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Anaesthesia
& Intensive Care
For FCAI, FRCA & EDAIC
Part: 1 - Intensive Care Medicine
Modified by
AYMAN EDAROUS
Pathogenesis of VAP:
It is thought to be caused by entry of infected secretions into distal bronchi.
Patients are usually immunosuppressed, and their oropharynx becomes colonised with
organisms, especially G-ve bacteria.
Oral and nasal tubes cause trauma, leading to infections such as sinusitis.
The natural protections like cough reflex, tracheobronchial secretions, mucociliary linings,
saliva, and nasal mucosa are less effective in these patients.
The pathogens enter the lower lung through mechanical routes such as around the
endotracheal tube cuff, suction catheter, and ventilation tubings.
General measures: Use of sterile equipment, regular hand washing, using barrier nursing such as
gloves and an apron, and minimal contact with patient usually reduce the incidence of any infection
in ICU.
Specific measures: This include reducing the load of pathogens and their entry into lower
respiratory tract.
• Reducing Aspiration
*Patients nursed in 30-45o degree head-up position
*Use of ETT with subglottic secretion drainage port with regular subglottic suction.
*Regular Monitoring /4 hr and maintainence of ETT Cuff Pressure (20-30 cmH2O).
**Scores can range from 0 to 12 with a score of ≥ 6: good correlation with the presence of VAP.
Sepsis:
Life-threatening Organ Dysfunction caused by Dysregulated Host Response to Infection.
- Septic Shock:
Subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher
risk of mortality.
More than 1 h may be required for resuscitation to be completed, but initiation of resuscitation and
treatment, such as obtaining blood for measuring lactate and blood cultures, administration of fluids
and antibiotics, and in the case of life-threatening hypotension, initiation of vasopressor therapy, are
all begun immediately.
Apply Vasopressors
If blood pressure is not restored after initial
fluid resuscitation, then vasopressors should
be commenced within the first hour to
achieve mean arterial pressure (MAP) of ≥ 65
mmHg.
Acute Phase:
*Lasts for up to 7 days from Onset.
*Hypoxemia, Infiltrates on the Chest Radiograph, and in Pulmonary Compliance.
*Leakage of Protein-rich fluid into the Alveoli, Haemorrhage, and Diffuse Neutrophilic Alveolar
Infiltrate with resultant Endothelial and Epithelial Injury.
Proliferative Phase:
*Can occur from day 5 onwards.
*Characterised by persistent Hypoxaemia, Dead Space, and Lung Compliance.
*Accompanied by Interstitial Fibrosis, Proliferation of type 2 Alveolar Cells, and disruption of Capillary
function due to Microvascular Thrombus Formation.
*In some these changes resolve and clinical improvement follows; others progress into the Chronic or
Fibrotic Stage.
Chronic Phase (Fibrotic Stage):
*Not clearly defined.
*May starts as early as day 14 and can Last Weeks
*Widespread Pulmonary Fibrosis and Loss of the normal Lung Structure leads to worsening Lung
Compliance and an in Dead Space.
*Clinically there is a in CO2 excretion which may be accompanied by an improvement in
Oxygenation.
**All of the above happen in a heterogenous way throughout the Lungs with some parts worse
affected than others.
Further Diagnosis:
- Serum Amylase (> 3X), Lipase (> 3X), Tryptase .
- CT scan early if diagnosis uncertain, at 48-72
hours for Prognostication and Management.
-MRCP, Endoscopic ultrasound (EUS) and USS
(diagnosis of gallstones).
Complications of Pancreatitis:
Patients with severe pancreatitis can have systemic
and local complications, including:
Pleural effusion, ARDS, ileus, Gastric ulceration,
Renal failure and cardiovascular compromise.
Prognostic Methods:
*APACHE II score: [Physiological Parameters and a Chronic Health Evaluation]
Score greater than 8 predicts a severe episode of pancreatitis,
maximum score 71.
*Ranson's Score:
Developed from an American of alcohol induced pancreatitis.
*Balthazar CT Severity Index.
*BISAP score.
Management:
Early identification and management of
organ failure and aggressive resuscitation to
optimise tissue perfusion is important in
cases of severe pancreatitis.
- Assessment of Circulation: MAP, UO, Pulse Oximetry, Acid-Base Status, CO and CVP.
- Specific Renal Investigations: Urea and Creatinine, Potassium, Liver Function Tests, Creatinine
Kinase(CK)/urinary Myoglobin, Urinary Sodium, Urine plasma:osmolality ratio, Urine Microscopy, U/S
renal tracts.
- Glomerular Filtration Rate (GFR) [Overall index of Renal Function].
-Rate at which Substances are Filtered from the Blood of the Glomeruli into the Bowman’s
Capsules of the Nephrons.
-Calculated by the clearance of specific substances which have a constant plasma concentration,
are freely filtered by the glomerulus, and are not subsequently secreted, reabsorbed or
metabolised. The clearance of substances from the plasma are used as an index of GFR.
-Creatinine clearance is the most common in clinical use.
RRT circuit and how does it work to remove fluid and solutes:
Intermittent RRT: less expensive, simpler to run, requires less time, rapid fluid and solute removal is
possible. However, critically unwell patients may become haemodynamically unstable, and
hypotension may cause further renal injury.
Continuous RRT: slower and more expensive than Intermittent, and requires premixed fluids and
anticoagulation. Slower fluid and solute removal reduces risk of haemodynamic instability.
Peritoneal: inefficient at removing large amounts of fluid/solute. Increases intra-abdominal pressure,
which may splint diaphragm in unwell patients, so contraindicated in critical care.
-Veno-Venous circuit -pump driven, reliable high flow rates. Commonly used now.
-Arterio-Venous circuit –driven by patients own BP. Less reliable, associated with catheter related
complications, so rarely used now.
Mechanism of Fluid Removal (Ultrafiltration):
Produced by creating a positive pressure in the blood compartment of the dialyser and is facilitated
by creating a negative pressure in the dialysate compartment. The resulting trans-membrane
pressure is the driving force for ultrafiltration.
Pharmacological
Unfractionated Heparin:
-Typically a bolus followed by a prefilter infusion.
-Cost effective, can be fully reversed with protamine.
-Requires monitoring of APTT.
Low Molecular Weight Heparin:
-Lower incidence of heparin-induced thrombocytopenia.
-Longer half-life than UFH, only partially reversed by protamine.
Prostaglandins:
-Inhibit platelet function. Can be used alone, or with heparin (synergistic effect).
-Short half-life, so administered as infusion.
-Potent vasodilator, so can reduce MAP.
-May inhibit hypoxic pulmonary vasoconstriction, so may cause/worsen hypoxaemia.
-Expensive.
Sodium Citrate:
-Infused prefilter.
-Chelates calcium and inhibits clot formation.
-Calcium infusion required post filter.
-Cause metabolic derangements (hypoCa, hypoMg, hyperNa, metabolic alkalosis, or acidosis).
Motor Dysfunction:
- Progressive Motor Weakness, usually Symmetric, Ascending from the Legs.
- Reflexes: Areflexia (reflexes may be preserved in AMAN)
- Cranial Nerves: Facial Palsy and Bulbar Weakness.
- Eyes: Ophthalmoplegia, Ptosis and Diplopia.
- Respiratory Failure: secondary to Respiratory Muscle Weakness.
Sensory Dysfunction:
-Pain is most severe in the shoulder girdle, back, buttocks, and thighs.
-Paraesthesia and Numbness usually begins in the toes and fingertips and progresses upward but
generally does not extend beyond the wrists or ankles.
-Loss of vibration, proprioception, touch, and pain distally may be present
Autonomic Dysfunction:
-Tachycardia, Arrythmia, Labile Blood Pressure, Orthostatic Hypotension.
-Urinary Retention, Paralytic Ileus and Hyperhydriasis.
Diagnosis:
- GBS should be suspected in all patients with unexplained motor weakness or a new sensory
deficit affecting the limbs
History: of recent Gastrointestinal or Respiratory infection should be sought.
Examination: Symptoms and Signs (SEE BEFORE).
Investigations:
- Daily measurement of Vital Capacity.
- Lumbar Puncture/ CSF analysis: Protein and Normal WBC.
- Electrophysiological Studies: aid diagnosis and help to differentiate GBS from other
neuropathies. Each subtype has different electrophysiological features.
- Muscle biopsy: may help to distinguish GBS from a primary myopathy in unclear cases
- MRI: May show spinal nerve root enhancement with gadolinium
- Stool Cultures may show Campylobacter jejuni infection.
- Blood Tests: Anti-Ganglioside Antibody. Anti-GM1 antibodies are associated with a worse
prognosis and Anti-GQ1 antibody is associated with MFS.
IV Immunoglobulin (IgG):
The initial treatment of choice
IV 0.4mg/kg OD for 5 days.
Much more convenient than plasma exchange, same efficacy and Less Side Effects.
It should be commenced within 2 weeks of the onset of symptoms.
Side Effects (Rare): nausea, fever, headache, a transient rise in liver enzymes, encephalopathy,
meningism and malaise. Serious SE; skin reactions (e.g. erythroderma) and hypercoagulability.
Contraindications:
*IgA deficiency (increased incidence of Anaphylaxis) and Previous anaphylaxis to
immunoglobulin therapy. IgA levels must be checked in all patients prior to administration of
immunoglobulin.
* Renal impairment as renal function may deteriorate further with immunoglobulin therapy.
*Severe congestive cardiac failure is also a relative contraindication
The Prognosis:
Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12
months.
Patients may have persistent weakness, areflexia, imbalance, or sensory loss.
Some patients may have permanent neurologic sequelae including bilateral foot drop,
intrinsic hand muscle wasting, sensory ataxia, and dysaesthesia.
The mortality rate is approximately 10%, usually from complications such as cardiac arrest
secondary to autonomic dysfunction, sepsis, pulmonary embolism and respiratory infection.
Poorer Prognosis Is Associated with:
Older Patients
Preceding Campylobacter Jejuni Infection
Need For Mechanical Ventilation
Rapid Progression of Symptoms
Extensive disease.
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 35
7- Status Epilepticus
(a) What is the WHO definition of status epilepticus (SE)? How may it be classified?
(b) What are the systemic effects of SE?
(c) What are the causes of SE?
(d) Describe the pharmacological treatment options for SE.
(e) Describe the non-pharmacological options for treatment SE
Classification:
**N.B. These are usually accompanied by a neuromuscular blocking agent in order to facilitate
tracheal intubation for the purpose of airway protection
-Neuromuscular blocking agents may stop overt seizure activity but patient may continue to have
NCSE
*N.B. In the case of the eclamptic fit, first line treatment is 4g MgSO4 IV over 15minutes, followed by
infusion as necessary. Benzodiazepines and other anti-epileptics are not used in this scenario.
Supportive care includes airway maintenance and protection with opening manouvres, recovery
position to avoid aspiration, adjuncts or formal protection with intubation via a cuffed, ETT.
- Identify and correct any underlying cause e.g. hypoglycaemia or electrolyte disorders, antibiotics if
infection considered likely, if known cerebral tumour consider IV dexamethasone to reduce swelling
- Treat hypotension with IV fluid therapy initially taking care not to overload (N.B. be wary of
neurogenic pulmonary oedema or raising ICP);
Vasopressor agents can be used to prevent fluid overload
- Ensure patient is not at risk of injuring themselves or others whilst actively seizing
- Aim to achieve and maintain normothermia
(c) Critical Illness Neuro-myopathy (CINM): All of Patient meets criteria for ICUAW; Patient meets
criteria for CIP; Patient meets criteria for probable or definite CIM
Rehabilitation: Should begin early during ICU admission, and continue throughout hospital stay and
after discharge; Phased physical and mobilisation therapy,
-Beginning with passive limb movement.
-Occupational therapy.
-Cycle Ergometry.
-Electrical Muscle Stimulation.
- All equipment and bed spaces should be cleaned with Chlorine containing antisepsis daily and after
every toilet use.
- Good antibiotic stewardship- avoiding high risk antibiotics in high risk patients, stop unnecessary
antibiotics and have guidelines for narrow spectrum antibiotics.
- Careful use of proton pump inhibitors - Restoring enteral bacteria with live culture yoghurts
- Enteral infusion of emulsified faeces has been described
- Immunoglobulin is being trialed with positive results.
Common pathogens:
-MRSA – methicillin-resistant Staphylococcus aureus
-CNS – coagulase negative Staphylococcus
-Enterococcus spp.
-Pseudomonas aeruginosa
-Acinetobacter baumannii
-ESBL – extended spectrum beta-lactamases
Antimicrobial Stewardship:
This refers to a coordinated programme that promotes the
appropriate prescribing and use of antimicrobials (including
antibiotics) in order to:
Reduce microbial resistance.
Decrease the spread of infection caused by multi-drug
resistant organisms.
Improve patient outcomes.
Risk of Malnutrition
Physical Signs
*Loss of Subcutaneous Fat
*Muscle Wasting,
*Peripheral Oedema and Ascites.
*Methods such as Triceps Skin-fold Thickness and Mid-arm circumference are
poor predictors because of the presence of Peripheral Oedema.
-Volitional Tests of Strength are often not possible in the sedated patient or in the presence of
critical illness poly-neuromyopathy.
-Laboratory indices, for example Serum Albumin or Urea Excretion, are occasionally utilized to
indicate nitrogen balance but are unreliable in the context of critical illness.
-Indirect Calorimetry is the Gold Standard in assessment of energy expenditure.
Normal Daily Nutritional Requirements:
* Water 30ml/kg
* Energy 30 kcal/kg
* Nitrogen 0.2 g/kg
* Glucose 3 g/kg
* Lipid 2 g/kg
* Sodium 1 mmol/kg
* Potassium 1 mmol/kg
* Calcium 0.1–0.2 mmol/kg
* Magnesium 0.1–0.2 mmol/kg
* Phosphate 0.2–0.5 mmol/kg.
The Metabolic Changes in Critical Illness that make Early Feeding preferable:
- Glycogen store utilization (Fasting hours)
- Insulin resistance Hyperglycaemia
- Cortisol Sodium and Water Retention (Stress Response)
- Catabolism:Protein Breakdown
- Increase Basal Metabolic Rate (BMR) by 40%
- Impaired Immune Function
- Poor wound healing
- Muscle Weakness
- Impaired Thermoregulation
- Increase Ventilator Dependent Days
a) Why should this patient receive early nutritional support and what are the clinical benefits?
b) List the factors that increase the risk of the development of VAP. (10 marks)
c) What measures may reduce the risk of development of VAP? (7 marks).
• A screening tool should be used to assess nutritional state. The Nutritional Risk Score (NRS-2002) is
validated in ICU; a score >5 is indicative of a patient at high risk.
• Benefits
o Reduced length of ICU and hospital stay
o Reduced morbidity and mortality
o Reduced risk of muscle atrophy
♣ Improve weaning
o Improved immune function
♣ Reduced risk of infection
o Improved GIT blood flow (if enteral)
♣ Improved healing
• Weigh up risks vs. benefits of enteral nutrition (EN) vs. parenteral nutrition (PN)
• Multidisciplinary approach required. If end ileostomy formed and no issues with bowel continuity,
EN is preferable.
• Nutritional requirements
o Calories - 25-30 Kcal/Kg/Day
o Protein - 1.2-2 g/Kg/Day
• This patient is at high risk of re-feeding, therefore starting at 50% requirements for two days and
increasing by 300Kcal/day is appropriate
o 1.5 Kcal/ml feed running initially at 30ml/hr to increase after two days
o Close monitoring of electrolytes required
• Disadvantages
o More expensive than oral nutrition
o Increased aspiration risk
♣ Increased potential for Ventilator Associated Pneumonia (VAP)
o May unduly stress ischaemic bowel
o May precipitate/ potentiate anastomotic leak
o Nasogatric tube required with potential for
♣ Incorrect placement and aspiration
♣ Skin breakdown/ local trauma
♣ Perforation of oesophagus, pharynx, stomach or bowel
o Intolerance
♣ Vomiting, excessive aspirates, abdominal distension, diarrhoea
o Malabsorption possible – resulting in unrecognised low caloric intake
Care Bundle:
A set of evidence-based interventions that, when used together, significantly improve patient
outcomes than if implemented individually.
Key Elements
- Each intervention should be widely accepted as good practice and widely applicable
- Should be adhered to for every Patient 100% of the time
- Can be used to measure Evidence Based Practice
- Each step able to be audited - done/not done/ local exclusion
- Audit focused on organizational aspects of performing intervention rather than how well
intervention performed
- Only compliant with bundle when every intervention completed or a step is excluded for pre-
defined reason.
Prevention of Delirium:
ABCDEF bundle:
-Spnotaneous Awakening Trial
-Spnotaneous Breathing Trial.
-Choice of Sedatives.
-Delirium Monitoring
-Early Mobility and Exercise
-Family engagement.
Management of Delirium:
Pharmacological Non-Pharmacological
Haloperidol: Medical Hx
- Reduces Hallucinations and Delusions Correct Visual and Hearing Impairments.
- Side effects: Extra-pyramidal side effects, Correct Metabolic Derangement.
Prolonged QT interval, Neuroleptic Diagnose and Treat Infection.
Malignant Syndrome Adequate Tissue Oxygen Delivery.
Adequate Analgesia.
Atypical Anti-psychotics [Olanzipine]: Remove Lines and Catheters promptly.
- Dopamine Receptor Antagonist and Medications
Serotonin Receptor Antagonists (5-HT2A) Avoid Deliriogenic Drugs were possible.
- Enteral administation required. Environmental
Orientate Patient Regularly.
Dexmeditomedine Reduce Noise and Reduce Sleep Disturbance
Mobilise Where Possible.
Heat is a form of energy- the total kinetic and potential energy of particles within a substance and
can be transferred from a hotter substance to a colder substance.
Temperature is a measurement of the quantity of heat energy; the tendency of a substance to gain
or lose heat relative to its surroundings; it is proportional to the mean kinetic energy of the particles
in the substance. 3 major scales for measuring temperature are Kelvin (SI unit), Celsius and
Fahrenheit.
Management
Identify and remove potential trigger factors, e.g. volatile inhalational agents in MH
Physical Methods
*Uncovering the patient
*Using cold towels/ice packs in axilla, groin, across the chest (avoid direct skin contact) *Cooling
blanket
* Invasive: cooled IV fluids, cool fluids into the peritoneum, bladder, pleura & stomach
*Intravascular cooling catheters, haemodialysis, cardiopulmonary bypass.
Pharmacological Methods
*Non- specific to reduce heat production- Sedative agents, neuromuscular blocking drugs
*Specific antipyretics- Paracetamol, NSAIDs
*Dantrolene- only specific indication is for use in MH but has also been described for treatment of
*Neuroleptic Malignant Syndrome
*For serotonin syndrome 5-HT2A antagonists such as Cyproheptadine may be used
*May include dopamine agonists, e.g. Bromocriptine for NMS.
Veno-arterial (VA-ECMO): allows gas exchange and haemodynamic support while blood
is pumped from the venous to arterial side
Arterio-venous (AV-ECMO): uses patient’s own arterial pressure to pump blood from
arterial to venous side, facilitating gas exchange.
-Vascular access
-Tubing
-Pump
-Gas exchange mechanism
Gas exchange mechanism
VA-ECMO:
- Refractory cardiogenic shock with underlying potentially reversible heart condition
- Weaning from cardiopulmonary bypass after cardiac surgery
- Bridge to cardiac transplantation or ventricular assist device
- Acute myocarditis
- Intractable arrhythmia
VV-ECMO:
- Aims to provide oxygenation and rest lungs, decreasing insult caused by mechanical
ventilation
- Any potentially reversible acute respiratory failure
- ARDS, associated with viral or bacterial pneumonia
- Graft dysfunction after lung transplantation
- Trauma (pulmonary contusion)
- Pulmonary embolism (if acceptable cardiac function)
Contraindications:
- Irreversible organ damage
- Multi organ failure
- Patients who are not candidates for transplantation
- Patients who cannot be anticoagulated (relative)
- Severe aortic regurgitation (VA-ECMO)
- Aortic dissections (VA-ECMO)
- Patient / proxy refusal
- Patients with “do not resuscitate” orders
- Severe bleeding and PVD increases risk of complications
- Haemorrhage
- Infection
- Lower limb ischaemia
- Abdominal compartment syndrome likely secondary to massive fluid resuscitation in
an effort to achieve adequate ECMO flows
- Clot formation
- Stroke
- Renal failure
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 70
- Nosocomial infection
- Mechanical mishaps e.g. Pump / oxygenator / circuit failure / breakage
Normal pressures within the heart that can be demonstrated with a PAC?
- As the PAC is floated through the right atrium a characteristic waveform is seen as
long as there is a competent tricuspid valve.
- This waveform represents venous return to the right atrium during ventricular
systole and right ventricular end-diastolic pressure.
- Normal right atrial pressure lies between 0-7/8 mmHg.
- As the PAC floats into the right ventricle the tracing changes.
- Ventricular systole is represented by the prominent upstroke and downstroke, while
ventricular diastole is represented by a more gradual upstroke that consists of an early
rapid filling phase, a slow filling phase and an atrial systolic phase.
- Two pressures are measured from the RV pressure waveform: the peak right
ventricular systolic pressure and the right ventricular end-diastolic pressure.
- Normal right ventricular systolic pressure varies from 15 to 25 mmHg and normal
right ventricular end-diastolic pressure varies from 3 to 12 mmHg.
- As the PAC passes through the pulmonary artery, the PAWP will be found when the
inflated balloon wedges in a distal branch of the pulmonary artery.
- This creates a static column of blood between the catheter tip and the left atrium.
- Pressure at both ends of the column equilibrates- therefore pressure at the distal
end of the catheter is equal to the pressure of the left atrium.
- Normal PAWP is between 6-15mmhg.
- The PAWP will represent the left ventricular end diastolic pressure as long as there is
no obstruction to flow between the left atrium and left ventricle.
The values and derived/calculated values that can be measured with a PAC:
Values that can be obtained from a PAC include pressures and waveforms for:
- Central venous pressures
- Right atrial pressure
- Right ventricular systolic and diastolic pressures
- Pulmonary artery systolic and diastolic pressures
- Pulmonary artery wedge pressure
Measurements may be derived or calculated:
- Left ventricular end diastolic volume
- Left ventricular end diastolic pressure
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 73
- Stroke volume
- Cardiac output via thermodilution
- Pulmonary vascular resistance
- Systemic vascular resistance
Late:
Infection
Venous thrombosis, pulmonary emboli
Catheter migration
Catheter embolization
Myocardial perforation
Nerve injury
The pros and cons of pulmonary artery catheters on the intensive care unitPros of
PAC in ICU:
As for the indications for PAC use
- For the use in diagnosis of complex conditions
- To measure the responses to therapy
- Can be used to answer a question that is not answered by standard monitoring and
whose answer could affect treatment choice
Cardiac output is the volume of blood ejected by the left ventricle per minute (equals Stroke volume
x heart rate). Influenced by preload, contractility and afterload
Preload is the end diastolic ventricular wall tension (tension at the point of maximal filling) – mainly
determined by venous return
Afterload is tension developed in ventricular wall during systole – largely determined by SVR
Systemic vascular resistance is all the forces that oppose blood flow through the systemic vasculature
– mainly determined by vasoconstriction in the arteriolar bed
Advantages
less invasive than PAC, less skill required as PAC not needed to be accurately positioned.
In general good agreement with CO measurements from PAC
Dynamic continuous measurement
Measures extra-vascular lung water – shown to correlate in severity of ARDS, no of ventilator days,
ICU duration and mortality
Can stay in patient for up to 10 days (unlike PAC – 72 hours)
No CXR required
Claimed to be cheaper
Patients usually already require a CVL and arterial line
Mechanism of Action:
The Intra-aortic balloon pump (IABP) is a mechanical device
that increases myocardial oxygen perfusion while at the same
time increasing cardiac output Coronary Blood Flow and
therefore Increasing Myocardial Oxygen Delivery.
It consists of a cylindrical polyethylene balloon that sits in the
aorta, approximately 2 centimeters from the left subclavian
artery and Counterpulsates:
That is, it actively deflates in systole, increasing forward
blood flow by reducing afterload through a vacuum effect.
It actively inflates in diastole, increasing blood flow to the
coronary arteries via retrograde flow. These actions combine
to Decrease Myocardial Oxygen Demand and Increase
Myocardial Oxygen Supply.
A computer-controlled mechanism inflates the balloon with
helium from a cylinder during diastole, usually linked to either
an electrocardiogram (ECG) or a pressure transducer at the distal tip of the catheter; some IABPs,
such as the Datascope System 98XT, allow asynchronous counterpulsation at a set rate, though this
setting is rarely used.
Helium is used because its low viscosity allows it to travel quickly through the long connecting tubes,
and has a lower risk than air of causing an embolism should the balloon rupture.
Procedure
*Percutaneous tracheostomy can be performed under local
anaesthesia but in the ICU it is usually performed under general
anaesthesia.
*Patient supine and the neck extended.
*Requires 2 people for the procedure: 1 to maintain the airway at
the top end , and 1 to perform the tracheostomy
*Ultrasound scanning of the neck reveals any abnormal vessels
near the surgical site.
* Landmarks are marked, including the suprasternal notch, cricoid
cartilage and tracheal rings when palpable.
*The components of the tracheostomy set and other equipment
are checked
*Lidocaine with Adrenaline 1:200,000 up to 10 ml is infiltrated into the
surgical site.
Steps
*Small transverse incision is made at the level of the 2nd tracheal ring (the midpoint between cricoid
cartilage and suprasternal notch in patients with normal anatomy).
*Blunt dissection is carried out until the trachea is felt with a finger.
*The existing endotracheal tube is withdrawn over the endoscope until the cuff is near the vocal
cords. The procedure can also be done with an LMA
*A Bonfils semi-rigid scope (or similar) or a flexible fibreoptic scope is used to visualise the airway
with display of images on a monitor
*The introducer needle and cannula is inserted into the trachea preferably below the second
tracheal ring in the midline under endoscopic visualization
*Following removal of the needle, a J-tipped guide-wire is inserted.
*A small starter dilator is inserted into the trachea to open a tract and is then removed.
A guiding catheter is then inserted over the guide-wire and followed
by an appropriate dilator (e.g. single-tapered dilator;
A tracheostomy tube of appropriate size is then inserted over the
loading dilator via the stoma
The entire procedure is performed under continuous endoscopic guidance to help reduce the risk of
malposition and false passage.persistent stoma and tracheal stenosis.
Basic principles were agreed by the National Tracheostomy Safety Project that would underpin
guideline development for patients with surgical airways:
Patients with tracheostomies or laryngectomies may be considered to have airways that are difficult
to manage, either leading to the formation of the airway stoma itself or as a result
Distinct bedside information and algorithms were required for patients with a potentially patent
upper airway and those with a laryngectomy. Bedside Information cards displaying whether the
patient had a tracheostomy or laryngectomy, type of tracheostomy, size or tube and date insertion.
This allows first responders to rapidly assess management options
It was recognised that separate algorithms were needed for patients with a potentially patent
upper airway and those with a laryngectomy
Overall style of the algorithms was to be based on the highly successful flow charts produced by DAS
to build on the success of previous guidance, highlighting how effective emergency management
requires careful advanced planning and a multi-disciplinary team approach
Oxygenation of the patient takes priority (not necessarily securing the airway immediately and
definitively, unless required for oxygenation)
Generic algorithm developed that would cover the vast majority of common and easil reversible
clinical situations that arise whilst accepting that a number of special circumstances do exist
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 86
Competencies and training are likely to be divided between those of the primary and secondary
responder. The primary responder (typically a nurse, junior doctor or allied health professional)
needs to be guided to detect airway problems, to assess tracheostomy and airway patency and to
provide basic emergency oxygenation. The secondary responder (typically an anaesthetist,
intensivist, head and neck surgeon or specialist practitioner) will have skills in conventional airway
management and will also be guided to use skills in managing the tracheostomy or stoma
The 'GREEN' algorithm for emergencies involving a patent upper airway. Contrast this with the
'RED' algorithm.
Green Algorithm: National Tracheostomy Safety Project 2012
Paired with green sign placed over bedspace of tracheostomy patient
For Tracheostomy patients (who have an anatomically connected and potentially patent upper
airway)
Date of insertion / Type / Size of tube documented
Step 1: Call for help
Step 2: Look listen feel at site of tracheostomy – Is the patient Breathing?
Step 3: If no start CPR, If yes apply high flow oxygen to face and tracheostomy site
Step 4: Assess tracheostomy patency;
Remove speaking valve
Remove inner tube
Suction catheter down inner tube
Step 5: If tracheostomy patent suction airway and continue ABCDE assessment. If tracheostomy not
patent:
Step 6: Deflate cuff and look, listen,feel
Step 7: Remove tracheostomy
Step 8: Primary Oxygenation: Bag mask ventilation (BMV) via face. If fails: BMV via tracheostomy
Step 9: Secondary Oxygenation: Oral Intubation (may be difficult). If fails: attempt intubation of
stoma (Size 6.0 ETT + Bougie)
For both Green and Red Algorithms, capnography or Mapleson C circuit should be used
Bedside equipment
• Humidification equipment
• Suction with selection of appropriate suction catheters
• Spare tracheostomy tubes
One the same size
One tube one size smaller
• Clean pot for spare inner cannula
• Sterile water for cleaning the suction tube
• Scissors (and stitch cutter if tracheostomy tube is sutured)
• Water soluble lubricating jelly
• Sterile dressing pack
• Tracheostomy dressings
• Tracheostomy tapes
• Personal protective equipment (gloves, aprons, eye protection)
• Sterile gloves for performing deep suction
• Nurse call bell: the patient may be unable to call for help verbally
• Communication aids: the patient may not be able to verbalise
• Bedside equipment checklist
Emergency equipment
• Basic airway equipment – oxygen masks, self inflatingbags, oral and nasal airways
• Advanced airway equipment – laryngeal mask airways and laryngoscopes with appropriate tubes
(arrest trolley or similar)
• Capnography (should be available immediately in critical care)
• A fibreoptic ‘scope (should be available immediately in critical care)
• Tracheal dilators
• Bougies
The Key items to elicit in the history in the patient presenting with an oral poisoning syndrome:
- Risk assessment: Obtain specific history from patient / ambulance crew / relatives / collateral
history – including last time seen prior to ingestion and time found
- Timing of ingestion / amount taken / other ingested substances including alcohol
- Check clothing / look for empty packets of medication or any written notes
- History of previous episodes or underlying medical conditions including psychiatric disorders
- Aim to identify substance or substances
- Any suggestion / evidence of seizure activity / other injuries sustained
Describe the methods by which a drug can be removed from the body in the case of poisoning
Gastric Lavage: significant morbidity and mortality with no data of improved outcome against or
with activated charcoal.
- Induced emesis: Not recommended
- Whole bowel irrigation: only consider in poisoning with sustained release or enteric coated
preparations
Increased Elimination
Alkaline diuresis enhances elimination of weak
acids. Sodium bicarbonate is administered to
keep urinary pH between 7.5 – 8.5
Haemodialysis
Usefulness dependent on properties of ingested
drug. Substance needs to have a low molecular
weight < 5000 Da / low protein binding / low
water solubility and a low volume of distribution
Useful for ethylene glycol / methanol / lithium /
theophylines and salicylates
What are the peripheral and central manifestations of TCA poisoning? (4 marks)
Peripheral effects:
Sinus tachycardia and cardiac arrhythmias
Hot dry skin
Dry mouth
Dilated pupils
Urinary retention
Central
Ataxia / Nystagmus / Divergent squint
Drowsiness
Increase tone / Hypereflexia / Extensor plantars
Seizures
Agitation / confusion / hallucinations
What is the role of sodium bicarbonate in the management of TCA overdoses? (3 marks)
- Most efficacy of use comes from clinical experience.
- Animal studies demonstrate it narrows the QRS complex, improves systolic BP and controls
ventricular arrhythmias
- Indicated if QRS duration > 100msecs or Ventricular arrhythmia
- Initial loading dose of 1-2ml/kg 8.4% sodium bicarbonate as a bolus which can be repeated after 5
minutes if no improvement in ECG changes followed by an infusion
What are the causes of the morbidity and mortality when seen in amphetamine OD?
Sudden death – sympathomimetic effects precipitate dysrhymias – likely in pts with undiagnosed
cardiomyopathy, viral myocarditis or congential cardiac conditions eg WPW or Brugada
Hyponatremia and cerebral oedema – dilutional hyponatremia from drinking large amts water
Presents with confusion, convulsions and can progress to coma and death from coning –
Liver failure – centrilobular necrosis and steatosis – can lead to fulminant hepatic failure and
encephalopathy
Genetics: variant polymorphisms of the iso-enzyme CYP-2D6 exist, resulting in ultra-rapid extensive
metabolisers, and slow metabolisers; ultra-rapid metabolisers produce the toxic NAPQI more
effectively and are therefore more at risk of toxicity.
Examination:
*Looking for ALF features – jaundice etc
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*GCS
*Nutritional state
?Any other drug toxic signs
Investigations:
*Paracetamol levels (with respect to drug ingestion timings)
*LFTs / Tox screen / Coag / glucose / lactate / U&E / Ammonia
*ECG, Pregnancy test
Resuscitation:
?Intubation
*Lung protective ventilation
*Volume resuscitation and CVS support
*Sugar / nutrition / GCS support
*Temperature control
Treatment:
*WEIGH THE PATIENT
*Specific to the Paracetamol OD
*Decontamination with activated charcoal (if
<4 hours)
*Toxbase for other substances
*NEW MRHA guidance (single treatment line, LD over 1 hour, now NO contraindications to NAC)
*N-acetylcysteine mainstay of treatment (150mg/kg LD over 60 mins, the 50mg/kg over 4 hours,
100mg /kg over 16 hours)
*Start NAC if staggered OD is suspected, regardless of paracetamol level
*If single OD, treat if 4 hr level > 100mg/l, or 15 hour level > 15mg/L
*Check NEW treatment nomogram (no longer high and low risk lines)
General
*Nutrition / VTE prophylaxis / ventilator care bundles
*GI prophylaxis
*Good nursing care
*Prognosis and Disposal
*Various scoring systems (Kings / MELD / APACHE etc)
Features of the King’s College Criteria for liver transplantation in acute liver
failure:
2 Main criteria for referral depending on underlying mechanism of damage:
Paracetamol vs Non-paracetamol related.
Investigations:
Arterial Blood Gases:
likely to show Hypoxaemia, high serum Lactate and reduced AV difference due to impaired Oxygen
Delivery and reduced tissue Oxygen utilisation in CO poisoning
Nasendoscopy:
Nasopharyngeal Oedema and Swelling of Cords;
Bronchoscopy will show evidence of particulate matter and exudate, Carbonaceous Debris, Mucosal
Pallor, Ulceration and Erythema. There may also be evidence of Haemorrhage
Chest X-ray:
Early X-raymay be normal but later may show diffuse Atelectasis, Pulmonary Oedema and
Bronchopneumonia
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26- Burns and Fluid Calculation
A 23 year old woman is brought into A&E with severe dermal burns limited to her chest, face and
hands. She is 60kg. Her GCS is 14.
(a) List the reasons a burns patient may require intubation and ventilation (20%)
(b) What difficulties may you encounter with routine monitoring in these patients? (10%)
(c) What are the referral criteria for a burns patient to a specialist centre? (15%)
(d) Describe the ‘Rule of 9 & Parkland formula. Estimate the fluid resuscitation required by the patient
(e) List the complications that can result from severe burn injury. (15%)
(f) What are the key principles of ICU management in a patient with severe burns? (20%)
Difficulties may you encounter with routine monitoring in these patients? (10%)
Difficulty applying monitors, for example, ECG electrodes unlikely to stick on burns, Oxygen
saturation probes likely to be sore on burnt skin
Use alternative sites, for example nose, ear, lips
Use skin staples or subcutaneous needles attached to crocodile clips for ECG monitoring
End tidal C02 may not reflect PaCO2 as increased dead space in inhalational injury
Blood pressure- invasive access versus non-invasive BP cuff application
IV access, peripheral or central for medication, fluids or CVP monitoring may be difficult and might
require sutures to keep in place.
Late
*Infection, especially skin, significant cause of mortality
from burns
*Pulmonary fibrosis
*Chronic pain
*PTSD, depression, sleep disorders
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27- Coma and altered Consciousness
(a) Define the state of coma. How may coma states be classified? (3 marks)
(b) What are the different causes of coma? (4 marks)
(c) How can coma be differentiated from persistent vegetative state (PVS), minimally conscious state (MCS), or
locked-in syndrome? (3 marks)
(d) Describe the spectrum of states of altered consciousness (3 marks)
(e) What disorders may mimic coma? (3 marks)
(f) What investigations may be helpful in identifying the cause of the coma? (4 marks)
Define the state of coma. How many coma states can be classified? (3 marks)
- Coma can be defined as unarousable unresponsiveness or the absence of any psychologically
understandable response to external stimulus or inner need.
- Coma can be classified into 4 groups:
Coma with intact brainstem function, no meningism and no lateralising signs
Coma with intact brainstem function and lateralising signs
Coma with meningism (with or without intact brainstem function and lateralising signs)
Coma with signs of focal brainstem dysfunction
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How can coma be differentiated from persistent vegetative state (PVS), minimally conscious state
(MCS) or locked-in syndrome? (3 marks)
Coma is a state of unarousable unresponsiveness. The patient is unaware of self and environment
and does not respond to vigorous stimulation.
Patients with PVS are in a state of partial arousal and may briefly respond to sound or visual stimuli.
They withdraw to noxious stimuli but are unable to interact or respond voluntarily or purposefully
when stimulated. It is a chronic condition, diagnosed after 30 days of persistent altered
consciousness.
Patients in MCS display deliberate or cognitively mediated behaviour. They may intermittently follow
commands or have intelligible but inconsistent verbal output. Patients can evolve from coma or PVS
to MCS.
Patients with locked-in syndrome have intact cognition but complete paralysis of voluntary muscles
in all parts of the body. Can communicate using blinking / up-and-down eye movements.
Describe the spectrum of states of altered consciousness (3 marks)
There is considerable overlap between intermediate states on the spectrum of altered consciousness
Clouding of consciousness: a state of reduced wakefulness or awareness, characterised by impaired
attention and memory. Patient is easily distracted and sometimes hyperexcitable, startled by stimuli.
Acute confusional state: impairment of consciousness in which stimuli are intermittently
misinterpreted. Patients are drowsy, disorientated in time and occasionally place and person and
have poor short-term memory.
Delirium: acutely developing impairment of consciousness, attention, disordered thinking – fear,
disorientation, visual hallucinations, delusions and misperceptions of sensory stimuli. Can be
interspersed with lucid intervals. Commonly due to metabolic, toxic, or endocrine derangements.
Very common in hospitalised patients. Follows a fluctuating course and rarely lasts more than a
week.
Obtundation: mental blunting with apathy and inactivity. Patient is drowsy with reduced alertness,
has a decreased interest in the environment and responds slowly to stimulation.
Stupor: similar to deep sleep or unresponsiveness. Patient can be aroused by episodes of repeated,
vigorous stimuli. As stimulation decreases, patient lapses back into a state of decreased
responsiveness. Even when aroused, communication is by monosyllabic sounds and simple
behaviour.
What investigations may be helpful in identifying the cause of the coma? (4 marks)
Glucose
Urea and electrolytes
Full blood count
Arterial blood gas
Blood cultures if pyrexial / hypothermic / suspect infection
Urine screen for drugs and toxins
CT brain – detects intracranial haemorrhage, hydrocephalus and structural abnormalities
MRI brain superior in early detection of ischaemic strokes
CT venogram and angiogram may be required to exclude basilar artery thrombus or sinus venous
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thrombosis
EEG to rule out non-convulsive status epilepticus
Lumbar puncture if infection or inflammation suspected.
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28- Necrotising Fasciitis
(a) What is necrotising fasciitis (NF)?
(b) What pathogens may potentially be responsible for causing necrotising fasciitis?
(c) What are the risk factors for developing NF?
(d) How may it be diagnosed?
(e) Describe the management of NF
Necrotizing fasciitis (NF) is a progressive, fulminant bacterial infection of subcutaneous tissue that
spreads rapidly through the fascial planes causing extensive tissue destruction.
NF can affect any part of the body and is the most serious
presentation of necrotizing soft tissue infection (NSTI); it is a
rare but potentially fatal condition.
- Type III is a Gram-negative monomicrobial NF. The most common Gram-negative responsible are
Vibrio spp., such as V. damselae and V. vulnificus
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Surgery
I.V. drug use
Childbirth
Burns
Muscle injuries
Management of NF:
- Early diagnosis, aggressive resuscitation, surgical debridement, antibiotic therapy, and supportive
intensive care are necessary for managing patients with NF. Effective communication between the
intensivist, surgeon, anaesthetist, and microbiologist is essential.
- The aim of resuscitation is to establish an adequate tissue perfusion and oxygen delivery. Invasive
arterial pressure monitoring and central venous access may be required; goal-directed therapy
targets for haemodynamic resuscitation in patients with sepsis secondary to NF are as suggested by
the Surviving Sepsis Campaign.
- Several studies have shown that the most important factor affecting mortality is timing and
adequacy of initial surgical debridement. Debridement removes the source of infection and toxins,
and furthermore, removal of infarcted tissue improves the subsequent penetration of antibiotics.
Multiple debridement’s may be required.
Empiric therapy requires an antibiotic combination that covers the variety of organisms that may
cause NF. A broad-spectrum agent such as Tazocin or a Carbapenem, can be combined with
Clindamycin. If Group A streptococcus alone is responsible, antibiotics may be rationalized to a
combination of Penicillin and Clindamycin. When MRSA is suspected, Linezolid is preferred to
Vancomycin as it inhibits exotoxin production.
- The use of i.v. immunoglobulin is based on the theoretical mechanism that it can bind
staphylococcal- and streptococcal derived exotoxin, so limiting the systemic cytokine release
associated with systemic inflammatory response syndrome. There is very limited evidence which
suggests a decreased mortality from using IVIG in group A streptococcal NF.
For synergistic infections, particularly involving Clostridium spp., hyperbaric oxygen switches off toxin
production.
- These patients need managed in a critical care setting, with facilities for organ support.
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29- Heparin Induced Thrombocytopaenia (HIT)
(a) What is the mechanism of action of (i) unfractionated heparin? (ii) LMWH? (20%)
(b) List the potential causes of thrombocytopaenia in an intensive care patient. (20%)
(c) What is heparin induced thrombocytopaenia? (20%)
(d) How may it be diagnosed? (20%)
(e) What are the alternatives (their modes of action) to heparin for short-term anticoagulation
Mechanism of action of (i) unfractionated heparin? (ii) low molecular weight heparin:
- Heparin inhibits antithrombin-III
A pentasaccharide on the heparin molecule binds to AT-III producing a conformational changein its
reactive site.
This enhances AT-III’s neutralizing of factors VIIa, IXa, Xia, XIIa and thrombin and prevents them
forming complexes.
Inactivation of thrombin inhibits fibrin formation and activation of factors V, VII.
- Heparin molecule dissociates then and can be reused.
- Heparin induces a vascular endothelial tissue factor pathway inhibitor (TFPI) which antagonises TF-
VII complex.
- Heparin may inhibit VW dependent platelet function.
- Heparin inhibits platelet aggregation in high doses.
ii) LMWHs bind and neutralize factor Xa. They are too small to bind well to AT-III and thrombin
simultaneously. Different preparations have different AntiXa/Antithrombin activity ratios.
- Decreased Production
BM suppression
Postviral (rubella, mumps, varicella, parvovirus, hepatitis C, and Epstein-Barr virus)
Viral (HIV)
Chemo or radiotherapy (eg. Nodal)
Congenital or acquired bone marrow aplasia/hypoplasia eg. Fanconi’s
Alcohol toxicity
B12, folate deficiency
- Increased Destruction
ITP, SLE- autoimmune antiplatelet antibodies
Drugs- Heparin, quinine, valproate, linezolid, rifampicin, ranitidine
Alloimmune- transfusion, transplantation
DIC
TTP-HUS- idiopathic, Shigella
Antiphospholipid
HELLP
Physical destruction eg. CPB
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Dilutional
Spurious-
Insufficient anticoagulation- clumps counted as leukocytes by machine
G2a/3b inhibitors
Satellitism (clumping around leukocytes)
Type 1- Non-immune- may be a direct effect of heparin- and inconsequential. Results in a slight fall in
platelet count, within the first 2 days after heparin initiation. It often returns to normal with
continued heparin administration
Type 2- Immune- antibodies against the heparin-platelet factor 4 complex- and serious. Incidence
2.6%. RFs- UFH, female, long duration, surgical patient. Occurs 5-10 days after starting. Major clinical
manifestation in thrombosis.
What are the alternatives (and their modes of action) to heparin for short-term
anticoagulation? (20%)
Direct thrombin inhibitors- Bivalirudin, Argatroban, Lepirudin
Factor Xa inhibitors- Fondaparinux
Heparinoid- Danaparoid
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30- Management of Ischaemic Stroke (CVA)
(a) How may the clinical presentation of stroke may used to distinguish between an infarct of: (i) Anterior
Circulation (ii) Partial Anterior Circulation (iii) Lacunar Area (iv) Posterior Circ.
(b) What risk factors do you know for ischaemic stroke?
(c) What are the exclusion criteria for lysis of a cerebral infarction?
(d) Describe the non pharmacological management of a cerebral infarction
(e) What are the aims of critical care in management of ischaemic stroke?
Partial anterior circulation (PACS) – 2 out of 3 components of TACS or pure higher cortical
dysfunction or pure motor or sensory deficit not as extensive as for lacunar syndromes
Lacunar syndrome (LACS): Pure motor or sensory deficit affecting at least 2 of face, arm or leg
Sensorimotor deficit
Ataxic hemiparesis
Dysarthria, clumsy hand syndrome
Acute onset movement disorder
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31- Brainstem Death (BSD) and Testing
A 35 year old woman is apnoeic on the ventilator following a large SAH and the decision is taken to
perform brainstem death testing after speaking to the family.
(a) What are the preconditions for brainstem death testing (BSD)? (20%)
(b) Describe the principles of the apnoea test component of BSD testing - describe the physiology for
maintenance of oxygenation. (20%)
(c) List the other components of the BSD tests. (20%)
(d) What additional investigations apart from brainstem death tests may confirm brainstem death?
(e) What are the physiological consequences of brainstem death?(20%)
- The apnoea test is only performed when all other test for BSD have shown absent response.
- Inspired oxygen is increased to 100% for at least 5 minutes before hand. - An arterial blood sample
if then taken to assess pH, paO2, and paCO2. Minute ventilation is then decreased to allow the
paCO2 to rise to more than 6kPa and the pH to fall below 7.4. Higher levels of paCO2 may be needed
in patients with chronic retention of CO2.
- The patient is then disconnected from the ventilator for 5 minutes and observed for respiratory
effort.
- A repeat blood gas is then taken- a PaCO2 gain of 0.5kPa or more demonstrates adequate
respiratory stimulus. The patient is reconnected to the ventilator at the end of the test.
Oxygenation is maintained throughout this period by insufflating 5L/min of oxygen via a tracheal
catheter to avoid hypoxia. This means that the test will only assess the stimulation of respiration to
arterial carbon dioxide tension alone. If saturations fall, CPAP or recruitment manoeuvres can be
carried out.
BSD testing should be carried out by two doctors with at least 5 years registration with one of the
two of consultant grade.
Pupillary response to light: the pupils don’t respond to direct or consensually to sharp changes in the
intensity of light. This tests CN 2 afferent and 3 efferent
Corneal reflex: there is no response following direct stimulation of the cornea with a cotton bud.
Test cranial nerve 5 afferent and 7 efferent
Vestibulo-ocular reflex: no eye movements are seen following slow injection of at least 50mls of ice
cold water to the external auditory meatus. Normal response would be eye movement away from
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the ear injected. This tests CN 8 afferent and 3, 4, 6 efferent.
Motor response: no motor response with supraorbital pressure. Tests CN 5 afferent and CN 7
efferent
Gag Reflex: No contraction of the soft palate following direst stimulation of the uvula. Tests CN 9 and
10.
Cough Reflex: no response to bronchial stimulation at the level of the carina by suction catheter.
Tests CN 9 and 10
Apnoea Test: As above
Occasionally it may be difficult to perform BSD testing, for example with facial trauma. In these
situations ancillary testing may be needed to confirm the diagnosis.
Tests are divided in three groupings;
Blood flow in the larger cerebral arteries: Four vessel angiography
Transcranial Doppler
Magnetic resonance angiography
CT angiography
Brain tissue perfusion: Cerebral scintigraphy
Xenom CT
Position emission tomography
Neurophysiology: EEG
Evoked potentials
A number of changes occur as brain damage progresses, the subsequent organ damage
associated with cardiovascular derangement is well recognised.
Sympathetic storm: Hypertension and bradycardia are initially seen as ICP rises and the brainstem
becomes ischaemic. Critical ischaemia and infarction of the brainstem causes intense autonomic
activity and a surge of catecholamine release- causing increases in heart rate, BP, CO and PVR.
Myocardial ischaemia, conduction abnormalities and arrhythmias can also occur at this point. As
brain stem infarction causes death of the vasomotor centres, sympathetic activity is lost and
hypotension develops which will lead to asystole if untreated.
Endocrine system: Failure of the hypothalamic-pituitary axis leads to a decline in plasma hormone
concentrations. ADH, thyroid hormone, cortisol and insulin levels all fall. Lack of ADH leads to
diabetes insipidus which untreated leads to electrolyte abnormalities and hypovolaemia. Lack of T3
is associated with loss of cardiac contractility and accumulation of lactate. Low cortisol levels impair
the donor stress response and contributes to cardiovascular collapse. Lack of insulin leads to
hyperglycaemia.
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Immunological effects: There is increasing evidence that part of brainstem death causes
immunogenicity of solid organs by a variety of mechanisms which may contribute to rejection of the
donor organ in the recipient.
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32- Brainstem Death and Physiological Changes
a) List the main adverse cardiovascular changes associated with brainstem death.
b) What are the physiological goals (with values) required to ensure optimisation of this donor?
c) Outline the measures and drugs that may be used to achieve these goals. (8 marks)
Following brainstem death, cardiovascular changes occur secondary to increasing ICP and cerebral
herniation.
In summary:
• Catecholamine damage – secondary to coning.
• Arrhythmias – secondary to catecholamines, altered autonomic tone, acidosis, electrolyte
disturbance.
The physiological goals (with values) required to ensure optimisation of this donor:
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The measures and drugs that may be used to achieve the physiological goals:
1) Blood pressure management: vasoactive solutions can be stopped/weaned and short acting drugs
used to control hypertension (e.g. Esmolol, GTN, Sod. nitroprusside)
3) Thyroxine (T3) administration can improve cardiac function in the haemodynamically unstable
donor
5) TTE and oesophageal Doppler: guide fluid, inotrope and vasopressor therapy
6) Lung protective ventilation strategy: as post brain stem death there is an active inflammatory
process that render lungs vulnerable to damage. Uses minimal FiO2 to achieve
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33- Donation after Brainstem Death (DBD)
You have confirmed brainstem death in a patient in the ICU with a catastrophic brain injury. The
organ transplant coordinator has been informed.
Distinguish between the terms DCD and DBD in reference to organ donation
DCD: Donation after Cardiac Death
Classified by the Maastricht Classification
Either controlled or uncontrolled cardiac arrest
Viability of organs depends on the warm ischemic time
-Sustained phase of profound vasodilation, hypothermia and hypotension requiring careful fluid
resuscitation, warming blankets and vasopressor/catecholamines
-Renal function benefits from generous fluid administration-may adversely affect lung retrieval
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-Systemic heparinization prior to aortic cross clamping
-If lungs to be retrieved: withdrawing of the ETT and a maximum tidal volume to be given prior to
stapling of trachea
Distinguish between the terms ‘opt in’ and ‘opt out’, indication the current situation in the UK
Opt in: informed consent presumes the patient is not willing to donate unless either; individual has
made clear statement of intention before death by registering with the national organ registry or
indicating a clear willingness to donate to relatives or friends or consent is obtained from relative or
nominated individual after death
Opt out: Presumed consent presumes consent is given unless the individual has made a clear
statement of refusal to donation, normally in writing. This varies in the different countries that have
this method
‘soft’ approach: relatives can refuse donation on behalf of the deceased
‘hard’ approach: relatives cannot refuse donation if the individual has not previously registered
refusal
The UK’s current model is ‘opt in’ however in recent years due to the shortfall of donated organs and
concerns that not all potential donors are being considered an ‘opt out’ model is being considered.
Role of (i) the patient (ii) family members in supplying consent for organ retrieval (DCD or DBD)
The patient
-Human Tissue Act 2004 gives primacy to the individuals wishes
-This wish to donate may be recorded or stated in a number of ways
-Verbally
-By having a Donor Card
-In writing
-Via accessing the NHS Organ Donor Register
Family members
-To define the known or likely wishes of an individual. If the wishes of individual are unknown-
authority for decision making passes to a nominated representative
-No authority at law to overturn the known wishes of an individual
-In Scotland families who object required to sign a disclaimer if they wish to over-ride patient’s
wishes
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Critica pathways for organ donaf1on*
POSSIBLE DECEASEDORGAN DONOR
A patient with a devastating brain injury or lesion OR a patient with circulatory failure
AND apparently medically suitable for organ donation
Tr eat ing ph y s ician
Donation after Circulatory Death (DCD)/ ,, to 1dentifyfrefer a potential donor Donat.ion after BrainDeath (DBD)
POTENTIAL DCD DONOR POTENTIAL DBD DONOR
A. A person whose circulatory and respiratory Reasons why a potential donor A person whose clinical condttion is suspected to
functions have ceased and resuscitative does not become a utilized donor fulfill brain death criteria.
measures are not to be attempted or continued.
System
or
• Failure to identify/refer a potential or eligible donor
B. A person in whom the cessation of circulatory
• Brain death diagnosis not confirmed (e.g.
and respiratory functions is anticipated to occur
within a time frame that will enable organ does not fulfill criteria) or completed
recovery. (e.g. lack of technical resources or clinician
to make diagnosis or perform confirmatory tests)
J,
! • Circulatory death not declared within the appropriate
time frame. ELIGIBLE DBDDONOR
ELIGIBLE DCD DONOR
• Logistical problems (e.g. no recovery team)
A medically suitable person who has been A medically suitable person who has been
• Lack of appropriate recipient (e.g. child, blood type,
declared dead based on the irreversible absence declared dead based on neuroloigc criteria as
serology positive)
of circulatory and respiratory funcitons as stipulated by the law of the relevant jurisdiction.
stipulated by the law of the relevant jurisdiction, Donor/Organ
within a time frame that enables organ recovery. • Medical unsuitability (e.g. serology positi,ve neoplasia)
• Haemodynamic inslabilily Iunanticipated cardiac '¥
y
arrest ACTUAL DBD DONOR
ACTUAL DCD DONOR
• Anatomic al, histological and/or functional A consented eligible donor:
A consented eligible donor. abnonnalities of organs A. In whom an operative incision was made
A In whom an operative incision was made • Organs damaged during recovery with the intent of organ recovery for the
with the intent of organ recovery for the
• Inadequate perfusion of organs or thrombosis purpose of transplantation.
purpose of transplantation. or
or Permission
B. From whom at least one organ was
B. From whom at least one organ was • Expressed intent of deceased not to be donor
recovered forthe purpose of transplantation. recovered for the p urpose of transplantaiton.
y
• Relative's refusal of permission for organ donation
• Refusal by coroner or other judicial officer to allow
..,
donation for forensic reasons UTILIZED DBD DONOR
UTILIZED DCD DONOR
An actual donor from whom at least one organ
An actual donor from whom at least one organ
was transplanted.
was transplante d.
34- Donation after Circulatory Death (DCD)
In terms of organ donation, the rates of donation after circulatory death are expected
to rise markedly over the next decade.
(a) Define and classify the term “donation after circulatory death”.
(b) Distinguish between the terms warm and cold ischaemia.
(c) Define ‘stand down time’ for various organ retrieval
(d) What are the contraindications to donation after circulatory death?
(e) Outline the donation process, including the staff groups involved.
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‘Stand Down Time’ for Various Organ Retrieval
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Medical staff
Assessment for donation potential
Medical staff
SN-OD
Organ donor register
Family (assent)
Lab staff (tissue typing etc)
Consent and authorisation
Involvement of recipient centres
Medical staff
SN-OD
Maintenance of donation potential / donor optimisation
Mobilisation of retrieval teams
Notification of donor recipients & their respective teams
Medical staff – optimisation of donor
SN-OD and paramedical staff
WLST, diagnosis of death, transfer to theatre for retrieval (within constraints of stand
down times)
Critical care and theatre staff
Retrieval team(s) with transport staff
Cold perfusion, packaging, departure of retrieval teams
Last offices / clerical input
Mortuary staff
Portering staff
Post donation debrief
Contact with family
Medical, nursing, paramedical staff
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35- Post Cardiac Arrest Care and Cooling
You have been asked to admit a 75 year old man to ICU who has had an OOH VF arrest
for ventilation and therapeutic hypothermia.
(a) What were the major changes in the ILCOR 2010 resuscitation guidelines for adult cardiac arrest?
(b) What is induced hypothermia and what is the proposed mechanism by which it exerts its effects?
(c) What are the adverse systemic consequences of hypothermia? (15%)
(d) Outline the principles of management of therapeutic hypothermia (30%)
(e) Describe a scoring system by which neurological outcome may be predicted post critical care
admission (15%)
The Major Changes in the ILCOR 2010 Resus. Guidelines for Cardiac Arrest in Adults
removal of rescue breaths
early CPR
minimally interrupted CPR; less than 5 seconds
CPR during charging of defibrillator
use of cpr feedback devices
role of praecordial thump de emphasised
drugs no longer recommended via trachael route
drugs recommended via IO route if IV cannot be established
less focus on early intubation unless expert assistance available
capnography recommended for intubated patient
atropine removed from PEA algorithm
amiodarone and adrenaline recommended at 3rd shock/cycle in shockable algorithm
recognition of potential of USS in cardiac arrest e.g. FEEL algorithm
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reduces ICP
reduces CMRO2; 7% for every degree of cooling
reduces reperfusion injury;
free radical release, excitatory amino acid production, calcium shifts
decision to cool - meets criteria for cooling, feasible in centre, intubated and ventilated
aim to cool within 2-4 hours for 12-24 hours
metastatic malignancy 10
non metastatic malignancy 3
sepsis 5
dependent functional status 5
pneumonia 3
creatinine >130 3
age > 70 2
acute MI -2
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36- Management of MI
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GOOD LUCK FOR ALL