burns patients?
Increased nutritional requirements due to hypermetabilism - may last up to 2 years
increased protein catabolism
Stress ulceration
What haematological complication are burns patients at risk of?
VTE
What is a bronchopleural fistula?
An abnormal communication between the bronchial tree and pleural space, which causes an air leak from the lunk
It manifests as a persistent air leak or a failure to re-inflate the lung despite chest tube drainage for 24 hours.
How are air leaks from the tracheobronchial tree classified?
The Robert David Cerfolio classification
- Continuous - the leak is present throughout the respiratory cycle. Seen in those receiving mechanical ventilation or who have a BPF
- Inspiratory
- Expiratory
- Forced expiration
What are the causes of BPF?
- Most commonly post pulmonary resection with increased risk in right sided procedures, uncontrolled pleural/pulmonary infection, pre-op steroids, radiation, diabetes, malignancy, mechanical ventilation for > 24 hours
- Other causes includer
- trauma
- ARDS
- infection
- necrotising lung disease
- iatrogenic
- persistent spontaneous pneumothorax
- complication of mechanical ventilation
What are the clinical features of a BPF?
- Dyspnoea
- hypotension
- SC emphysema
- Cough with expectoration of purulent material
- Shifting of the trachea and mediastinum
- persistent air leak in a MV patient
- persistent bubbling of ICD
How is a BPF diagnosed?
- CXR - increase in intrapleural space, new air/fluid level, tension pnuemothorax
- Bronchoscopy - can confirm and localise by visualisation of continuous return of bubbles on bronchial washing
- CT chest - imaging modality of choice
- Others - vetilation scintigraphy
How does BPF differ from pnuemothorax?
A BPF is a direct communication between the central bronchial tree and the pleural cavity
A pneumothorax is a peripheral communication between a ruptured bleb or alveolar duct and the pleural cavity
What are the potential physiological consequences of a BPF in a mechanically ventilated patient?
Continuous air leak leading to delayed healing
- Inability to apply PEEP
- Loss of effective tidal volume secondary to inability to maintain adequate alveolar ventilation
- failure of lung re-expansion
- inappropriate cycling of the ventilator
- delayed weaning from the ventilator
How is a BPF managed?
Initial management
- treat tension pneumothorax, major bronchial stump dihiscence will need immediate re-suturing, pulmonary flooding will need affected side down posture
General - large chest drain, suction to drain, treat infection
Ventilated pts - minimise PEEP, TV, insp time and resp rate, encourage spont vent, extubate if able
How are large persistend BPF’s managed?
Independent lung ventilation using DLT and 2 ventilators
Bronchoscopic repair if < 8mm
Surgery - thoracoplasty, stump stapling, pleural abrasion and decortication
ECMO
What are the ICU consequences of a large BPF?
- Difficulty weaning
- Hypoxia/hypercarbia
- Inability to apply PEEP
- Prolonged use of sedatives
- Need for further surgery
- Potential need for DLT/2 ventilators
- High M+M
How can arrhythmias be classified?
May be classified according to
- Heart rate - i.e. brady or tachy
- Origin of arrhythmia - i.e SVT or VT
- Regular vs irregular
What are the causes of AF?
- Hypovolaemia
- Sepsis
- Metabolic disturbances e.g. hypokalaemia, hypomagnesaemia
- Hypoxia
- Ischaemia
- Thyrptoxicosis
- PE
How is AF managed?
ABCDE approach
1. DCCV if there are adverse signes e.g. SBP < 90, pulmonary oedema, reduced GCS/syncope, chest pain
2. Treat underlygin cause e.g. electrolyte disturbances, sepsis
3. Rate control vs cardioversion
Rate control with beta blocker or CCH e.g. diltiazem/verapamil e.g. if AF > 48 hours
Chemical cardioversion with amiodarone or electrical - may be unsuccessful if underlying cause is not treated.
What is atrial flutter?
A type of SVT that is caused by the presence of a re-entry circuit within the right atrium
The atrial rate approaches 300 bpm and the AV node blocks the rapid flutter waves producing a lower ventricular rate e.g. 2:1 (rate ~150) or 3:1 (rate ~ 100)
How is atrial flutter treated?
It’s normally unresponsive to vagal manoeuvres
Adenosine may reveal the underlying rhythm but will not cardiovert it
Rate control to increase the AV block, or chemical or electrical cardioversion may be required
What is atrioventricular nodal re-entrant tachycardia?
AVNRT is a type of SVT and is the commonest cause of palpitations in patients with a structurally normal heart
It’s paroxysmal often provoked by alcohol or caffeine
The resultant tachycardia is regular and ranges between 140-280 bpm
There are typically 2 functional pathways located aorund the AVN: a slow, posterior, pathway and a fast, anterior, pathway. One allows antegrade conduction and the other retrograde.
What are the different types of AVNRT?
- Slow-fast AVNRT (80-90%) - slow anterograde and fast retrograde conduction. P waves often hidden within corresponding QRS complexes or seen as a pseudo-R wave just after the QRS in V1 or V2
- Fast-slow (~10%) - fast anterograde and slow retrograde conduction. QRS-P-T complexes are seen (P waves within the ST segment)
- Slow-slow (< 5%) - slow anterograde and slow retrograde conduction via fibres in the left atrium. P wave seen in mid-diastole, often just before the QRS complex meaning may be mistaken for sinus tachycardia.
How do you treat AVNRT?
- Vagal maneouvres
- Adenosine may cardiovert rhythm
- Beta-blockers
- Flecainide or amiodarone are second line.
What is an atrioventricular re-entrant tachycardia?
AVRT is an SVT caused by a re-entrant circuit that is anatomically distinct from the AVN and can cause pre-excitation of the ventricles. This can degenerate into tachycardia because there is no AVN to delay conduction. The commonest cause of AVRT is WPW syndrome.
What is Wolf-Parkinson-White syndrome?
It’s caused by aberrant conduction via the Bundle of Kent, a congenital accessory pathway. Impulses may be conducted in a antereograde or retrograde fashion, but more commonly are bidirectional.
What are the ECG changes seen in WPW?
The ECG changes (which may only be present intermittently) include:
- Delta waves
- PR < 120 ms
- QRS-T wave discordance (i.e the T wave deflection is in the opposite direction to the QRS)
- Presence of tall R waves and T wave inversion in the precordial leads mimicking either RV or LV hypertrophy
What are the two types of WPW?
Type A or type B
Type A = positive delta wave in precordial leads, dominant S wave in V1 (left-sided pathway)
Type B = negative delta wave in V1 (right sided pathway)
Describe the conduction of impulses through the AVN in WPW
AVRT is often triggered by premature beats and the features of pre-excitation are lost. Conduction through the AVN may be either:
- Orthodromic (~95%) - antegrade with retrograde conduction through the accessory pathway resulting in narrow complexes, rate 200-300, no visible p waves, pattern mimics AVRNT
- Antidromic - retrograde, with antegrade conduction through the accessory pathway resulting in broad complexes, rate 200-300
How is AVRT managed?
- Vagal manoeuvres
- Adenosine may cardiovert the rhythm
- CCBs are first line if adenosine unsuccessful
- DCCV is necessary in the presence of adverse signs
What happens if AF develops in patients with WPW?
The accessory pathway allows for rapid conduction directly to the ventricles, bypassingthe AVN.
The complexes are broad and the rate is well over 200bpm
treatment with AVN blocking drugs e.g. adenosine, beta-blockers and CCBs may increase conduction via the accessory pathway and cause degeneration into VT or VF.
Procainamide or DCCV are preferred.
How do you differentiate VT from SVT with abberancy?
A broad complex tachycardia is more likely to be VT if there is:
- AV dissociation (P waves superimposed on T waves or between QRS complexes)
- Extreme axis deviation (lead 1 is positive, lead aVF is negative)
- QRS > 160ms
- Fusion beats (hybrid of sinus + ventricular complexes
- Capture beats (normal conduction or an atrial impulse through the AVN)
- Concordance across the precordial leads
- Notching seen near the top of the S wave - Josephson’s sign
What are the causes of long QT interval?
- Congenital
- Romano-Ward syndrome (AD|)
- Jervell-Lange-Neilson (AR, a/w/ congenital deafness) - Electrolyte disturbance
- hypokalaemia, hypomagnesaemia, hypocalcaemia - Drugs
- antiarrhymics e.g. sotolol, amiodarone
- antibiotics e.g. erythromycin, fluconazele
- psych drugs e.g. TCAs, SSRIs, phenothiazines - Myocardial ischaemia
- SAH
- Hypothermia
How are anti-arrhythmic drugs classified?
Commonly by using the Vaughn Williams classification
Class 1: sodium channel blockers, reduce the rise of phase 0.
- Type 1a - prolong the absolute refractory period e.g. procainamide
- Type 1b - shorten ARP e.g. lignocaine, phenytoin
- Type 1c - ARP unchanged e.g. flecainide
Class 2: beta blockers; reduce AVN conduction, prolong phase 4, reduce contractility
Class 3: potassium channel blockers; prolong phase 3, increase duration of phase 4, reduce contractility e.g. amiodarone, sotolol
Class 4: calcium channel blockers; reduce SA and AV node automaticity e.g. verapamil.
Describe the phases of a myocardial action potential
0 - depolarisation (fast Na+influx). Rapide increase in membrane potential from -90 to +20
1 - Repolariation (K+ efflux)
2 - Plataeu phase (K+ efflux balanced by calcium influx through slow L-type ca2+ channels)
3 - Repolarisation (L-type ca channels close)
4- RMP restored by Na/K ATPase (Na efflux/K influx)
How does adenosine work?
It’s an endogenous nucleoside with rapid onset and ultra-short duration of action
It acts on A1 receptors.causing transient AVN block and is used in the diagnosis and treatment of SVT.
It may cause severe bronchospasm and should be avoided in asthmatics.
What is normal core temperature?
Flucuates between 35.5 and 37.5
What is hypothermia?
Core body temp < 35 degrees.
Mild - 32-35
Moderate - 28-32
severe - < 28
How is heat lost from the body?
Radiation (40%) Convection (30%) Evaporation (15%) Conduction (5%) Respiration (10%)
What are the mechanisms by which a person may become hypothermic?
- Increased heat loss
- trauma: exposure, open body cavities, wet, neurogenic shock
- surgery
- anaesthesia
- immersion
- burns
- decreased thermogenesis - hypothyroidism, hypoadrenalism, elderly, malnutrition
- Impaired thermoregulation
- Drugs impairing thermoregulatory mechanisms e.g. anaesthetic agents
- Drugs impairing behaviour
- hypothalamic impairment that may occur as a result of any CNS pathology
- Altered hypothalamic set point e.g. sepsis, burns
What are the risk factors for hypothermia?
- Extremes of age
- Low socio-economic status
- Trauma
- Surgery
What are the cardiovascular complications of hypothermia?
- initial catecholamine surge causes hypertension and tachycardia with increased CO
- Widespread peripheral vasoconstriction
- decreasing temperature is subsequently accompanied by bradycardia
- Below 33 the ECG may show J waves (positive deflection at the J point) roughly proportional to the degree of hypothermia
- Bradyarrythmias esp AF are common
- Below 28 the heart become susceptible to developing VT/VF
- Asystole occurs at core temps < 20
What are the respiratory complications a/w hypothermia?
Depression of the normal ventilatory responses, with progressive bradypnoea
Cough reflex is lost and the pt develops profound bronchorrhoea
Apnoea occurs < 24 degrees
What are the neurological complications a/w hypothermia?
CNS depressant effect - reduced GCS, confusion and lethargy
Tendon reflexes are diminished and lost < 28 degrees
Coma ensues and pupils are fixed and dilated below 30
The EEG is isoelectric at temps < 20
What are the renal complications a/w hypothermia?
- The initial profound vasoconstriction results in cold diuresis in response to the apparent increase in central intravascular volume - the ensuing hypovolaemia becomes clinically apparent as the patient is rewarmed.
- Hypothermia impairs ADH secretion and increases resistance to its action, worsening the polyuria
What are the gastrointestinal effects of hypothermia?
Gastric motility is impaired
Hepatic blood flow is reduced, slowing drug metabolism
What are the metabolic/endocrine complications of hypothermia?
- The BMR reduces by 7% for every 1 degree drop in core temp
- there is reduced oxygen consumption, co2 production, and glucose and fat metabolism
- there is metabolic acidosis with accompanying hyperkalaemia, hypermagnesaemia and hyperglycaemia
- shivering occurs - which increases BMR by a factor of 5-at a maximal at 35 degrees and decreases as temp drops further. It ceases completely when hepatic glycogen stores are exhausted and muscles stiffen (< 32)
- hypothermia causes pancreatitis and increases insulin resistance
What are the haematological complications a/w hypothermia?
- There is thrombocytopenia due to sequestration, bone marrow depression and consumption
- A progressive coagulopathy develops, eventually resulting in DIC (enzymes in the coag-cascade are temp sensitive)
- Blood viscosity increases as temperature drops
- WCC drops and immunity is impaired
How would you manage a person with hypothermia?
ABCDE approach
1. Resus - pulse check may be difficult, echo may help
For hypothermia-associated cardiac arrest defib is unlikely to be successful in VF - give up to three shocks and then try again after temp > 30; avoid ALS drugs until temp > 30 - double dose intervals at core temps 30-35. You are not dead until you’re warm and dead (temp > 32)
2. Manage the hypothermia
3. Treat any underlying cause
4. Manager complications of hypothermia
how should you rewarm a hypothermic patient?
In acute hypothermia rewarming can occur quite rapidly at 2-3 degrees per hour
- Passive rewarming - remove wet clothes, dry pt, increase ambient temp, blankets, hat, encourage mobilisation if possible
- Active external rewarming - forced air blankets, radiant heaters
- Active internal warming - warm IV fluids, warm inspired gases, peritoneal or intravesical lavage with warm water, central venous heat exchange catheters, extracorporeal methods
What complicationds occur when rewarming a hypothermic patient?
- Afterdrop - vasodilatation and release of cold blood from peripheries into the core may cause a second drop in temperature, not usually clinically significant.
- Acidosis and hyperkalaemia - consequence of reperfusion
- Shock (multifactorial). Hypovolaemia as a result of vasoconstriction and subsequent cold diuresis, cardiogenic shock due to myocardial depression, distributive shock due to vasodilatation on rewarming.
What’s the evidence for therapeutic hypothermia post cardiac arrest?
In 2002, 2 RCTs in the NEJM of TH after OOHCA demonstrated significant improval in neurological outcomes. As a result the International liaison Committee on Resuscitation (ILCOR) recommended that all unconscious patients who have suffered an OOHCA where the rhythm was shockable should receive 24 hours of TH to 32-34 degrees. The UK resus council extrapolated this to include all cardiac arrests regardless of underlying rhythm.
- however, in 2013 the TTM trial (NEJM) compared targeted temp management to either 33 or 36 degrees. There was no difference in neuro outcome or all-cause mortality between the 2 groups. Interestingly, there was no difference in the incidence of adverse events.
When is therapeutic hypothermia used and when is it not used?
- OOHCA
- Perinatal hypoxia
- Deep hypothermic arrest for aortic root surgery
It’s not used following TBI - increases mortality.
