Surgical Critical Care For MRCS 3

Surgical Critical Care
For MRCS part 3
BY
Dr. MMM
Surgical Critical Care 2
ITU general
ITU versus HDU
Which patients should be admitted to an HDU (High Dependency Unit)?

Patients for administration to HDU are typically those who need a higher level of
monitoring and/or nursing than is available on a general ward but who do not
ventilation :
 High-risk surgical patients(with medical co-morbidities), for monitoring /
support.
 Patients/who have undergone major/complex surgical procedures, e.g. hepatic
resection, oesophagectomy.
 Patients at risk of veveloping multiple-organ failure/dysfunction, e.g.
pancreatitis.
 Patients able to step down from ITU care.
What are the selection criteria for admitting a patient to an ITU (Intensive
Therapy Unit) ?
 Patients requiring or who are likely to require advanced respiratory support.
 Patients requiring support to two or more organ systems.
 Severe disease states in which intensive monitoring and treatment is required
(septicaemia, head injury, etc)
 Homeostatic disorders (severe fluid and electrolyte imbalance,
thermoregulatory failure).
 Patients who are undergoing specialized therapeutic techniques and/or
monitoring.
What factors need to be considered when assessing suitability for admission to

intensive care?
1. The diagnosis. 2. Age.
3. Severity of the illness. 4. Co-existing disease.
5. Prognosis. 6. Availability of suitable treatment.
7. Response to treatyment. 8. Anticipated quality of life.
9. Patient's wishes.
How would you decide if a patient should be admitted to ICU or HDU?

HDU is suitable for patients with impairment of a single organ system who require
detailed monitoring but not mechanical ventilator support.
ICU should be reserved for patients who require, or have a high probability of
requiring, mechanical ventilator support require detailed and/or invasive monitoring,
and have impeding multiple organ system failure.
Differences between care in HDU and ITU:

In the UK, there is usually one nurse per patient on ITU and one per two patients in
HDU. This represents the increased level of care required on ITU.
The majority of patients on ITU will be mechanically ventilated and need full care for
all daily needs.
An ITU has dedicated doctor (or group of doctors) on duty within the unit at all times
who is free of commitments elsewhere.
What are the problems in admitting emergrncy patients to ICU?

These patients are usually older, with often an incomplete knowledge of their past
medical history. They are less well optinsea for surgery. They may be multiple trauma
patients.
What parameters would you measure in a seriously ill patient that may help in
determining the requirement for ICU?
Many centres have developed an early warning scoring system that measure
physiological parameters.
These scoring systems help alert junior staff as to whether a patient may require
admission to an ICU. Parameters that are particularly useful include:
 Heart rate.  Blood pressure.
 Respiratory rate.  Temperature.
 Conscious level.  Oxygen saturations.
 Urine output.  Blood PH.
What other factors need to be taken into account in assessing suitability for
admission?
The diagnosis and severity of illness need to be taken into account so that maximal
benefit can be provided for the right patient.
It is important to differentiate between the sick patient for who may have a good
prognosis from the moribund patients with terminal diagnosis.
The wishes of the patient and their future quality of life should be taken into account.
What is 'multiple-organ failure' (MOF)?

 A syndrome characterized by the significant failure of two or more organs.
 Usually starts with minor or moderate abnormalities in organ function
(multiple-organ dysfunction syndrome, or MODS). Failure to control the
situation at this stage may lead to MOF.
 5 main organ system (with various definitions for specific organ system
failure):
 Cardiovascular.  Respiratory.
 Renal haematological.  Neurological.
 Additional features include:
 Polyneuropthy.
 Gastrointestinal failure (ileus).
 Musculoskeletal failure (muscle wasting, myositis).
 Skin'failure' (pressure sores).
 Endocrine failure (hypoadrenalism, abnormal thyroid function tests).
Definitions of system failure:

Cardiovascular failure:
 HR > 140 b/min.  Systolic BP < 100 mmHg.  ± cardiac arrest.
Respiratory failure:
 Airway compromise.  SpO2 < 90% on > 40% O2.  ± Resp. arrest.
Renal failure
 Urine output < 120 ml in 4 h with associated hyperkalaemia/acidosis.
Central nervous system dysfunction:
 GCS < 9 or a fall of 2 points.
 Seizures, new or sustained > 10 min (status epilepticus).
Scoring systems
What is the purpose of scoring systems?

 Scoring systems provide a way of evaluating the severity of illness, assessing
response to treatment and predicting the outcome from various conditions.
 They aid the comparison between patients and units.
In general, what types of illness scoring are used in the critical care setting?
 Scores to estimate patient outcome and to guide clinical management.
 Scores to stratify patients for audit and research purposes.
What is level 1, 2 and 3 care?

1. Acute postoperative care.
2. HDU.
3. ITU
Can you give some examples of each type ?

1. Scores to estimate patient outcome and to guide clinical management:
 RTS- Revised Trauma Score.
 ISS- Injury Severity Score.
 MEWS-Modified Early Warning System.
2. Scores to stratify patients for audit and research purposes:
 APACHE II score: Acute Physiology And Chronic Health status
Evaluation.
 POSSUM: Physiological and Operative Severity Score for the
enUMeration of morbidity and mortality.
What are the characteristics of an ideal scoring system?

It should be:
 Validated.
 Easy to use reliable.
 Be able to predict the outcome for specific cases.
In the case of the invasive treatment unit ( ITU):
 It should predict the non-survivors for whom admission is futile.
What scoring system are you aware of?

 Glasgow coma scale (GCS).
 Acute physiology and chronic health evaluation (APACHE).
 Simplified acute physiology score (SAPS).
 Mortality probability models (MPM).
 Revised trauma score (RTS).
 Injury severity score (ISS).
 Abbreviated injury score (AIS).
Briefly describe the GCS?

It gives a score from 3 to 15, with 3 being the worst.
It is used to describe the level of consciousness of a patient, and is particularly useful
in the management of head injuries.
There are three components:
 Motor response scored out of 6.
 Verbal response scored out of 5.
 Eye reponse scored out of 4.
The best score for each component is always taken, e.g. if a patient has a left
hemiparesis but has normal function on the right the motor score would be 6.
What is the most commonly used disease severity scoring system in the UK?
The acute physiology and chronic health evaluation II system (APACHE II).
How is this system used?

It combines 12 physiological parameters with age and chronic health score.
Physiological parameters included are:
1. Temperature. 2. Blood pressure.
3. Heart rate. 4. Respiratory rate.
5. Oxygen therapy required. 6. Arterial Ph.
7. Serum sodium. 8. Serum potassium.
9. Creatinine. 10. Packed cell volume.
11. White blood cell count. 12. Neurological score.
Data are entered on admission to the ICU and then after 24 hours.
The resulting score provides an index of disease severity and a percentage risk of
death.
What is the predicted risk of death with an APACHE score of >40 ?

Risk is 100%.
Brifly describe the APACHE sore ?

The APACHE score is made up of the some of three scores: A, B and C:
o A: a score based on acute physiological variables would include:
1. Rectal tempreture. 2. Mean arterial pressure.
3. Heart rate. 4. Respiratory rate.
5. Arterial Ph. 6. Na+.
+
7. K . 8. Creatinine.
9. white cell count. 10. GCS.
o B: ascore for increasing age.
o C: a score for chronic health by system.
The larger the sum ( A+ B+C) the pooper the outcome
When should APACHE scoring be done in the ITU setting ?

Within the first 24 hours of admission.
What is the effect of a reduced APACHE score following treatment on outcome ?

Despite reduction of the APACHE score with treatment the outcome is unaltered. The
initial physiological disturbance is the main determinant of outcome.
Give examples of some of the commonly used scoring systems

APACHE II:
- It is the most commonly used scoring system in the UK .
- The score is assimilated from 12 physiological parameters, plus the
Glasgow Coma Score, and is then weighted for the patient's age, general
health and diagnosis.
Increasingly, specialist scoring systems are used for patients who have undergone
surgery, and currently:
POSSUM or the Portmouth corrected version, P-POSSUM:

- Physiological and Operative Severity Score for the enUmeration of
Mortality and morbidity.
- These scores use a combination of physiological parameters and pre-
existing illness with an operative score, which includes:
 Operation type.  Malignancy.
 Contamination.  Blood loss.
- Both have been shown to be better predictors of mortality in surgical
patients than APACHE II.
- P-POSASUM has superseded POSSUM in many areas of general surgery
since POSSUM was found to over-predict deaths in the low-risk
categories.
- However, while remaining useful as an audit tool, P-POSSUM and
POSSUM should not be used pre-operatively.
What are the drawbacks in using scoring systems?

The principal drawbacks of using any of these scoring systems are that:
o The conclusions drawn can only be as good as the data collected.
o It is well recognized that units collect data in different ways, and incomplete
data collection is a major problem. The validity of comparing two units, which
have differeing data capture techniques and staff, is questionable at best.
No scoring system has yet been devised that will predict with certainty the outcome
for an individual patient, and thus they must not be used as a basis for limiting or
discontinuing treatment.
What are the limitations of IUT scoring systems?

 Intra-and interobserver error.
 Accuracy of data.
 Insufficient data.
 Systems such as the ISS require data that may not all be available early on in
the clinical course.
 Over-reliance on scores rather than clinical judgement.
Respiratory
Airwy & Intubation
How would you define airway obstruction?

Partial or complete occlusion of the upper or lower respiratory tract, upper airway
obstruction being more common than obstruction below the larynx.
In what situations does it occur?

Upper airway obstruction commonly occurs in:
 The unconscious patient who is unable to maintain there airway due to the
tongue falling backward.
 Laryngiospasm.
 Tumours.
 Soft tissue swellings.
 Oedema.
 Infection (epiglottitis and diphtheria).
 Foreign objects as well as blood and vomit.
Lower airway obstruction may occur due:
 Pulmonary secretions, mucus pluuging, in anaethesia.
 Pulmonary oedema.
 Pneumothorax.
 Haemothorax.
What are the clinical features of airway obstruction?

 Hypoventilation.
 Increased work of breathing: accessory muscles of breathing are often
employed, tracheal tug may be seen, see-saw paradoxical movement of the
abdomen and the chest may also be noticeable.
 Change in noise of breathing: complete obstruction is silent; partial
obstruction is noisy (e.g. stridor).
 Tachypnoea.
 Tachycardia.
 Lower respiratory signs will be present if there is lower airway obstruction,
but this will depend on the cause of the lower airway obstruction.
How would you clinically assess an airway?

 Look: for
 Accessory muscle movements.
 See-saw movements of abdomen and chest.
 Foreign bodies in airway
 An in late stages central cyanosis.
 Listen: for
 Breath sounds.
 Stridor.
 Grunting and gurgling.
 Feel: for
 Airflow at the nose and mouth.
 Cest movement.
What are the immediate management possibilities?

 Suction/finger sweep: to remove secretions and debris.
 Chin lift or jaw thrust (safest in trauma).
 Airway adjucts: oro/nasopharyngeal airway.
 Definitive airway: orotracheal intubation, nasotracheal intubation and surgical
airway.
 Oxygen therapy.
What methods are there of managing a compromised airway?

A compromised airway should always be secured and intervention needed will
depend on the cause.
Unconsciousness leads to airway compromise owing to loss of muscular control of the
neck or tongue muscles.
In these circumstances, simple emergency measures, such as:
 Jaw thrust or chin lift, will usually open the airway.
 Guedel airway or nasal airway will ensure a patent route while this is
maintained .
Where definitive airway control is needed, the usual first-line treatment is by:
 Endotracheal intubation with a cuffed tube (uncuffed in children). This is
usually the domain of the anaethetist.
 Laryngeal mask airway (LMA) can be used, but should be avoided in the
emergency situation, since there is still a risk of aspiration with an LMA.
When intubation is difficult the anaethetist may use a bougie to guide the tube or
even a fibreoptic laryngoscope.
In the event of an airway not being attained by these measures, then emergency
surgical techniques are needed.
 Needle jet insufflations:
It is the quickest.
Using a 12- or 14-gauge cannula inserted via the cricothyroid membrane.
This is connected to high-flow oxygen and a Y connector; the cycle is 4
seconds of insufflations followed by 1 second of exhalation.
This technique will maintain oxygenation for around 20-40 minutes, but CO2
levels soon rise, and this is not a definitive airway.
Definitive surgical airways are cricothyroidotomy and tracheostomy.
 The cricothyroidotomy can be performed as an emergency.
 Emergency tracheostomy should be avoided, if possible.
 Elective tracheostomy can be performed as an open technique or
percutaneously using a guide wire and dilators.
Are there any contraindications to the airway adjuncts?

 Oropharyngeal airway should not be used in patients with a gag reflex.
 Nasopharyngeal airway should not be used in patients with suspected basal
skull fracture.
A patient in A&E has a completely obstructed airway that an experienced

anaethetist cannot traverse. Describe how you would ontain an emergency
airway?
A cricothyroidotomy:
- It can be performed using local anaethetic, if the patient were still conscious, or
omitting it if in extremeis.
- A fully prepared insertion tray must be ready.
- The patient is positioned supine with the neck extended.
- A 2-3 cm transverse incision is made over the cricothyroid membrane and
deepned until it comes into view, the membrane is incised with a scalpel, placing
the scalpel handle in the hole and turning it sideways to open the hole.
- A cricothyroid tube is now inserted and the patient ventilated through this, finally
suturing the skin around the tube to ensure a snug fit.
In elective practice, when would you perform a tracheostomy?

The indications for elective tracheostomy are:
- To relieve upper airway obstruction as a definitive procedure, such as in vocal
cord paralysis, laryngeal tumours, chronic traumatic scarring, congenital atresias
and laryngeal trauma.
- To improve respiratory function by reducing anatomical dead space and allowing
regular effective aspiration of bronchial secretions.
- In respiratory paralysis, where it allows positive pressure ventilation to be used,
such as elective long-term ventilation and coma.
- As a preliminary to certain head and neck surgery.
Describe the steps of an elective tracheostomy?

1. The patient is consented and taken to the operating theatre, where under a
general anaesthetic, the patient is positioned supine with the neck extended.
2. The neck is prepared and draped.
3. A horizontal incision through skin and platysma is made at the level of the
third tracheal ring.
4. The strap muscles are retracted exposing the trachea and the thyroid isthmus.
5. The isthmus is divided and oversewn for haemostasis.
6. The tracheal rings are carefully identified and a vertical incision made through
the third ring.
7. The anaesthetist is asked to withdraw the endotracheal tube to a point above
the incision.
8. The incision is wided by removing a semicircle of cartilage on each side, and a
tracheostomy tube is inserted and secured .
9. As the tube is inserted, the anaesthetic should change the ventilator to the
tracheostomy and withdraw the endotracheal tube.
10. The wound is closed loosely around the tracheostomy.
What are the complications of tracheostomy?

Complications of tracheostomy occur at the time of creation or with tube
management:
 At the time of the procedure, bleeding from the thyroid isthmus can occur but
should be controlled by oversewing.
 Subcutaneous emphysema can occur after the tube is sited, especially if the
skin is closed too tighly.
 Blood can enter the trachea as the hole is made, leading to aspiration, and
suction should be judiciously used to avoid this.
 Infections around the tracheostomy site are not uncommon, and should be
swabbed and treated as appropriate.
 The first tube change should be performed with care, since misplacement can
lead to airway compromise, but also anterior displacement can led to erosion
of the brachiocephalic vein, ehich is often fatal.
 Tracheal stenosis can occur from prolonged cuff use, or with healing and
scarring at a late stage.
Acute lung injury
What is 'acute lung injury' (ALI)?

Acute repiratory fsilure characterized by:
1. Diffuse pulmonary infiltrates.
2. Progressive hypoxaemia.
3. Reduced lung compliance.
4. Normal hydrostatic pressures.
Diagnostic criteria:
1. Bilateral pulmonary infiltrates on chest x-ray.
2. Pulmonary capillary wedge pressure<18 mmlHg.
3. PaO2/Fio2< 300mmHg (40kPa)=ALI.
4. PaO2/FiO2<200mmHg(26kPa)=ARDS.
The most severe form of ALI is acute repiratory distress syndrome ( ARDS)
Acute respiratory distress syndrome
How would you define acute repiratory distress syndrome (ARDS)?

The adult respiratory distress syndrome is pulmonary oedema with a normal central
venous pressure and pulmonary artery wedge pressure, i.e the oedema is not
cardiogenic in origin.
It characterizes a type I respiratory failure and is typified by diffuse pulmonary
infiltrates, refractory hypoxaemia, stiff lungs and respiratory distress following a
recognized precipitating cause.
What are the criteria for diagnosing ARDS?

The criteria include:
The appropriate clinical setting with a history of a precipitating condition such as
sepsis.
On chest x-ray, bilateral infiltrates with no clinical evidence of clinical heart failure,
fluid overload or chronic lung disease would be seen with:
 Refractory hypoxaemia (PaO2 < 8kPa, FiO2m >0.4, paO2/paO2<0.25)
 Pulmonary artery wedge pressure < 18mmHg
 paO2/FiO2< 200mmHg
What are the criteria for the diagnosis of ARDS?

 Bilateral pulmonary infiltrates on chest X-ray
 PaO2/FiO2 ratio<200.
 Pulmonary artery wedge pressure<18mmHg
What are the causes of ARDS?

Systemic:
 Sepsis.  Trauma.
 Burns.  Massive blood transfusion.
 Post-cardiac arrest.  Pancreatitis.
 Anaphylactic shock.
Pulmonary:
 Lung infections.  Pulmonary trauma.
 Smoke inhalation.  Near drowning.
 Aspiration.
What clinical condition are commonly associated with the development of

ARDS?
The most common conditions include:
 Severe sepsis (50%).
 Trauma (30%).
 Gastric aspiration (10%).
 Other important causes include:
 Multiple trauma.  Fat embolus.
 Massive blood transfusion.  Acute pancreatitis.
What pathophysiological processes underline ARDS?

The underline processes are incompletely understood but acharacteristic feature is
diffuse alveolar-capillary damage.the disruption of the alveolar –capillary units can be
divided into three phases: exudative, proliferative and fibrotic.
In the exudative phase:
 Acute phase plasma protein fill the alveoli.
 Endothelial injury is thought to be mediated by cytokines (TNF, platelet
activating factor and interlukins 1, 2, 6 and 8).
 Activating neutrophils also damage the endothelium by releasing proteolytic
enzymes and oxygen radicals.
 This first phase lasts afew days and progresses into aproliferative phase.
In the proliferative phase:
 There is activation and proliferation of type 2 pneumocytes and fibroblasts,
which migrate into the alveolar space and produce granulation tissue and
collagen.
 This result in remodelling of the pulmonary vasculature with occlusion of the
vascular lumen.
In the fibrotic phase:
The lungs become scarred and further collagen is deposited.
What is pathology seen in ALI \ ARDS?

 Caused by astimulus to the local or systemic inflammatory response.
 Causes include :
 Shock
1. Sepsi, particulary gram –negative bacteria.
2. Haemorrahage.
3. Trauma: multisystem trauma, direct lung trauma, near drowning, smoke
inhalation.
4. Cerebral: head injury, cerebral haemorrage.
5. Embolism: fat, air, amniotic fluid.
6. Others:
 Acute pancreatitis.
 Disseminated intravascular coagulation.
 Cardiopulmonary bypass.
 Massive blood transfusion.
 Eclampsia.
 Oxygen toxicity.
 Occur 12-72 hours after precipitating insult.
 Early change: interstisial and alveolar oedema,containing red blood cells,white
blood cells,proteins and hyaline membrane.
 Late changes: interstitial fibrosis with proliferation of alveolar type II cells,
obstruction and destruction of the microcirculation of the lung.
 Multiple-organ failure is acommon outcome.
What is the pathophysiology of ARDS?

The localosed or systemic insult results in release of interleukins (e.g. IL-1, 6and 8)
and tumour necrosis factor α (TNTFα). These mediators cause white cell activation,
adhesion and migration from peri-alveolar capillaries into alveoli. In addition,
endothelial and alveolar cell damage results in increased permeability, pulmonary

oedema and alveolar collapse.
What are the principles of treating ALI/ARDS ?

 Treatment is primarily supportive.
 Treat the underlying cause if possible.
 Try to maintain PaO2 > 60mmHg, but try to keep FiO2 between 0.5 and 0.6 (to
avoid oxygen toxicity).
 Ventilation strategies:
o Positive end-expiratory pressure (PEEP).
o Inverse ventillation ration (inspiraotry phase > expiratory phase ) –
re-opens collapsed alveoli.
o Prone position ventillation.
 Drugs:
o None conclusively shown to be of benefit.
o Nitric oxide: reduces pulmonary hypertension, reduces shunting,
improves gas exchange.
o Prostacyclin.
o Surfactant.
o Corticosteroids.
What are the aims of mechanical ventilation for ARDS?

 Prevent alveolar collapse and recuit collapsed alveoli by using high positive
end-expiratory pressures.
 Use low tidal volumes and low peak insipatory pressures to reduce lung
damage that may caused by ventilation.
What is the mortality from ARDS?

This depends on underlying cause, age of patient.
 When the under-lying cause is trauma mortality is typically 30-40%.
 When ARDS is secondary to sepsis mortality is around 60%.
 However, the highest mortality for ARDS is when it occurs secondary to
aspiration pneumonia when the mortality is 90%.
Principles of cardiovascular monitoring
What non-invasive means of cardiovascular monitoring do you know?

The lead II ECG shows rate and rhythm.
The pulse oximeter monitors arterial blood oxygen saturation and heart rate.
Blood pressure can be measures using an automated sphygmomanometer.
What invasive means of cardiovascular monitoring do you know?

An arterial line can be used to directly measure blood pressure.
Catheters may be used to measure either CVP or pulmonary artery wedge pressure.
A transoesophageal Doppler probe can estimate CO.
Pulse oximetry
What information can be gained from pulse oximetry?

 Oxygen saturation (SaO2) of haemoglobin.
 Pulse rate.
 Peripheral perfusion.
What factors might make pulse oximetry unreliable ?

 Patient movement.
 Electrical interference (diathermy).
 Venous congestion.
 SaO2 below 50%.
 Coloured nail polish.
 Carboxyhaemoglobi (SaO2 falsely high).
 Methaemoglobin, bilirubin (SaO2 falsely low).
 Methylene blue dye (decrease SaO2 temporarily).
 Ambient light.
Note that fetal haemoglobin (HbF) and polycythaemia have no effect on readings.
How does pulse oximetry work?

 Pulse oximetry relies on the principle that absorbance of light by a ubstyance
depends on the concentration of the substance and the distance the light travels
through it (Beer-Lambert Law).
 2 light-emitting diodes produce beams at red and near infrared frequencies
(660 nm and 980 nm), which are picked up by a photodetector on the opposite
side.
 Diodes flash approximately 30 times per second.
 A microprocessor analyses light absorption during arterial flow and ignores
non-pulsatile components of the signal (tissues and venous blood).
What are the problems and complications of arterial pressure monitoring?

o Over- and under-dampening which may be due to a clot, air bubbles or a very
compliant diaphragm and tube.
o Incorrect zeroing: the transducer must be placed at the level of the right
atrium.
o Haematoma and distal ischaemia.
o Arterial thrombus.
o Inadvertent drug injection.
o Disconnection and haemorrhage.
o Infection.
What are the complications of central venous access?

1. Arterial puncture and trauma. 2. Pneumothorax.
3. Haemothorax. 4. Air embolism.
5. Haematoma. 6. Catheter embolism.
7. Dysrhythmias. 8. Cardiac perforation and tamponade.
9. Damage to surrounding structures (e.g. thoracic duct, trachea and thyroid).
10. Infection (local, bacteraemia and rndooocarditis).
Key learning point

FiO2 is key
Note that either SaO2 or PaO2 is absolutely meaningless wothout knowledge of the
concentration of inspired oxygen or oxygen flow (e.g. FiO 2).
 A saturation of 95% on air may be considered reasonable but the same
saturation on high-flow oxygen with a non-rebreather reservoir bag could
indicate very poor gas transfer. Likewise,
 PaO2 of 12.0 kPa on room air would be considered normal but the same PaO2
on 100% humidity O2 through an ET tube reflects sever respiratory failure.
Therefore, pulse oximetry doesn't assess ventillation and other test such as end-tidal
Co2 and capnography should be used for this purpose.
What is A-a gradient?

Put simply, the A-a gradient is a measure of how well oxygen is transferred from the
alveolus to the blood and is defined as:
A-a gradient = PAO2 – PaO2
Where PAO2 = partial pressure of oxygen in the alveolus. And
PaO2 = partial pressure of oxygen in arterial blood.
PaO2 is obtained form ABGs and PAO2 is estimated from the alveolar gas equation:
PAO2 = {(760-47)  FiO2- PaCO2} / 0.8
Where FiO2 is expressed as a fraction.
A normal A-a gradient on air is estimated by:
(age + 100)/4
A higher gradient indicates shunting and/or a ventillation-perfusion mismatch.
Arterial blood gases
How do you take an arterial blood sample?

1. Clean procedure.
2. Radial artery (preferably the non-dominant hand-use Allen's test to ensure
dual blood supply to the hand) or femoral artery.
3. 2 ml heparinised syringe.
4. Gentle asapiration after seeing flashback.
5. Keep sample cool until analysis.
6. Firm pressure on artery to prevent haematoma.
Can you interept the two blood gas sample results?

Sample 1 Sample 2
 Ph 7.081.  PH 7.275.
 Pco2 2.76.  Pco2 12.98 Kpa.
 Po2 14.10Kpa.  Po2 4.44 Kpa.
 Base excess -22.4 mmol/l.  Base excess 15.8 mmol/l.
 HCO3- 8.4 mmol/l.  HCO3- 33.9 mmol/l.
 SaO2 94.9%.  Sao2 55.1%.
 Haemoglobin 13.2 g/dl.  Haemoglobin 18.2g/dl.
Sample 1 :
Metabolic acidosis, low Pco2, indicating compensatory respiratory alkalosis to
moderate the metabolic acidosis, eg diabetic ketoacidosis.
Sample 2:
Respiratory acidosis, high bicarbonate and base excess, suggesting metabolic
compensation. The high haemoglobin and hypoxia suggest chronic respiratory failure.
What are the potential errors in arterial blood gas sampling ?

 Over-heparinisation of the sample (increased acidosis).
 Air in the syringr (raises Po2, lower Pco2).
 Delayed analysis without cooling (decreased Po2 and PH, increased Po2 , due
to metabolism by white cells).
Oxygen delivery
How can oxygen be delivered to a patient?

Variable performance devices:
 Nasal cannulae.
 Face mask:
 At litres/minute, approximate Fio2= 0.25 – 0.30.
 At 6-10 litres/minute, Fio2 = 0.30 – 0.40.
Fixed performance devices (constant fiO2):
 Venture mask: nozzle designed to entrain air with oxygen; affords specific
FiO2 depending on nozzle used.
 Reservoir bag: FiO2 close to 1.0; mostly used in trauma.
 Continuous positive airway pressure (CPAP).
 Invasive ventilator support.
What is the danger of oxygen therapy in a patient who has chronic carbon
dioxide retension?
 Uncontrolled use of oxygen may cause apnoea.
 Some patients with chronically raised carbon dioxide rely on hypoxia to
stimulate repiration. If this drive is abolished through the use of high
concentrations of oxygen, this can lead to apnoea.
 Correction of hypoxia may reverse the normal compensatory hypoxic
venoconstriction, leading to worsening V/Q mismatch.
What are the potential complications of oxygen therapy?

 Absorption atelectasis: nitrogen is slowly absorbed and therefore splints the
alveoli; high concentrations of oxygen flush out the nitrogen. Oxygen is
absorbed rapidly and the alveoli collapse.
 Pulmonary toxicity: oxygen irritates the mucosa of the airways directly,
leading to loss of surfactant and progressive fibrosis.
 Retinopathy: due to retrolenticular fibroplasias.
 Risk of fibres and explosions.
Artifical ventilation
What are the indications for artificial ventilation?

 Respiratory failure (repiratory rate > 30 breaths/minute, high PaCO2 ),
exhaustion.
 Head injury / coma (to reduce intracranial pressure).
 Severe shock.
 Loss of chest wall integrity (trauma).
 Peripheral neuromuscular disease (Guillin –Barre syndrome).
 To reduce the work of breathing , e.g. in cardiac failure.
Can you name some indications for mechanical ventilation?

 Correction of hypoxia / hypercapnia in respiratory failure.
 Protect the airway in the " drowsy" patient (Glasgow coma scale, GCS< 8).
 Allow effective suctuining of respiratory secretions.
 To improve oxygen delivery to tissues.
What are the complications of artificial ventilation?

Cardiovascular complications:
 Decrease in venous return.
 Increase in pulmonary cascular resistance, leading to decreased right and left
ventricular output.
Pulmonary effects:
 Barotrauma results in :
 Pulmonsry interstitial emphysema.  Pneumomediastinum.
 Penumoperitoneum.  Pneumothorax.
 Tension pneumothorax.
High peak inflation pressure > 40 cm H2O are associated
with an increased incidence of barotrauma.
 Alveolar cellular dysfunction occurs with high airway pressures. The resultant
surface dependent leads to ateletasis.
 High airway pressures results in alveolar overdistension (volutrauma),
increased microvascular permeability and parechymal injury.
 High-inspired concentration of oxygen (FiO2 > 50%) result in free-radical
fromation and secondary cellular damage. These same high concentrations of
oxygen can lead to alveolar nitrogen washout and secondary atelectasis.
 ARDS
Renal, hepatic and gastrointestina effects:

 Positive pressure ventillation is resposnsible for an overall decline in renal
function with decreased urine volume and sodium excretion + water retension
(release of vasopressin)
 Hepatic function is adversely affected by decrease in cardiac output,increased
hepatic vascular resistance and elevated bile duct pressure.
 The gastric mucosa doesn't have autoregulatory capability. Thus, mucosal
ichaemia and secondary bleedingmay resulte from a decrease in cardiac output
and increased gastricvenous pressure.
What is assissted ventillation?

It can be split into non-invasive & invasive ventillation.
Non-invasive ventillation:
1. CPAP (continous positive airway ventillation)
 Delivered by an airtight mask over the nose and mouth.
 It provides a continous pressure in the airway, thus splinting open
alveoli and improving recruitment, reducing the work of breathing.
2. Pressure support:
 It can be delivered by a CPAP mask. Closely monitors the airflow in
the circuit and provides a positive pessure increase when it can
drastically reduce the work of brathing and may be termed BIPAP
(bilevel positive airway pressure).
Invasive ventillation:
It provides the most reliable way of providing a constant FiO 2 to the patient, along
with reducing the anatomicaldead space and in some cases increasing the efficiency of
ventillation.
1. CPAP: may be adminsted invasively.
2. BIPAP: and/or pressure support maybe adminstered invasively.
3. IPPV: is an obligatory ventillatory mode requiring apnoea. It is the most used
form of ventillation in acute trauma or surgery where patients are
anaesthesized and paralysed at the same time.
4. SIMV (simultaneous intermittent mechanical ventillation):
These methods allow spontaneous repiratory effort by the patient to contribute
to the ventilator process.
A predetermined tidal volume and frequency of brathing is set on the machine.
If there is no respiratory effort from the patient then the machine delivers a
breath of the preset parameters.
However, if the patient attemps to breath alone the number of machine
delivered breaths is reduced, allowing the patient to "fill in the gaps".
A further subdivision of invasive ventillation:

Volume controlled:
 A less sophisticated method of ventillation, this allows the use toset a tidal
volume that must be delivered regardless of the airway pressures involved, and
thus increase the risk or baroteauma to the lungs. Pressure limits can be used
to help prevents this. Volume-controlled ventillation does provide a constant
minute volume.
Pressure controlled:
 A more sphisticated method of ventillation, it allows the user to set a peak
inspiratory pressure (PIP).
 Inhalation occurs until this PIP is reached, after which passive exhaation is
allowed.
 The delivered volume with each respiration is dependent on the pulmonary
and thoracic compliance.
 A major advantages of pressure-controlled ventillation is a decelebrating
inspiratory flow pattern,in which inspiratory flow tapers off as the lung
inflates. This usually results is more homogenous gas distribution throughout
the lungs and a decrease in the incidence of barotrauma.
 However, tidal volume aren't constant in this method of ventillation, although

mixed modes with volume-assured, pressure-controlled ventillation are now
available on some ventillators.
What is PEEP?
It stands for positive end-expiratory pressure and is used to ensure a positive pressure
at the end of expiration, splinting open alveoli and preventing the usual alveolar
collapse. This decrease the work of breathing by obviating the initial force on
inspiration required to open the alveoli and overcomes the surface tension of alveolar
water.
High levels of PEEPincrease the risk f barotrauma.
How is the patient weaned from artificial ventilation?

1. Gradual and progressive reduction of support can be initiated using SIMV as
outlined above.
2. Alternatively, the patient may be disconnected from the ventilator for
increasing periods of time to allow spontaneous repiration. The capability to
cough effectively is essential before extubation.
What are the indications for tracheostomy ?

1. Surgical access.
2. Relief of airway obstruction.
3. Protection of tracheobronchial tree.
4. Suction and removal of secretions.
5. Prolonged ventilation (> 10-14 days , slow to wean off).
What are the criteria for extubation?

It is important to assess and consider the general condition of the patient before
considering extubation.
Various criteria have been proposed:
 Repiratory rate <45 breaths/min.
 Tidal volume 4-5 ml/kg.
 Vital capacity 10-15 ml/kg.
 PO2> 8KPa on 40% Oxygen.
 PH> 7.3.
 Stable cardiovascular system.
 No severe abdominal ditension.
 No major metabolic disturbances.
 Co-operative patient.
If ratio of repiratory rate : Tidal volume is < 80 , this usually indicates a successful
extubation.
What are the hazards of ventilation?

The hazards include:
 Barotraumas including: pneumothorax and pneumomediatinum.
 Air embolus.
 Subcutaneous emphysema.
 Dcreased cardiac output.
 Nosocomial pneumonia.
 Parenchymal lung damage.
Respiratory failure
Define repiratory failure and what are its clinical signs?

PaO2 less than 8 kPa while breathing air without intracardiac shunting .
Signs:
 Cyanosis.  Tachypnoea.
 Use of accessory muscles.  Inability of speak in sentences.
 Depressed level of consciousness.  Signs of hypercapnia.
What do you understand by respiratory failure?

Respiratory failure occurs when ventilation is unable to meet the required oxygen
demand or when the CO2 produced cannot be adequently removed.
Respiratory failure may be classified into two types:
Type 1:
I. PaO2 ( < 8 kPa), PaCO2 normal 1. Ventilation-perfusion mismatch.
2. Pulmonary embolism.
3. ARDS.
Type 2:
II. PaO2 (< 8 kPa), PaCO2 (>7 kPa) Impaired gas exchange e.g. chest
trauma, pneumothorax,
head injury
Can you do the same for instances where PaCO2 is reduced or normal ?
 Collapse / consolidation ( e.g.pneumonia).
 Pulmonary contusion.
 Asthma.
 Cardiac disease ( e.g. left ventricular failure).
 Pulmonary embolism.
Can you list some causes of repiratory failure where the PaCO 2 is raised ?
o Depression of respiratory centre: sedatives, trauma and raised intracranial
pressure.
o Chest wall problem: flail chest and kyphoscoliosis
o Neuromuscular disease: Guillain-Barre and poliomyelitis.
o Severe obstructive airways disease.
What arew the signs of impending respiratory arrest?

 Respiratory rate > 30.
 Tachycardia > 120.
 Hypotension.
 Sympathetic activation : sweaty, clammy and agitated.
 Fall in PaO2.
 Rapid desaturation when oxygen withdrawn.
The following arterial blood gas results were obtained from a young man with an
isolated chest injury following a road traffic accident. Can you comment?
1. pH : 7.24. 2. PaO2: 8 kPa.
3. PaCO2: 9 kPa. 4. Bicarbonate: 29 mmol/l.
There is an acidosis and the raised PaCO2 suggests that this is respiratory in origin .
The low PaO2 with a raised PaCO2 could be explained by hypoventilation secondary
to a large flail chest injury.
What is the definition of base excess obtained from blood-gas analysis?

This is the amount of acid ( mmol) required to restore 1L of blood to normal pH at
37˚C and PCO2 of 5.3 kPa. Normal range is -2 to +2 mmol/l
How can you treat respiratory failure?

 Treat underlying cause.
 Oxygen.
 Respiratory stimulants , eg doxapram .
 Continuous positive airway airway pressure (CPAP).
 Intermittent positive-pressure ventilation (IPPV).
 Extracorporeal membrane oxygenation (ECMO).
What treatment strategies are available in the management of ARDS?

All types of respiratory failure are treated by increasing the concentration of inspired
oxygen.
1. Techniques such as PEEP or CPAP are utilized to recruit consolidated alveoli
and hold them open, increasing the area available for gaseous diffusion.
2. Reversal of the inspiratory : expiratory ratio is beneficial.
3. Prone ventilation allows alveoli previously compressed under the effect of
gravity to be opened up.
4. Nitrous oxide is potent vasodilator and has a predilection for acting on the
pulmonary circulation, its action is to dilate the pulmonary vessels near to
working alveoli, thus maximizing the blood supply to ventilated lung.
5. Newer strategies include partial liquid ventilation using perfluorocarbon
compound, which reduces the work of breathing by reducing surface tension,
particulary in colllaped dependant lung areas; it also decreases lung
inflammation.
6. Some centres have used extracorporeal membrane oxygenation as a salvage
method in ARDS resistant to other modalities.
Explain the four types of hypoxaemia?

I. Anaemic:
Hypoxaemia occurs due to inadequate amounts of haemoglobin for oxygen
carriage.
This may be:
 Anaemia. or
 May also occur in situations, such as carbon monoxide poisoning, where
carboxyhaemoglobin preferentially binds oxygen.
II. Stagement:
 An effect of poor tissue perfusion either:
 Centrally from low cardiac output.
 Peripherally from local perfusion defects
III. Histotoxic:
A block to the cellular utilization of oxygen is present.
This is typified by the effects of cyanide inhibiting the cytochrome pathways.
IV. Hypoxic:
A broad category that includes hypoventilation, impairment gaseous diffusion in
the alveoli and V/Q mismatch.
How is breathing controlled?

Breathing is regulated by two mechanisms: Auotmatic and voluntary.
Automatic regulation:
Controlled by the brain stem: sensory information is relayed to the brain stem from:
 Central chemoreceptors near the surface of the medulla.
 Peripheral chempreceptors in the carotid and aortic bodies.
 Proprioceptor in the lung, intercostals muscles and diaphragm.
Voluntary regulation:
The central chemoreceptors respond to changes in PaCO2.
The peripheral chemoreceptors respond to changes in H+ and O2.
The response to O2 is only significant at low partial pressures ( < 70 mmHg).
Tracheostomy
What are the indications for tracheostomy ?

1. A definitive airway is required but orotracheal and nasotracheal intubation is
not possible.
2. Prolonged intubation is required.
What types of tracheostomy is most commonly performed in the intensive care

unit setting?
 Percutaneous tracheostomy as this is less traumatic and can be performed with
transfer to theatre.
How soon after a tracheostomy should the tube be changed and why?
No sooner than 3 days as it takes this long for a fistula to form so that rewplacement
may be done safely.
How should a tracheostomy be maintained ?

 The tracheostomy site needs to kept clean to avoid infection.
 Humidified oxygen should be used.
 Regular tracheal suction will be necessary.
What are the potential complications of a tracheostomy ?

1. Haemorrhage at the time of insertion.
2. Infection.
3. Misplacement.
4. Blockage.
5. Trachea-oesophageal fistula.
How do you place a CVP line and what is a normal CVP?

The two common routes for replacement of central venous lines are via the right
subclavian vein or the right internal jugular vein. The right subclavian route will be
described.
o The procedure is explained to the patient and consent obtained, in practicable.
o The patient is attached to a cardiac monitor.
o The central line is flushed down each port with saline and three-way taps
attchaed to each lateral lumen.
o The patient is positioned supine with the head turned fully to the left.
o The bed is tiled head down.
o The area of the light neck and anterior chest is widely prepared with skin
antiseptic and draped to reveal the area beneath the mid-clavicle.
o After infiltration with local anaesthetic, a large-gauge needle with attached
syringe is advanced through the skin immediately beneath the clavicle at its
junction of middle and lateral thirds.
o The needle is advanced with suction on the syringe, aiming for the
suprasternal notch at about 30˚to the skin.
o As the needle advances, it will enter the subclavian vein and venous blood can
easily be withdrawn into the syringe.
o Many sets now have hollow-barrelled syringes so that a guide wire can be
passed directly down through the syringe and needle to enter the vein.
o The guide wire is passed to a sufficient length to enter the lower superior vena
cava.
o The needle is withdrawn.
o The skin at the point of entry is nicked with a blade and a dilator is passed
over the wire to enlarge the track through the soft tissues.
o The central line is then passed over the wire into the subclavian vein.
o When sufficient length has been passed, the guide wire is withdrawn.
o The channels usually three-are aspirated, flushed and heparin/saline locked.
o The catheter is then securely sutured in place and covered with a transparent
occlusive dressing.
o A chest x-ray is organized to check catheter placement and to check for
complications, after which the line may be used.
o If advanced too far, it is a simple job to withdraw it by the appropriate amount
and rescure it.
A normal CVP reading is between 8 and 10 cm water, although an absolute value is
not as important as trends in the readings.
CVS
Central venous pressure
How is the Central Venous Pressure (CVP) measured?

1. CVP may be assessed clinically by looking for the jugular venous waveform.
 In a normal healthy person, reclining at 45˚, the manubriosternal joint may
be up to 5cm above the right atrium.
 Thus, the venous waveform either may or may not be just visible above
the clavicle.
2. The CVP may also be measured by invasive means, by inserting a central line
into the right usually via the subclavian or internal jugular vein.
3. Other routes include via the cephalic and femoral veins.
What is a normal range for the CVP?

The normal range is 0-10 mmHg, (1-13 cm H2O).
The reference point (zero point) is the surface marking of the right atrium. This
equates to the mid-axillary line if the patient is lying flat.
The range is dependent on the function of the right side of the heart. The actual
numerical measurement of CVP pressure is less useful than its response to fluid bolus
challenging.
What are the complications of a CVP line?

The complications may be divided into early and late.
Early complications: related to insertion and include:
1. Haematoma.
2. Haemorrhage.
3. Air embolus.
4. Pneumothorax.
Late complications: include:
1. Thrombophlebitis.
2. Catheter infection.
What does the CVP tell us about the heart?

The CVP only gives information about the filling pressure of the right atrium.
In diastole, this filling pressure in the heart is called the preload. The preload causes
the ventricular muscle to stretch and this is proportional to the force of contraction
according to Starling's law. Thus, an increased force of contraction will increase the
cardiac output.
The relationship between the CVP and force of contraction only applies if there is no
intrinsic lung disease or right heart pathology (e.g. valvular disease or corpulmonale).
CVP waveform:
 The a wave is caused by atrial contraction.
 The x descent follows atrial relaxation.
 The c wave is formed by the instrusion of the tricuspid valve leaflets into the
atrium at the start of ventricular systole.
 The v wave is a measure of the venous return to the atrium. It marks the point
of ventricular systole but it isn't caused by it.
 The y descent occurs when the tricuspid valve opens & the atrium empties.
The waveform can be affected by various conditions:

 Atrial fibrillation (AF): absent a wave (lack of coordinated atrial contraction).
 Tricuspid regurgitation: large v wave caused by a jet blood coming into the
atrium during ventricular systole as a result of an incompetent valve.
 Tricupid stenosis: large a wave caused by atriovenous outflow obstruction.
Slow y descent results from slow atrial emptying.
 Complete heart block: "cannon" a wave caused by uncoordination of atria and
ventricles, leading to occasional contraction where the atrium contracts against
a closed tricuspid valve.
Is absolute CVP a useful measurement? In what circumstances might CVP not

repressent overall filling?
Absolute CVP depends on ensuring that the is properly positioned each time that it is
measured (at 45o or at least the same angle for all measurments with the transducer
set at the same height). It isn't as useful a clinical tool as the response of the CVP to a
fluid challenge.
In circumstances where the right heart isn't functioning normally (partiularly in
valvular heart disease) or the overall myocardial compliance (e.g. right-sided heart
failure or pulmonary hypertension) is affected, the CVP may not be give a true
reflection of the patient's filling. In these cases, the parameter has to be considered in
the light of other physiological parameters and a PAFC may be considered.
How can you tell if your patient is adequently resuscitated now you have a
central line?
The patient should be fluid challenged.

After reading the CVP, a bolus of 200ml of crystalloid is infused and the CVP
recorded. Three patterns occur.
In A: the CVP rises a little and then goes back to its previously low value, denoting
continued hypovolaemia.
In B: A CVP that rises and then after 15 minutes or so settles down to a normal value
is indicative of normovolaemia.
In C: the CVP rises and stays high-this indicates overfilling.
Swan-Ganz catheters
What do you use a Swan-Ganz catheter for?

A Swan-Ganz catheter measures pressures in the pulmonary artery and, indirectly, left
heart filling pressure.
Blood can be aspirated from its ports to measure saturations in the right atrium and
right ventricle. It can also be used to measure CO and estimate SVR.
This is a flow-directed catheter that is floated through the heart on an inflatable ballon
until it wedges in a branch of the pulmonary artery. When the ballon is inflated, there
is a continous column of blood between the tip of the catheter and the left atrium, so
that the wedge pressure reflects left atrial pressure.
What can a pulmonary artery catheter measure?

Pressure measurements can be taken from the central veins, right atrium, right
ventricle and pulmonary artery as the catheter is floated through these structures.
When the balloon is wedged in one of the pulmonary arteries measurement of the left
atrial pressure may be taken.
In addition, one can measure cardiac output using a thermodilution technique based
on the modified Fick principle.
What are the indications for inserting a Swan-Ganz catheter ?

 Measurement of PAWP to assess fluid status and optimize CO: oliguria,
hypotension, right ventricular infarction, shock, adult respiratory distress
syndrome (ARDS) to differentiate between cardiac and non-cardiac
pulmonary oedema.
 Measurement of CO amd SCR to guide inotropic therapy in shock.
 Measurement of right heart blood SaO2 to diagnose of left to right shunts.
How do you place a Swan-Ganz catheter ?

The inflated balloon on the catheter's tip lets it float in the lumen. As the Swan-Ganz
catheter is advanced through the right heart, the pressure tracings from its identify
where it is (right atrium, right ventricle and pulmonary artery). Advancing the
catherter further causes it to " wedge" in the pulmonary artery. The balloon should
always be deflated between PAWP measurements.The tracing during the insertion of
aSwan-Ganz catheter is shown in the figure
What variables does a PAFC actually measure and which are derived?
 The PAFC can also measure the tempreture of the blood and is used to
measure changes in temperature in order to calculate cardiac output.
 It also allows true mixed venous blood sampling, which in turn allows
calculation of oxygen delivery and uptake; other derived variables include the
systemic vascular resistance.
What conditions must prevail for the PAFC reading to be valid?

A PAFC, as its name suggests, measures the pressure in the small vessels of the
pulmonary artery system. As there are no valves between it and the left atrium, its
pressure recording is deemed to represent left atrial pressure, and thus is extrapolated
to left ventricular pressure and filling .For these assumptions to be valid ,there must
be no obstructions between the catheter and the left atrium, so that it is truly a
continuous colum of blood, there must be no flow, as that would indicate a pressure
gradient and invalidate the readings.
Can you describe the principles of the thermodilution trchnique to measure

cardiac output?
The technique involves injecting a known volume and temperature of cold normal
saline into the right atrium.
The saline mixes with the blood in the right atrium and ventricle and passes into the
pulmonary artery where fall in temperature is detected, thus causing a drop in
temperature which is proportional to the cardiac output (dilution curve).
From these measurements, one can calculate systemic vascular resistance and oxygen
delivery.
What are the complications of inserting a Swan-Ganz catheter ?

1. Complications of central venous cannulation (as outlined above).
2. Dysrhythmias. 3. Heart block.
4. Valvular damage. 5. Perforation.
6. Knotting. 7. Thrombosis.
8. Pulmonary infarction. 9. Arterial laceration.
Why is the clinical use of Swan-Ganz catheters conversial ?

The conversy of the use of Swan-Ganz catheters arose because studies in the mid-
1990s found that patients who received a Swan-Ganz catheter had a higher mortality
than patients who did not receive a Swan-Ganz catheter .However, it was argued that
patients who received Swan-Ganz catheters were, by definition, sicker than those for
who they are not indicated, therefore patients receining Swan-Ganz catheters were
more likely to havew a greater mortality. Further studies, including meta-analyses of
randomized controlled trials on Swan-Ganz-guided strategies found a modest risk
reduction in mortality: the risk reduction appeared greatest in surgical patients. There
are still no consensus guidelines for clinical practice.
Pulmonary artery wedge catheter
What can a pulmonary artery wedge catheter (PAWC) measure, and what can it
be used for?
It is 70-80 cm long catheter with 10-cm markings. It usually has 3 to 4 lumens:
 Distal.  Proximal.  Injectate.
 Lumen for balloon inflation.
Indications:
o Optimization of fluid therapy (especially if right atrial pressures do not reflect
left heart function , as in severe bundle branch block, pulmonary hypertension,
tamponade or pericarditis).
o Rationalization of inotropic support.
o Investigation of cardiac shunts.
o Measurement of cardiac output.
How do you insert a PAWC?

o Insert in the same fashion as a central venous pressure line.
o Use a septic Seldinger technique, with continuous visible pressure monitoing
o Correct positioning confirmed by pressure changes as PAWC is advanced
(central venous pressure, atrial, right ventricle and, finally, pulmonary artery
pressure).
o 'Wedge' pressure achieved when balloon occludes pulmonary vessel, so
creating a continuous column of blood to left atrium.
What measurements can be made using a PAWC?

Direct measurements:
 Mixed venous gases
 Pulmonary artery pressures
 Right atrial and ventricular pressures
 Right ventricular ejection fraction
 Right cardiac output
Indirect measurements:
 Systemic vascular resistance
 Peripheral vascular resistance
 Cardiac index(CI)
 Stroke volume index
Note that the usual pulmonary artery pressure is approximately a fifth of the systemic
pressure ( 15-30 mmHg systolic , 0-8 mmHg diastolic , mean 10-15 mmHg )
If venous access was very difficult, you might be called upon to perform a 'cut
down'. Which are the two commonest sites used ans describe the procedure?
The two commonest sites are the long saphenous vein at the ankle and the brachial
vein in the antecubital fossa. The long saphenous is used most commonly.
The vein is constant at the ankle, being located 2 cm above and anterior to the tip of
the medial malleolus.
After skin preparation and local anaethetic, if time permits and the conscious state of
the patient dictates, a small transverse incision is made in the skin directly over the
vein.
The vein itself is freed from surrounding tissue by gentle dissection with a haemostat
and the vein lifted free.
Two ties of 0 silk are passed beneath the vein:

1. The proximal one is looped and left free. whilst
2. The distal one is used to ligate the vein.
Using the proximal one to elevate the vein, a nick is made in the anterior surface and
the catheter is threaded into the vein and securely tied in place by the second thread.
Shock and inotropes
What clinical signs are suggestive of poor tissue perfusion?

1. Confusion. 2.  conscious level. 3. Tachycardia.
4. Cool cyanosed extremities. 5. Poor capillary refill. 6. Poor peripheral pulses.
7. Poor urine output (less than 0.5 ml/kg per hour). 8. Metabolic acidosis.
9. Rising blood lactate concentration.
What different inotropic agents are available ?

 Catecholamines (adrenaline (epinephrine), noradrenaline (noreepinephrine),
dobutamine, dopamine).
 Phophodiesterase inhibitors (enoximone, mirinone).
 Calcium.
 Glucagon (possibly via increased calcium influx).
 Cardiac glycosides (digoxin –weak , hardly used) .
What are their modes of action and common side effects?

 Β1- agonist increase the force of myocardial contraction.
 Phosphodiesterase inhibitors decrease cAMP breakdown, increasing
contractility.
 Side effects:
 Arrhythmia.
 Tachycardia.
 Hypertension.
 Exacerbation of ischaemia (ECG changes occu due to increased oxygen
demand).
 Hyperglycaemia.
What are the pharmacological mechanisms of action of inotropes work?

Inotropes increase myocardial contractility in a variety of ways. For example, digixon
increases intracellur calcium stores in the myocardium. Catecholamines stimulate the
myocardium through their action on β1 receptors on the surface of myocardial cells.
Others may act indirectly, e.g dopexamine increases the level of endogenous
noradrenaline by inhibiting its neuronal re-uptake.
How do you assess the need for inotropes ?

If there is hypotension in the face of a high PAWP which implies fluid overload or
cardiogenic shock, or if hypotension persists despite correcting hypovolaemia, then
inotropes, then inotropic are indicated.
When would you consider initiating inotrpic support on ITU?

The choice of inotropic depends on the clinical circumstances:
1. Low cardiac output states, eg ventricular dysfunction-consider adrenaline,
enoximone or dobutamine.
2. Vasodilatation, eg sepsis –use noradrenaline.
3. Raised pulmonary vascular resistance –use enoximone.
Receptots, position and action of inotropes?

 α-receptors: expressed in the vasculature; agonists cause vasoconstriction.
 β1-receptors: expressed in the heart, agonists are positively chronotropic
(increase heart rate) and positively inotropic (increase force of contraction).
 β2-receptors:expressed predominantly in the vasculature; agonists cause
vasodilataion.
Adrenaline:
Action on: α, β1, β2 – 'dirty drug'.
Used at cardiac arrest and turns patient into "heart-brain preparation" attemping to
spare the brain and myocardium from ischemia by causing massive peripheral
vasoconstriction (α effects) & strong chronotropia (β1 effects).
Noradrenaline:
Not an inotrope strictly because no increase in force of contraction.
Acts on: α.
Causes peripheral vasoconstriction, so increasing SVR. An inotrope given in the
context of septic shock.
Must be adminstered centrally.
At low doses, invasive arterial monitoring & urine output may be all that is required.
However in the context of sever sepsis with inotrope/multiple inotrope requirements,
some measure of SVR must be available to titrate the dose.
Dopamine:
Action on D-receptors in the gut & kidney.
 In small doses: renal arteries dilate, so, increasing urinary output. Splanchniic
flow increases.
 In medium doses: predominantly β1 effects resulting in a tachycarrdia and
increase fforce of contraction.
 In large doses: predominantly α effects, causing peripheral
vasoconstrictionand an increase in SVR.
Isoprenaline:
Actions on: predominantly β1 (with some β2 action).
A synthetic analogue of isoprenaline with its main advantage being that it causes less
of tachycardia, so increasing its usefulness. The drug is used for cardiogenic shock on
cardiac care units because β2 action offloads the heart and β1 action increases force of
contraction.
Nitrates (vasodilators – not inotropes):

Action venodilatation.
In circumstances where the heart needs to be 'offloads' such as pulmonary oedema or
left ventricular failure, nitrates can be used. Their action is to reduce SVR and
venodilate, thereby reducing both afterload & preload.
Note that if arterial vasodilataion is required, hydralazine may be used (this of course
reduces afterload alone).
A part from their effect on myocardial contractility, is there any other effect of
inotropes that is important to know about when selecting one to use?
Yes, inotropes also affect the peripheral vascular in different ways, e.g.
 Adrenaline and noradrenaline both have β1 inotropic effects.
 Adrenaline has β2 vasodilatory and α1 vasocostrictors effects in the periphery.
 Noradrenaline only has α1constrictor effects in the periphery.
 Dobutamine is a β2 vasodilator.
 Dopamine is an α1 vasoconstrictor.
However, it is important to realize that these receptor profiles are dose dependent.
 Adrenaline has exhibits β2 vasodilatory effects at a lower dose than it has α1
vasoconstrictor effects.
 Dopamine exhibits α1vasoconstrictor effects at much higher dose than its
β1inotropic effects .
What inotrope would you use in cardiogenic shock due to left ventricular
failure?
Dopamine.
What inotrope would you use in cardiogenic shock due to pulmonary embolism?
Noradrenaline.
What inotrope would you use in septic shock?

Noradrenaline.
What inotrpe would you use in anaphylactic shock?

Adrenaline.
Cardiac arrest
What types of cardiac arrest do you know?

Cardiac arrests are classified into:
1. Ventricular fibrillation (VF) arrests.
2. Pulseless electrical activity (PEA) arrests.
3. Asystoilc arrests.
How would you assess a collapsed and unresponsive patient on the ward?
 Check the patient's responsiveness –'shake and shout'.
 Open the airway –head tilt/jaw lift.
 Check the respiratory effort: look, listen and feel.
 If not breathing and unresponsive, make five attempts to give two full
effective breaths using a face mask.
 Call for help: ask someone to put out an adult cardiac arrest call via the
switchboard.
 Assess the circulation for 10 seconds at the carotoid.
 If circulation present, continue artificial respiration.
 If circulation not present, commence chest compressions at a ratio of 15
compressions to every two breaths.
How would you classify the reversible causes of cardiac arrest ?

The four 'T's and the four 'H's :
1. Tension pneumothorax. 2. Tamponade (cardiac).
3. Toxic /therapeutic disturbances. 4. Thromboembolic.
5. Hypothermia. 6. Hyper/hypokalaemia.
7. Hypoxia. 8. Hypovolaemia.
What interventions have been found to improve survival in cardiac arrest?

Early defibtillation: the probability of successful defibrillation decreases by
approximately 5% every minute from the onset of the arrest.
Basic life support: respiratory support and cardiac massage delay the onset of asystole
in a VF or PEA arrest.
Does this mean all other components of the cardiac arrest algorithm are
worthless?
No, it is just difficult to design studies to examine the effects of any single
interventions in cardiac arrest patients.
What drugs do you know that are used in a cardiac arrest situation ?
 Adrenaline.
 Atropine.
 Lignocaine.
 Calcium chloride .
 Sodium bicarbonate.
How should these drugs be administrated ideally in a cardiac arrest situation?

Ideally, these drugs should be administered by a central vein. However, peripheral
canulae are most commonly used and some drugs (adrenaline and atropine) can be
given endotracheally if no intravenous (i.v.) access is available.
What is the effect of adrenaline in cardiac arrest ?

It helps maintain coronary and cerebral perfusion through its α constrictor effects.
How would you treat a right-sided tension pneumothorax?

The diagnosis of a right-sided tension pneumothorax is made by the presence of signs
of circulatory embarrassment, tachypnoea, hyper-resonance to percussion, reduced
breath sounds and deviation of the trachea away from the side of the tension
pneumothorax.
 Tension pneumothorax is an emergency and should be treated immediately
with the insertion of a large-bore cannula into the second right intercostals
space in the mid-clavicular line. This decompresses the tension but a formal
chest tube is needed.
 The chest tube should be placed just anterior to the mid-axillary line in the
fifth intercostals space.
 It should be performed using an aspetic with Betadine ® skin preparation and
infiltration of local anaesthesia.
 An incision is made above the rib, with blunt dissection with artery forceps
down to the pleura.
 Once the pleura is breached, a finger is inserted and any lung tissue is swept
away.
 The chest tube is inserted (after discarding the trocar) with the aid of a pair of
artery forceps and the tube is positioned appropriately.
 The tube is then secured with a silk suture, dressed and attached to an
underwater seal drainage system.
Cardiopulmonary bypass
What are the indications for cardiopulmonary bypass?

 Cardiothoracic surgery:
 Coronary revascularization.
 Cardiac valvular surgery.
 Surgery on the thoracic aorta.
 Neurosurgery, eg for basilar artery aneurysm.
 Supportive treatment of critically ill patients, e.g. severe hypothermia, drug
overdose.
What are the components of a cardiopulmonary

bypass system?
Blood is drained from the superior and inferior vena
cavae by gravity into a venous reservoir, which is
then passed through an oxygenator and a heat
exchanger. This arterialized blood is returned via a
bubble trap and microemboli filter through the
aortic cannula to the systemic circulation. Blood is
also returned from suction system and cardiac vents
through a microfilter, into the circulation.
What are the complications of cardiopulmonary bypass?

The artery may be complications during cardiopulmonary bypass and complications
may also arise in the early late phases after bypass.
Complications during cardiopulmonary bypass:
 Disruption of the circuit: massive air embolism, hypoxia from pump failure,
venous congestion from misplaced or kinked lines.
 Coagulopathy and hypersensitivity reactions to heparin.
 Inflammatory response resulting from contact of blood with non-endothelial
circuit surfaces.
 Anaemia from haemodilution and red cell damage from pump.
 Hypothermia.
Early post-bypass complications:
 Cardiac arrhythmias (atrial and ventricular).
 Pulmonary (atelectasis, ARDS).
 Acute renal failure (uncommon).
Late post-bypass complications:
 Focal neurological deficits (may be temporary or permanent).
 Seizures.
 Coma/stupor.
 Respiratory injury.
 Mesenteric ischaemia.
 Pancreatitis.
Anaesthesia & Analgesia

Anaesthesia
What constitutes general anaesthesia?

General anaesthesia is the urias of muscle relaxation, reversible loss of consciousness
and blockade of painful stimuli.
What alternatives are there to a general anesthetic when performing surgery?

Alternatives to general anaesthesia depend on the site and duration of surgery. The
options are as follows
 Spinal anaesthesia: local anaesthetic and analgesic agents are injected directly
into the spinal canal, creating a level of anaesthesia below.
 Epidural anaesthesia: a catheter is inserted into the epidural space and local
anaesthetic mixures infused to give anaesthesia and later postoperative pain
relief.
 Epispinal: a combination of both spinal and epidural techniques.
 Regional nerve blocks: these can be used to operate on specified territories,
such as a brachial nerve block for the upper limb , an unckle block for the foot,
or perhaps most commonly a digital nerve block for operating on fingers and
toes.
 A Bier's block: a regional technique using intravenous prilocaine to
anaesthetize a limb that is under tourniquet to prevent systemic spread of local
anaesthetic agent .
 A field block: injection of local anaesthetic around the required area in a ring
creates a central area of anaesthesia , and is often used for ' lumps and bumps'
surgery.
 Topical: local anaesthetic agents will act topically. Cocaine paste in nasal
surgery , amethocaine drops for corneal anaesthesia , and EMLA (eutective
mixture of local anaesthetics) for skin anaesthesia are examples.
How is anaesthesia induced?

It is induced after pre-oxygenation by the use of an induction agent.
 In adults, an intravenous induction agent, such as sodium thiopentone or
propofol is usually used.
 In children, gas inhalation is often used, typically with isoflurane or the newer,
less pungent sevoflurane.
The induction agnet, when given intravenously is short acting, but a sufficient dose is
given to induce anaesthesia within 30 seconds and allow an airway to be secured,
after which inhalational agents may be used to maintain anaesthesia.
What types of muscle relaxants are there?

They are either depolarizing or non-depolarizing.
 The only depolarizing blocker in clinical use is suxamethonium.
It is 2 acetyl molecules stuck together.
This acts at the motor end plate and spontaneously reverses under the action
of pseudocholinesterase after about 5 minutes.
 The non-depolarizing relaxants:
Includes atracurium, vecuronium and pancurium, although there are others.
These don't reverse spontaneously except atracurium which undergoes
Hoffman degradarion and need to be reversed by neostigmen which is
administered with glycopyrolate or atropin to prevent accumulation of

acetylcholine eslewhere causing problems.
What is LMA?
It stands for laryngeal mask airway which is a relatively new device.
It is placed without the use of laryngoscope and lies across the larynx to provide a
relatively secure airway, however, it doesn't protect completely against aspiration
problems.
Can you tell me any commonly used local anaesthetics that you have been used?
 Lidocaine.
 Bupivacaine.
 Prilocaine.
 Cocaine.
 Recently induced local anaesthetics include ropivacaine and levo-bupivacaine.
How do local anaesthetics work?

They inhibit entery Na+ ions thorugh sodium channels in cells with excitable
membranes, so blocking an action membrabes, so blocking an action potential.
They are weak bases and are so able to bind ti hydrogen ions.
How does lignocaine work?

o It works as a local anaesthetic by decreasing the transit increase in sodium
permeability of exciable membranes, which increases the threshold for
electrical excitability.
o It also works as a class I anti-arrthymic by slowing the rate of depolarizing of
the cardiac action potential, thus suppressing cardiac automaticity.
Depolarization is slowed and action potential duration is shortened with minimal
shortening of the refractory period. Thus, the proportion of time for which fibers are
refractory is increased.
What are different types of local anaesthesia?

I. Ester class
Only still cocaine still in frequent use for topical anaesthesia.
II. Amide class
 Lidocaine ( formerly called lignocaine ): short acting, usually available as
0.5%, 1 % and 2 % solutions.
 Prilocaine : highest therapeutic index, safest agent for intravenous blockade.
 Bupivacaine: longer acting than lidocaine. Often used in epidurals.
Levo-bupivacaine now used extensively for local infiltration to minimize
wound pain postoperatively .
Local anaesthetic Max. dose mg/dl Max. dose mg/dl Common uses
eout adrenaline With adrenaline
Lidocaine 3 5 (infilteration)  Local infilteration.
 Short acting nerve
blocks.
 Epidurals.
Bupivacaine 2 3 (don't use  Local infilteration
(Marcaine) adrenaline in spirals (either alone or in
or epidurals). combination with
lidocaine).
 Epidurals.
 Spinals.
Prilocaine 6 6  Regional nerve blocks.

Bier's block.
What is Marcain Heavy ?

This is bupivacaine prepared in a dextrose solution to increase its viscosity and
weight.
It is used in spinal anaesthetisia to keep the local anaesthetic localized around the
spinal cord for longer .
Care must be taken with its use in this context because patient positioning is crucial.
If the patient is too flat, a high concentration of bupivacaine can gravitate to the high
cervical cord and brain stem, causing problem with respiration and maintenance of
blood pressure ( 'a total spinal').
What precautions and maximum doses apply to local anaesthetic infilteration?

 Implied or written consent.
 Precautionary intravenous access.
 Avoidance of intravascular injection.
 Availability of resuscitation equipment.
 Monitoring of patients for 30 minutes post-infiltration.
Lidocaine maximum dose:

 4 mg/kg plain 1% lidocaine, i.e. 28 ml (280 mg) for a 70 kg patient.
 7 mg/kg 1% lidocaine with adrenaline, i.e. 50 ml (500 mg) for a 70 kg patient.
(1% lidocaine = 10 mg/ml; low-concentration adrenaline is used – 1:200,000).
Bupivacaine maximum dose:

 2.5 mg/kg plain 0.25% bupivacaine, i.e. 70 ml for a 70 kg patient (or 35 ml of
0.5% bupivacaine).
 3.2 mg/kg 0.25% bupivacaine with adrenaline, i.e. 90 ml for a 70 kg patient
(or 45 ml of 0.5% bupivacaine + adrenaline)
(0.25% bupivacaine = 2.5 mg/ml; adrenaline, 1:200,000).
How would you calculate the safe maximum dose of a local anaesthetic such as
1% lidocaine?
It is important to consider a number of factors when considering toxicity of a local
anaesthetic.
These include the site and rate of injection as well as the intrinsic toxicityof the agent
itself.
 1% of a local anaesthetic contains 10 mg/ml.
 The safe dose of lidocaine is 3 mg/kg.
In a 70 kg male, a total of 210 mg can be administered.
So 21 ml of 1% lidocaine can be safely given.
How does adding adrenaline affect the action of a local anaesthetic?

Adrenaline promotes local vasoconstriction slowing the absorption of the local
anaesthetic.
The effect of this is to prolong the duration of action of the local anaesthetic and
reduce the risk of systemic toxicity.
Adrenaline shouldn't be used near terminal arteries such as the fingers and toes, as a
reduction in blood flow rsults in increasing the risk of ischaemia.
What are the effects of local anaesthetics and how do you manage them?
Local effects:
 Inflammatory response (especially esters).
 Neuropathy (if injected intraneurally).
 Neurotoxicity (especially high concentrations of lidocaine.
Systemic effects:
1. Central nervous system toxicity, :occurs in 3 phases):
 Excitation phase: tinnitus confusion, circumoral tingling, light
headedness.
 Convulsion phase: grand mal seizure.
 CNS depression: drowsiness, collapse, coma, apnoea.
2. Cardiovascular system toxicity:
 Excitation phase: hypertension, tachycardia.
 CVS depression: hypotension.
 Cardiovascular collapse.
How would you manage a patient exhibity toxic effects of a local anaesthetic?
Management is essentially supportive as there is no reversal agent .
 It is important to assess the airway, breathing and circulation.
 Stop injecting the L.A. and give the patient oxygen.
 Be prepared to intubate if necessary.
 Rapid fluid infusion to help cardiovascular collapse. The patient may require
inotrpic support.
 Seek approprtiate help.
Local anaesthesia & infection:
Infection promotes an acidic environment in the tissues with a great deal of

anaerobic metabolism.
Local anaesthetics penetrate the cell membrane in an uncharged form . In such an

acidic environment the molecules become charged and cannot therefore penetrate
the membrane and exert their effect.
Local anaesthetic infiltration can also spread cellulitis in the tissues.
Postoperative analgesia
What are the pronciples of post-operative pain management?

Management of post-operative pain should be tailored to the individual patient.
It is important to choose the appropriate drug and mode of delivery.
Provision of post-operative pain relief can be divided into:
Pre-operative, this includes:
 Pre-emptive analgesia with NSAIDS or nerve blocks.
 Epidural analgesia given 48 hrs before lower limb amputation has been shown
to reduce the incidence of phantom limb pain.
 Pain is sunjective phenomenon and patients councelling is important (has been
reduce post-operative pain).
Intra-operative:
 Judicious use of opioids, regional nerve (including central & peripheral nerve)
blocks and wound infiltration with local anaesthetic agnets.
Post-operative:
 Pain can be managed by either opioids or non-opioid methods.
Can you expand on the methods of postoperative pain relief?

It should be delievred according to an analgesia ladder, starting with the least potent
agent and working upwards.
It is important to maintain adequate levels of analgesia rather than to provide
analgesia solely on demand. A multi-modal approach is though to be superior to
single modal techniques.
Methods of providing post-operative pain relief may be broadly divided into:
 Drug therapy.
 Regional anaesthetic techniques.
 Psychological methods.
Drug therapy, it would encompass opioid and non-opioid methods.
 The opioid drugs, for example, include morphine, diamorphine and pethidine.
 The non-opioid drugs include most commonly NSAIDs and paracetamol (±
combination).
Regional anaesthetic techniques: It includes:
 Central.
 Neuraxial blocks e.g. epidural (usually a combination of opioid and local
anaesthetic).
 Spinal nerve blocks (fentanyl or diamorphine and bupivacaine).
 Peripheral nerve blocks (intercostal, brachial or local infilteration.
Psychological methods:
 They are important and include psychoprophylaxis and relaxation techniques.
When considering these methods one needs to take into account the route of
adminstration;
 Parenteral (I.M., I.V., continous infusion, patient controlled analgesia (PCA)).
 Non-parenteral (oral, buccal, sublingual, rectal, transdermal, intra-articular,
spinal TENS (trans-cutaneous electrical nerve stimuation) and inhalational).
What are the advantages of PCA?

 It provides rapid prompt drug delivery.
 Studies have shown that it gives greater patient satisfaction and improved
ventillation compared with conventional routes of analgesia adminstration.
Route of administration:
An intavenous cannula is connected to a rate-limited giving set, which in turn is partly
controlled by a handset given to the patient.
By pressing the handset button, the patient receives a bolus of intravenous analgesic –
usually an opiate- on top of bachground infusion.
The machine is regulated to prevent overdose.
A similar method of patient controlled "top up" has also been introduced for
epidurals.
What are the physiological benefits of good post-operative pain control?

It produces a stressor effecct on the body.
Thus effective analgesia will reduce this reponse and therefore benefit the respiratory,
cardiovascular, gastrointestinal and genitourinary system.
With good pain relieft there is:
 Improved respiratory function as a result of reduced splinting of the
diaphragm and subsequent increased alveolar ventillation. This further educes
the risk of hypoxia.
 Reduced sympathetic stimulation, so decreasing cardiac work and systemic
vascular resistance. This in turn improves splanchnic and renal perfusion.
 Reduced incidence of deep veous thrombosis, due to more rapid patient
mobilization.
 Reduced incidence of post-operative ileus and urinary retention.
What is the analgesic ladder?

It is a stepwise approach to pain control, in which each analgesic is categorized
according to potency as mild, moderate or strong.
It is an attempt to rationalize analgesic prescribing and suggests that a patient's pain
should be treated in a stepwise manner, moving up or down the ladder one step at a
time as a patient's pain changes.
Its benefits:
 It prevents sudden, irrational changes in analgesia.
 It stops the subsequential use of different analgesics of the same potency being
used in worsening or uncontrolled pain.
 It provides a mechannism of reduction in analgesia when pain is improving.
What techniques may be used in a child who has had a circumcision?

At the time of procedure, the anaesthetic may employ a caudal block by injecting L.A.
into the spinal cord via the sacral foramen. This provides effective means of analgesia
for this type of procedure, alternatvely, a local anaesthetic penile block may be used
inserted at the time of the operation.
Postoperatively; non-steroidal anti-inflammtory suppository may be inserted before
the patient recovers from anaesthesia and simple oral analgesia taken thereafter.
Compare the use of traditional on demand IM analgesia with PCA.

Trditional on demand I.M.:
The advantages:
 IM morphine are convenience and safety.
 At doses commonly used, there are few side effects and adequate analgesia is
usually maintained for several hours with each injection.
The disadvantages:
 The patient must request the analgesia; some patients may be unwilling or
unable to do so, and suffer as a result.
 On a busy ward, there may also be a significant delay between requesting
analgesia and its adminstration.
 In shocked patients, opioid may accumulate IM owing to sluggish perfusion,
only to the rapidly absorbed when the circulation is restored, leading to
unpredictable side effects.
PCA:
The advantages:
 More stable blood level of opioid is achieved without the patient having to ask
or wait for a nurse to adminster it.
 There is a safety cut out to prevent patients being able to overdose.
The disadvantages:
 The patient must be able to understand the system and must have the phsyical
ability to press the button required; severly deformed rheumatoid hands can be
problematic, as are patients with dementia.
 This form of analgesia also requires an IV cannula, a pump and a handset to be
attached to the patient while they are trying to mobilize postoperatively.
 Blood opioid levels may fall quickely if no demands are made on the system,
so at night the patient may wake up in pain and take longer to achieve a
necessary level of analgesia than they received IM morphine.
Sedation
Indications for surgery:

1. Light sedation for minor procedures (e.g. manippulation of disslocation &
fractures, colonocscopy).
2. Anxiolytic & light sedative can be used as premedication before major
surgery.
3. Can be useful for a confused patient on the ward, although great care must be
taken to investigate the cause of the confusion (e.g. hypoxia sepsis) and watch
for repiratory depression.
4. Sedation is mandatory (if patient is not in arresst) on ET intubation.
What is sedative? How do a sedative, an anxiolytic & a anaesthetic differ?

Anxiolysis is relier of apprehension and uneasiness without alteration of awareness.
Amensia is loss of memory of an event or peoid and can be abterograde or
retrograde.
Sedation is depression of a patient's awarness of the environment and reduction of his
or her resposiveness to external stimulation:
 Conscious sedation is light sedation in which the patient maintains his or her
airway reflexes and abolity to cooperate.
 Deep sedation is a more profound depression of the response to stimulation in
which airway reflexes are not maintained.
Analgesia is relief of pain without sedaion or alteration of the state of awarnedd
(lthough analgesics may have a sedative effect).
Anaesthesia is a state of unconsciousness.
After adminstration of neuromuscular blockers to paralyze the patient either for

intubation or in ventilatory modes that require paralysis, adequate sedation is essential
to prevent the patient from being aware of the paalysis.
Further, in ventillatory modes that don't accommodate the patient's breathing effort
(e.g. IPPV), if onadequately paralysed and sedated, ventillation may be affected by
fighting against the ventilator.
An injured, stresssed and uncooperative patient may benefit from sedation, although
care must be taken in the context of a head injur; sedation in this context can help to
decrease the acute physiological stress respponse.
Sedation for MRI in children (must be done by paediatric anaesthetist).
Class of sedative:
Benzodiazepines (diazepam, lorazepam, midazolam):
The benzodiazepines act by stimulating GABA receptors in the CNS stimulation of
the receptor results n chloride influx, hyperpolarization and decreased neuronal
excitation.
Actions include:
 Anxiolysis and sedation.
 Amnesia (most profound with midazolam).
 Anticonvulsant.
 No analgesic properties.
 Respiratory & cardiovascular depression (much greater risk if adminstered
with centrally acting analgesic).
The major differences among the available agents concern the route of adminstration,
time of onset, duration of action, mechanism of metabolism and accumulation of
metabolites.
In non-intubated patients, they are titrated, starting at the lower end of the range of
recommended doses, followed by the adminstration of incremental doses until the
desired effect is achieved. These sedatives are also 1st line agents for acute seizure
management.
Midazolam:
Most commonly used benzodiazepine for minor procedures.
Water soluble.
Short half-life.
Profound amnesic effect in many patients.
Rapid onset.
Metabolized by hepatic microsomal system, so suitable for use in renal failure.
In overdose can cause respiratory & cardiac depression.
All patients having midazolam sedation should have intravenous access and pulse
oximetry; ECG monitoring & resuscitation facilities should be available. Patients
shouldn't drive or operate heavy machinery for 48 hours afterwards.
Lorazepam:
Water soluble.
Intermediate half-life.
Intermediate onset.
Suitable for infusion as little accumulation.
Cleared by hepatic conjugation.
Diazepam:
Not water soluble.
Intermediate to long half-life.
Can be given intravenously, orally or rectally.
Good anticonvulsant acutely.
Hepatic metabolites are active and have long half-lives, so not suitable for infusion.
Other sedatives: non-barbiturate and barbiturate:

Non-barbiturates:
Propofol:
 Non-barbiturates sedative.
 Subsituted isopropyl phenol compound prepared in a 10% lipid emulsion
(white emulsion).
 Anaesthetic induction agent: some short operations can be performed solely on
propofol without the use of a volatile agent.
 Rapid onset and short half life.
 Clearance not affected by renal or hepatic dysfunction.
 Respiratory & cardiovascular depressant.
 Good agent for sedation in patients receiving mechanical ventillation.
 Prolonged infusion in paediatrics is associated with lactic acidosis.
Etomidate:
 Non-barbiturates imidazole.
 Commonly used on rapid induction intubation alongsidde a muscle relaxant
such as suxamethonium.
 Rapid onset of action and a short but dose-dependent duration of action.
 Cardiovascular effects minimal.
 Can be used as a short term sedative for procedures.
 Depressses adrenal cortex in the long term- not suitable for infusion.
Barbiturates:
They act on GABA-a receptors in the brain and are also respiratory and cardiac
depressant as with most sedative & induction agents.
They are highly addictive drugs.
Thiopental:
 Commonly used induction agents.
 Given in alkaline solution so irritant to the tissues if it extravasates.
 Rapid onset and relatively short half life.
 If given in an infusion in the ITU (particulary in the treatment of intreactably
raised ICP), it accumulates in the body's fat stores so, when stopped, several
days must be given before any formal testing of brain or brain-stem function.
 -ve inotrope.
Phenobarbital:
 Older drug.
 Used in the past as an induction agent.
 Still used in some centers for intractable epilepsy & status epilepticus.
Opoids:
 They are agents thaty induce systemic analgesia, some anxiolysis and mild
sedation.
 They don't induce amnesia of any significant. Examples: morphin, fentanyl.
 Main type of analgesic used in surgery.
 Rapid onset and usually intermediate half life.
Sedation On ITU
What are the most common indications for sedation on ITU?

1. Mechanical ventilation.
2. Invasive procedures.
3. Pain/discomfort.
4. Underlying medical conditions:
o Raised intracranial pressure.
o Seizures.
o Low cardiac output state.
What are the undesirable effects of sedation?

 Inability to fully evaluate the patient's neurological status.
 Cardiovascular instability.
 More intravenous access required (therefore greater risk of infection).
 Decreased clearance of the drugs used for sedation may prolonge weaning
from ventilatory support.
Which sedative drugs are used on the ITU?

 Benzodiazepines: midazolam.
 Intravenous anaesthetic agents: propofol.
 Barbiturates: thiopentone in status epilepticus.
 Inhalational anaesthetic agents: isoflurane.
Nutrition & Fluids

Nutrition and the surgical patient
What are the indications for nutritional support?

o Patients who are unable to maintain adequate nutrition to maintain body
haemostasis.
o Medical and syrgical disorders likely to result in malnutrition, eg intestinal
fistulae, Crohn‟s disease.
o Postoperative starvation lasting more than 10 days.
When should nutritional support be considered in a surgical patient?

Nutritional support should be considered in any patient who is unable to have an
adequate dietery intake for more than 3 or 4 days.
What are the metabolic reponses to fasting?

The metabolic reponses include a fall in the insulin level and a rise in the plasma
glucagon level (in an attempt to maintain an adequate level of glucose for the brain).
Glucogen stores are also mobilised from the liver. In addition, there is breadown of
muscle and viscereal protein, which produces the amino acids, alanine and glutamine
which are precursors for hepatic gluconeogenesis. Breakdown of glycerol and
triglycerides to produce fatty acids is also seen.
.
What problems does malnutrition cause in a surgical patient?
the problems of malnutrition include:
 Poor wound healing.
 Gasrtromucosal atrophy.
 Loss of muscle mass.
 Reduced respiratory function.
 Reduced immune function.
 Reduced protein synthetsis.
whether these problems translate into increased post-operative morbidity is debatable
though more recently, studies have shown benefit of pre-op feeding only in patients
with severe malnutrition.
How would you assess the nutritional status of a patient?

 History.
 Examination:
 Clinical inspection: appearance through the loss of fat and muscle, and
respiratory muscle function.
 Anthropometric & Dynamometric:
 Dynamometric: hand grip strength.
 Anthropometric: triceps skinfold thickness, mild-arm muscle
circumference and lean body mass.
 Biochemical/haematological: serum proteins (e.g. albumin), liver function,
U+Es.
 Immune function.
What are the signs of malnutrition?

Early signs (loss of 15% body weight):
 Na+ and water retention leads to peripheral oedema.
Sever signs (loss > 15 % body weight):
 Loss of muscle mass & fat.
 Anaemia.
 Diarrhoea.
Pre-terminal signs:
 Decreased albumin synthesis and antibody production.
 Poor wound healing (paticularly zinc, mafnesium and selenium trace elements
important).
 Acidosis.
 Hyperkalaemia.
 Decreased cough reflex: leading to possible pneumonia.
How may nutritional support be delivrered ?

Enterally or parentelly.
Enteral feeding involves:
 Oral.
 Nasogastric (NGT) or nasojejunal tube (NJT).
 Percutaneous endoscopic gastrostomy (PEG).
 Percutaneous endoscopic jejunostomy (PEJ).
 Surgical jejunostomy.
Parenteral feeding can be either:
 Peripheral: through a long line. or
 Central: through a jujular or subclavian line.
Which type of feeding is preferable ?

Entral feeding is preferable to parentral for a number of reasons because:
 It is more physioliogical.
 It helps prevent traslocation of gut flora into the blood.
 It avoids the complications of central line insertion.
What are the indications for enteral feeding?

1. Sever catabolic states.
2. Malnutrition pre-surgery.
3. Postoperative oesophaggastric surgery.
4. The unconscious patient.
5. Anorexic elderly patient with inadequate intake.
6. Mild to moderate GI disease (pancreatitis, short gut syndrome, Crohn's
disease).
Monitoring:
1. Clinical. 2. Fluid balance.
3. Daily weights. 4. Electrolytes and twice-weekly trace elements.
In what instances would entral feeding be unsuitable?

In cases of complete small bowel obstruction, prolonged paralytic ileus with evidebce
of small bowel dilatation, severe diarrhoea and proximal small intestinal fistulae.
What are the complications of enteral feeding?

Complications of enteral feeding may be related to delivery of the nutrient to the
gastrointestinal tract or related to intubation of the gastrointestinal tract.
With regards to delivery:
 Diarrhoea is the most common complication , occuring in 5-10% of
patients.
 Aspiration and feed intolerance are two other well-known complications.
Complications related to the intubation of GI tract include:
 Blockage of the tube.  Displacement.
 Wound infection.  Fistula formation.
 Peritonitis.
What are the indications of TPN?
1. Aboslute or relative intestinal failure.
2. Hypercatabolic states.
3. Postoperative (in some selected cases particularly with prolonged
gastroparesis and failure of absorption).
Monitoring:
1. Weight. 2. U + Es, glucose, FBC, LFTs.
3. Fluid balance. 4. Temperature and signs of sepsis.
5. Trace elements.
What are the constitiuents of a parenteral nutrition diet?

Macronutrients:
 It is consisting mainly of energy sources.
 Many regiments have a combination of 50% carbohydrate and 50% lipid.
Nitrgen sources are present as a mino acids
Micronutrients:
 Vitamins, Electrolytes and Trace elements.
It is a mixure of hypertonic sugars + fat emulsion + nitrogen + electrolytes +

vitamines + trace element.
 > 50% CHO.
 30-40 % fat emulsion.
 1-3 g/kg body weight per day of fat.
 Nitrogen: synthetic crystalline amino acid preparation.
 Water: 30-45 ml/kg per day.
 Water 30 -35 ml/kg/ per day.
 Electrolytes: Na+, K+, Cl-, Ca++, Mg++, PO3---.
 Vitamines: A, D, E, K (fat soluble), B,C.
What are the basic components of total parentral nutrition (TPN)?

Water, potassium, sodium, energy, nitrogen, magnesium, phosphate, water-soluble
vitamins, trace elements and essential fatty acids.
What are the complications associated with TPN?

Complications associated with TPN may be related to insertion of the catheter and
include:
o Catheter-realted:
 Insertion.  Displacement.
 Infection.  Thrombosis.
 Occlusion.  Cannulation of the carotoid artery.
 Haematoma.  Pneumothorax.
o Metabolic complications include:

 Hypo/hyperglycaemia.
 Hyper/hypokalaemia.
 Hypo/hypercalcaemia.
 High and low sodium levels in addition to deficiences of trace elements,
vitamins, essential fatty, folate, zinc and magnesium.
 Hypercholraemic acidosis.
These metabolic complications only occur in approximately 5% of patients.
o Hepatobiliary:
 Abnormal liver function tests.
 Jaundice.
o Intestinal:
 Villous atrophy.
 Bacterial translocation / endotoxaemia.
o Refeeding syndrome:
 It is a rare but well documented complication.
 It is due to an over rapid shift of potasium and phosphate into the cells. It may
manifest itself with cardiac arrest and death.
Are there any contraindications to enteral feeding?
 Complete small bowel obstruction.
 Paralyric ileus.
 Proximal small intestinal fistula.
 Severe pancreatitis.
What are the nutritional requiremens of a 70kg man before and after surgery?
How does this change if he develops a pyrexia or sepsis?
Normal nutritional:
Requirmenrs approximately=
30 kcal/kg which roughly about 2000 kcal man
Postoperatively:
This increases to 35 kcal/kg
And increase by 10 % per degree increase in temperature.
In septic state:
Requirments = 40 – 45 kcal/kg.
In hypercatabolic state (such as sever burns).
Requirments as high as 60 % kcal/kg.
Intravenous fluids
How would you classify the fluid compartments in the body?

The body fluid compartments can be divided into extra-cellular and intra-cellular.
The intra-celluar fluid compartement accounts for ⅔ of the total body water.
The extra-cellular fluid compartement includes:
 The intra-vascular volume.
 The interstitial fluid volume.
In a 70 kg man:
 The intra-cellular fluid accounts for 28 litres.
 The extra-cellular fluid 11 litres.
 The plasma volume 3 litres.
What is the volume and composition of the body fluids?

Volumes and Electrolyte Copntent of Body Fluids
Volume Sodium Potassium Chloride Bicarbonate
(ml/day) (mmol/l) (mmol/l) (mmol/l) (mmol/l)
 Saliva 1500 30 20 35 15
 Stomach 2000 50 10 150 0
 Pancreas 1000 140 5 30 120
 Bile 1500 140 5 100 30
 Small bowel 3500 100 5 100 25
 Large bowel 500 80 15 50 0
 Sweat 0-500 50 10 50 0
 Diarrhea Variable 80 30 60 25
What are the clinical signs of dehydration?

 Dry mucous membranes.
 Decreased skin turgor.
 Tachycardia.
 Hypotension.
 Reduced urine output.
 Reduced level of consciousness.
 Suken fontanelles in young children.
Following a laporatory, what losses need to be taken into account and how do
you calculate these?
Basic fliud requirements = 25 ml/Kg/day
Insensible losses = 20 ml/hour
Pyrexia = Add 10 ml/hour for each degree above 37oc
Anticipated ileus = add 20 ml/hour first day
Third space losses = add 40ml/hour first day
Consider other losses , e.g. bleeding.
What are the daily requirements of an average 70 kg man in terms of potassium,

sodium, fluid volume and calories?
In the setting of intravenous fliud replacement, a daily intake of
 1-2 mmol/Kg body weight Na+.
 60 mmol of K+. Assuming normovolaemia,
 Daily I.V. fluid volume is 2500ml.
 Ongoing losses from the gastrointestinal tract , pyrexia or burns must be
replaced as well.
Adquate nutrition is most patients can be maintained by an intake of 1800-2000
calories per day. Patient who are hypercatabolic due to disease may need more.
What fluid would you use to replace the loss from a nasogastric tube?
Nasogastric tube aspirate is electrolyte-rich fluid containing large amounts of
potassium, sodium, chloride and bicarbonate. It should be replaced with as smilar a
fiuld as possible, i.e, Hartmann's solution or normal saline with added postasium.
What does Hartmann’s solution contain?

 Na+ 131 mmpl/l.
 Cl -
111 mmol/l.
 K+ 5 mmol/l.
 Ca 2+
2 mmol/l.
 HCO3 -
29 mmol/l (as lacrare).
 Osmolarity 278 mosmol/l.
Maintains composition of extracellular environment when large volumes
What are the contstituents of 5% dextrose, normal saline and Hatmann's

solution?
5% dextrose is soltuion of 50 g of anhydrotus glcuse in 1 litre of water with a calorific
value of 200 calories (4 cal/g).
This table shows the consittuents of each (all vaues given as mmol/L):
Osmolality Na+ Cl - K+ HCO3- Ca 2+ Dextrose
5% dextrose 280 5%
Normal salime 308 154 154
Hartmann's solution 267 131 111 5 29 2
Can you describe how 1 litre of 0.9% normal saline is distributed when infused
into a patient?
Following infusion:
 Only 25% of normal saline stays in the intravascular space.
 The remaining 75% redistributes into the interstitial space. hence only 250 ml
is „added‟ to the plasma volume.
How does this compare to infusing 1 litre of 5% dextrose?

In the case of infusing 5% dextrose, only 8% remains in the plasma and 92%
redistributes into the interstitial and intracellular compartments.
So for 1 litre of 5% dextrose, only 80 ml is „added‟ to the plasma volume.
How do colloids differ from crystalloids?

Colloids are fluids which exert an oncotic pressure either via protein particles
(natural colloids) or via synthetic particles (artificial colloids).
Crystalloids have approximately the same composition and osmolality of plasma, and
rapidly redistribute throughout the extra-cellular fluid compartments.
Plasma expanders have a high concentration of osmotically active particles so that
there is a shift of fluid from the interstitial tissue to the intra-vascular space.
What colloid solutions do you know?

Colloids solutions can be classified into natural and synthetic solutions.
The natural solutions include: fresh frozen plasma, purified protein fraction , human
albumin and plasma protein solutions.
The synthetic or artificial colloids include: the gelatins, hydroxyl ethyl starch and
dextrans.
Do the colloids interfere with cross-matching?

Gelatins such as haemaccel and gelofusin do not interfere with cross matching or
haemostasis. However, dextrans such as dextran 40 and dextran 70 are commonly
associated with coagulation abnormalities and interfere with blood cross matching.
The hydroxyl ethyl starch solutions such as hetastarch and pentastarch may interfere
with haemostasis if large volumes are transfused (dilutional coagulopathy).
What do you understand by the term third space fluid loss?

Third space fluid loss is the sequestration of sodium rich fliud into the interstitial
space as aresult of infection, inflammation or tissue trauma.
What are 'Haemaccel' and 'Gelofusin' and what are their consistuents?
They are synthetic colloids that are a solution of degraded bovine gelatins polygeline.
Haemaccel has the following ionic comopsition (all values given as mmol/L):
Na+ Ca2+ K+ Cl- PO4- and SO4-

145 6.3 5.1 145 Trace
Isotonicity is maintained by the polypeptides of the gelatin. Although Gelofusin is

droadly similar, it has approximately one-tenth of the concentrations of Ca2+ and k- .
Explain why 'Haemaccel' stays in the circulation longer than either normal
saline or dextrose?
Haemaccel is a synthetic colloid solution that generates an oncotic pressure, whereas
crystalloids, such as saline or dextrose, are salt solutions made up of small molecules
that do not generate an oncotic pressure.
As a result, when a crystalloid is introduced into the blood stream, it will attempt to
move by osmosis to an area with a higher oncotic pressure, which is the surrounding
extravascular tissues. Because colloids such as 'Haemaccel' generate their own oncotic
pressure, the osmotic gradient is lower and less fluid moves out of the circulation.
A patient with small bowel obstruction is oliguric, tachycardiac and hypotensive.

Outline your initial thoughts as you approach the bedside?
Patients with small bowel obstruction can sequester many litres of electrolyte-rich
fluid in their distended bowel causing hypovolaemia; there is a resultant oliguria
owing to decreased renal perfusion pressure and a tachycardia in an attempt to
maintain cardiac output.
Volumes of sequestered fluid are often underestimated and fluid replacement may be
insufficient and occasionally of the wrong type.
After assessing the patient to ensure no other cause of circulatory collapse has been
missed, and the sufficiany of fluid therapy assessed, fluid resuscitation of the patient
with crystalloid containing potassium is initiated.
A recent set of electrolyte results should available.
How will you monitor the adequancy of your fluid resuscitation?

In the first instance, monitoring is clinical and is by repeated observation of vital signs
for evidence of improvement.
If the patient is not catheterized, then they should now be catheterized.
If fluid resuscitation within the limits of clinical monitoring were insufficient, then
central venous pressure monitoring should be initiated to assist fluid management.
Describe the differences between osmolarity and osmolality . How would you
make osmolar and osmolal solutions?
 Osmolarity describes the concentration per litre of solvent.
 Osmolality quotes a concentration per kilogram of solution.
To make:
An osmolar solution of a substance:
 Dissolve the substance in 1 L of water, thus making the total volume greater
than 1 L.
An osmolal solution:
 Dissolve the substance in a small amount of solvent and then make the total
volume up to 1 L – thus, the concentration in an osmolal solution is higher as
the total volume is less.
Blood Groups
What do you understand about the ABO blood group system?

 The ABO blood group system consists of three allelic genes: A , B and O.
 The A and B genes control the synthesis of enzymes that add carbohydrate
residues to cell surface glycoprotiens and the O gene is an amorph that does
not transform the glycoprotein.
 There are six possible genotypes but only four phenotypes.
 Naturally-occuring antibodies are found in the serum of those lacking yhr
corresponding antigen.
Phenotype Genotype Antigens Antibodies Frequency
O OO O Anti-A, Anti-B 46%
A AA or AO A Anti-B 42%
B BBor BO B Anti-A 9%
AB AB AB None 3%
What is the blood grouping and ABO compatibility ?

 Blood group O = universal donor.
 Blood group AB = universal recipient.
Blood group Antigenes Antibodies Can give blood to Can give blood from
AB A and B None AB AB,A,B,O
A A B A and AB A and O
B B A B and AB B and O
O None A and B AB,A,B,O O
In blood grouping, a patient‟s red cell are grouped for ABO and Rhesus antigens, and
the serum is tested to confirm the patient‟s ABO group.
Tell me about the Rhesus ( RH) system?

 Rhesus antibodies are immune antibodies requiring exposure during
transfusion or pregnancy: 85% of the population is Rh-positive.
 90% of Rh-negative patients transfused with Rh-positive blood develop anti-D
antibodies.
 The two common alleles are D and d:
 If an individual (diploid) has both D allels (homozynous) or just one D allel
(heterozynous), they synthesise a glycolipid antigen (the Resus D antigen)
on the surface of their red cells.
 Unlike the ABO antibodies (anti- A and anti-B), the antibodies that recognises
the D antigen (anti-D) is not naturally occurring. It only arises as a result of
the immunization of Rh-negative person (dd) with the D antigen, usually via
Rh-positive (DD or Dd) blood, most commonly via transfusion or pregnancy.
Blood transfusion
What blood products are available for use in surgical patients?
Available blood products include:
 Packed cells ( storage life of 35-42 days).
 Plateltes concentrates (shelf life of 5 days) there are no viable platelets in
stored blood after 48 hours.
 Granulocyte concentrates.
 Fresh Frozen Plasma (plasma that has been separated from red cells within 6
hours of collection. It contains all the coagulation factors and can be stored for
up to 1 year, When thawed it should be used immediately).
 Cryoprecipitate (contains factor VII , fibrinogen and von Willebrand factor).
What are the complications of blood transfusion?

Complications of blood transfusion can be related to the mechanics of trans-fusion or
the transfusion itself.
Complications due to the mechanism of delivery include:
 Cannula site sepsis.
 Haematoma.
 Air embolism.
Complications of the transfusion itself:
The only „common‟ immediate complication is the major transfusion reaction
Early side effects associated with blood transfusion

Immunological:
 Haemolytic transfusion reaction.
 Anaphylactic.
 Febrile non-haemolytic reaction.
 Transfusion-related acute lung injury.
Non-immunological:
 Bacterial contamination.
 Endotoxins.
 Hypocalcaemia.
 Hyperkalaemia.
 Fluid overload.
 Air embolism.
 Clotting abnormalities.
Delayed adverse effects of blood transfusion

Immunological:
 Delayed haemolytic transfusion reactions.
 Graft versus host disease.
 Post-transfusion purpura.
Non-immonological:
 Infection.
 Transfusional iron overload.
What are the specific complications of massive blood transfusion?

Massive transfusion is defined as replacement of the entire circulating blood volume
within 24 hours and presents specific complications.
Massive transfusion of cold stored blood risks hypothermia, citrate toxicity,
hypocalcaemia from citrate binding and hyperkalemia from the k + that leaches out of
the red cells as they are stored. Most of these may be obviated by slower transfusion
of warmed blood.Stored blood contains little in the way of plateltes or clotting factors,
so massive transfusion with red cells alone includes a dilutional coagulopathy as the
platelet count falls. Threatment is by infusion of fresh-frozen plasma (FFP) and
platelets, if the count is low enough. Massive transfusion is a recognized contributing
factors to ARDS.
What infections can be transmitted by transfusions?

 Bacterial: Treponema pallidum (syphilis), Salmonella and Brucella.
 Viral: hepatitis A, B,C human immunodeficiency virus 1 and 2 (HIV-1 and
HIV-2 , respecrively ); parvovirus; cytomegalovirus; and Epstein-Barr virus.
 Protozoal: Plasmodium sp. (malaria); Toxoplasma; Trypanosoma cruzi
(Chagas‟ disease).
 Prion: new variant Creutzfedt-Jakob diseases (CJD).
Is there any alternative to help prevent adverse effects?

Yes, autologous blood transfusion.
This can be achieved by re-operative donation, acute normovolaemic haemodilution
(removal of blood prior to surgery with crystalloid replacement) or peri-operative red
cell salvage.
What are the possible benefits of autologous transfusion?

Autologous transfusion may reduce the risks of incompatibility, transfusion reactions
and exposure to possible transferrable infections. It may also reduce the burden on the
blood transfusion donor service.
Ho would you deal with an anaphylactic reaction when transfusing blood?

 Stop the transfusion immediately and remove the giving set.
 Maintain airway and administer 100% oxygen.
 Administer adrenaline (epinephrine) intramusculary (0.5 ml adrenaline
injection 1 in 1000), chlorpheramne (10-20 mg) slow intravenous injection
and hydrocortisone (100-300 mg) intravenously.
What factors would alert you to an incompatible blood transfusion?

In the conscious patient:
An incompatible transfusion presents as a haemolytic transfusion reaction (HTR) with
massive intravascular haemolysis of the transfused cells. This may manifest as:
 Rigors.
 Lumnar pain.
 Pyrexia. and fever.
 Hemoglobinuria.
 Hypotension.
 Renal failure.
 Activation of the clotting cascade and disseminated intravascular coagulation
may occur. It is a life-threatening event.
In the anaesthetized patient:
Recognition is often more difficult, but persistent hypotension and unexplained
oozing from the surgical site may be indicators.
If an immediate HTR is suspected, the transfusion should be stopped immediately,
and the identification details checked on both the patient and the donor unit.
Clerical error remains by far the most common cause of transfusion reaction.
The donor unit and a sample from the patient should be sent for immediate
compatibility testing. Supportive therapy should be instituted as required for the
patient.
This may well include inotropes and renal replacement therapy.Intravenous steroids
and histamines should be considered.
A delayed HTR may occur up to 3 weeks after transfusion with haemolysis occurring
in the sequestered cells in the spleen. symptoms include fever, rigors and myalgia,
accompanied by jaundice. A direct antiglobin test establishes the diagnosis.
How do we take and store blood for transfusion?

In the UK, blood donation is voluntary and unpaid. All donors undergo health
screening questions prior to donation to screen out individuals with behaviours at high
risk for HIV or hepatitis virus carriage.
 Recent malaria is a contraindication to donation, as is recent travel through a
malaria-endemic area. A finger-pick blood sample is used to ensure adequate
Hb levels .
 The donor lies recumbent with arm outstretched and blood pressure cuff
inflated on the upper arm.
 After skin cleaning with an alcohol wipe, a suitable vein in the antecubital
fossa is neebled and 450 ml of fresh blood is collected into a sterile plastic
pack containing 63 ml of citrate preservative as well as adenine , phosphate
and dextrose.
 The removed blood may be stored as whole blood or, more commonly,
processed into constituent fractions. It is usual to remove plasma to leave the
red cells with a haematocrit of ~70 percent. Other cellular components derived
include leucocyte poor red cells, washed red cells for patients who have had
previous anaphylactic transfusion reactions and platelet concentrates. The
plasma may then be further fractioned into fresh-frozen plama (200ml
obtained from 1 donor unti stored at -30OC), cryptocipitate (20 ml of
FFPsupernatant containing factor VII:C , VII:vWF and fibrinogen), clotting
factors concentrates (VIII, IX), albumin and immunoglobins.
Trauma
Metabolic response to trauma
Describe the body’s metabolic response to trauma?

The metabolic response is devided into three: the ebb, catabolic or flow, and anabolic
phases.
The ebb phase:
 It is the early acute response to injury and is seen in the first 12 to 24 hours.
 It is characterized by the mobilization of energy reseeves and changes in
cardiovascular activity.
 The changes which are seen during the ebb phase include changes in
homeostatic reflex activity (thermoregulatory and cardiovascular).
The patient:
 Is cold and clammy with poor tissue perfusion.
 Has a low cardiac output.
 Has a low core temperature.
 Is hypometabolic with lower energy expenditure.
 Has mild protein catabolism.
 Has elevated blood glucose, elevated catecholamines, elevated glucocorticoids
and glucagon levels.
 Has low insulin levels.
The flow phase:
 It signifies a period of increased metabolic rate and increased urinary nitrate
secretion.
 It is associated with weight loss and muscle wasting, reaching a maximum of
7-10 days after injury. However, this may be prolonged to many weeks if there
is multiple organ failure or sepsis.
The patient:
 Is warm and pink with normal tissue perfusion . There is evidence of
 Hypermetabolism.
 Raised core temperature.
 Increased energy expenditure.
 Increased glucose production.
 Profound protein catabolism.
 Elevated glucose catecholamines, glicocorticoids, insulin and glucagon
levels.
The anabolic phase:
 If recovery from the injuries occurs , an anabolic phase supervenes in which
weight gain occurs , protein and fat stores are replenished and metabolic rate
returns to normal.
 This phase may last for several monthsdepending on the extent of the initial
injuries.
Do wounds heal despite this protein breakdown?

Despite the large turnover of protein as described above, only in the worst cases of
persistent malnutrition do surgical traumatic wounds fail to heal, indicating that
whatever else goes on, the wound has primacy in terms of protein manufacture.
Where does the body derive its energy from?

Hepatic stores of glycogen are readily used up and from about 24 hours after injury
the energy requirements are met by triglyceride mobilization from adipose tissue.
There is an increase infree fatty acid oxidation producing ketone bodies, 3-
hydroxyburate and acetoacetate and adaptive responses occur that allow the brain and
other tissues to utilize them as energy substrates.
What is the endocrine response to trauma?

The endocrine response to trauma is widespread.
6 stress hormones in the response to surgery (A,C,G):
 A: ADH, Aldosterone.  C: Cortisol, Catecholamines.  G: Growth hormone, Glucagon.
The responses include:
1. Catecholamine release from the adrenal medulla, which produces inotropic
and chronotropic effects on the heart, peripheral vasoconstriction, increased
gluconeogenesis and lipolysis.
2. Cortisol levels are increased leading to increased proteolysis, gluconeogenesis,
lipolysis and acute phase proteins release.
3. Aldosterone release is also increased and causes increased renal sodium and
water retension.
4. Increased anti-diuretic hormone release from the posterior pituitary causing
increased water retension.
5. Other endocrine responses include:
 Increased glucagon secretion leading to increased glycogenilysis and
gluconeogenesis.
 A fall in insulin secretion.
 Growth hormone release is increased, this elevates hepatic glucose
output and decreases glucose uptake by tissues.
What happens to glucose metabolism in trauma?

Immediately after injury, plasma glucose levels rise as a result of increased
sympathetic outflow and circulating catecholamines.
The body‟s glycogen store is soon depleted. However, glucose levels are maintained
by the breakdown of protein and fat.
Recycling of lactate produced by anaerobic repiration, in the liver also produces
glucose . Other factors which serve to maintain an elevated blood glucose include
glucagon and corticosteroid secretion.
What are the effects of trauma on protein metabolism?

Protein metabolism is disturbed in the flow phase of injury.
The degree of disturbance is proportional to the magnitude of injury and the
nutritional status of the patient, so the more severe the injury, the greater the rate of
synthesis and breakdown of protein.
Malnutrition itself tends to depress synthesis. Following major trauma, approximately
20% of the body‟s protein store is lost in the first three weeks (mostly during the first
10 days). ⅔ of this loss is from skeletal muscle.
Which amino acids are particulary lost from skeletal muscle breakdown?
Two amino acids, alanine and glutamine account for approximately 60% of the
nitrogen released from the breakdown of skeletal muscle protein.
What is the role of these two amino acids?

 Glutamine is a primary energy source for immune cells and enrerocytes.
 Alanine is a major source for gluconeogenesis.
Can you describe the effects of trauma on lipid metabolism?

Following trauma, there is increased production of free fatty acids and glycerol from
triglycerides. This is mainly stimulated by beta-adrenergic mechanisms, although
glucagon, cortisol and growth hormone all make some contribution.
Free fatty acids act as a source of energy as they may be oxidized in both cardiac and
skeletal muscle. In addition, glycerol contributes to gluconeogenesis.
Can you describe the effects of surgery trauma on repiration?

1. Pain causes splinting and hypoxia leading to inadequate ventillation, basal
atelectasis and basal lung collapse.
2. Basal collapse increases risk of infection.
3. Hypoxia drives catabolic state and anaerobic repiration leading to a metabolic
acidosis.
Describe the metabolic changes that occur in the starving patient?

The changes that occur are aimed at maintaining lean muscle mass.
Glycogen stores last only for about 24 hours, after which catabolic muscle breakdown
benign. Metabolic rate falls, however, and protein catabolism decreases about 5-fold
from the 1-2 week point onwards.
There is a gradual increase in fat utilization as an energy source and adaptive
ketogenesis occurs by the 3-week point the brain can utilize ketone bodies as an
energy souece.
Lipolysis in the early weeks is inhibited by insulin but the insulin levels fall as
starvation continues. Stored triglyceride is hydrolysed for gluconeogenesis, whereas
fatty acids are used as fuel or converted to ketones for fuel in the liver.
There is a fall in the metabolic rate and in total body energy expenditure. The central
nervous system utilizes mostly ketones and gluconeogesis in the liver falls as protein
metabolism slows. Most of the energy comes adipose tissue, with a gradual protein
loss until all available fat is used.
What kills the starving patient?

Gradual but progressive protein wasting results in muscle weakness. This weakness in
respiratory muscles leads to atelectasis, pneumonia and ultimately death in the
majority of people in this situation.
Minimization of the systemic response to surgery.

Preoperative factors:
 Minimize fear & stress: to reduce sympathetic activity.
 Good high protein load.
 Correction & control of preoperative infection.
Operative factors:
 Good tissue handling.
 Minimmaly invasive surgery/minimal trauma.
 Shorten duration of abaesthesia.
Posoperative factors:
 Correction of hypovolemia.
 Correction of metabolic alkalosis/acidosis.
 Control of postoperative infection.
 Adequate and effective pain control.
 Correction of hypoxia.
 Increased arginine and glutamine intake, that improve nitrogen balance,
encourage weight gain, wound healing & immune function.
 Trace elements such as zinc to improve wound healing & immune function.
Why is urine output low in thr first 24 hours after syrgery? Why might a
metabolic alkalosis develop immediately after trauma?
After trauma, the activation of renin-angiotensin-aldosterone axis and the increase in
ADH secretion leads to a retention of sodium and water at the expense of pottasium.
Although the total body sodium may be elevated, a dilutional hyponatraemia is not
uncommon with an excess of serum ADH, leading to greater water than sodium
retention.
Furthermore, in catabolic cells with a degree of energy failure, sodium pump are
impaired, so sodium tends to drift into cells and thereby further decrease the plasma
sodium concentration. This sodium & water retention leads to a low urine output
(despite adequate filling) in the first 24 hours after surgery. Although the water
retention lasts for only 24 hours, the sodium retention may persist for much longer.
In many cases, postoperatively the patient may have an ileus, prompting fluid
extravasation into the gut lumen and intravascular depletion, leading to dehydration
and further compounding the low urine output state.
The most common acid-base imbalance is a metabolic alkalosis because aldosterone
promotes sodium retention at the expense of potassium, s potassium is excreted, so
are H+ ions in a co-transporter mechanism, leading to an alkalosis.
In more sever trauma, a metaolic acidosis can result as a lactic acidosis caused by
poor tissue perfusion and anaerobic metabolism.
Cardiac tamponade
A younth is brought in to A&E having been stabbed in the 4th left intercostals
space at the sterna edge. He is tachycardiac and hypotensive. What is the most
likely diagnosis ? What is the differential diagnosis?
A pericardial tamponade is the most likely diagnosis. The other leading differential
would be a tension pneumothorax.
In tamponade:
The pericardial blood decreases transmission of the heart sounds and the heart sounds
they sound muffled on auscultation.
 There is a raised juglur venous pressure as the raised intrathoracic pressure
decreases venous return, although this does not occur as dramatically as in
tension pneumothorax.
 Hyper-resonance of the hemithorax with decreased breath sounds would point
towards pneumothorax, as would tracheal deviation away from affected side.
 A further possibility is hypovolaemiafrom blood loss into a haemothorax,
which would produce the same picture of shock but the breath sounds are
louder due to conduction through the fluid. There tends to be an associated
pneumothorax.
What is the emergy management of pericardial tamponade?

In temponade there is a risk of an electromechanical dissociation (EMD) arrest so he
needs the pericardial space decompressing. This is most easily achieved by
pericardiocentesis.
 The skin is prepared, if time allows, and a syringe and long 12- or 14-gauge
needle is inserted through the skin under the left xiphicostal angle.
 The needle is at 45oC to the skin, aiming for the tip of the left shoulder.
 Suction is maintained on the syringe as the needle is achieved until the
pericardium is entered.
 Care must be taken not on to advance too far and aspirate from the ventricle.
Traversing the ventricular myocardium will be signaled by ventricular
ectopics and arrhythmias on the cardiac monitor. One attempt should suffice,
since there is no benefit in puncturing the ventricle many times.
Describe how you perform an anterolateral thoractomy

 The patient is anaestherized using a double lumen endotracheal tube.
 The patient is in the full lateral position with the appropriate side uppermost
and the body supported appropriately. The upper arm is normally supported in
an arm gutter.
 The skin is prepared and draped and the landmarks identified.
 The skin incision runs from a point midway between the lateral edge of the
vertebral body and the medial edge of scapula, and runs in the line of the ribs
to one fingerbreath below the tip of the scapula.
 The skin is incised and the underlying fat and fascia divided with diathermy.
 Latissimus dorsi is divided anteriorly and the anterior part of erector spinae is
divided posteriorly, if more room is required, serratus anterior shoud be left
intact.
 Slide a hand up under the scapula to identify the first rib and thence count
down to the sixth rib. The tissues overlying the upper portion of the 6 th rib are
divided using diathermy, leaving the bone intact.
 The periosteum is raised and astripper used over the rib edge posteriorly and
pulled anteriorly to detach the intercostals, asking your anaesthist to deflate
the lung as you go.
 Arip spreader is inserted and gently distracted. If more room is required asmall
portion of the rib may be excised posteriorly, the thoracotomy and deflated
lung now allow accessto the pericardia. Care should be taken not to damage
the the phrenic nerve as it runs down the pericardium.
 Penetrating cardiac injuries from a stab woud can usually be closed directly
using “Teflon” patches to buttres the sutures.
 Closure after haemostasis and chest drain placement (x2) is by 0 PDS around
the two previously distracted ribs, at which point the lung can be inflatd.
 The peristeum can then be closed with the same stitch, and fascia are repaired
in 2 layers with PDS.
 Subcutaneous and then subcuticular stitches are used to close the fat and skin.
The chest drains are connected to an underwater seal.
Care of the multiply injured
A patient is brought to the Emergency Department after a road traffic accident

with burns to his chest and arms, an obviously fractured femur and signs of a
base of skull fracture. Describe the first stages of your management.
Follow the ATLS guidelines in initiating a primary survey. Do not remove on to the
next step before all uncovered pathologies have been stabilized. Return to reassess if
the condition changes during the survey.
Primary survey:
 Airway with cervical spine control: note if the patient is talking and, if not,
whether they are spontaneously maintaining an airway.
 Breathing: assess bilateral air entry, repiratory rate, character and depth, and
monitor oxygenation with a saturation probe.
 Circulation: with haemorrhage control, assess carotid pulse rate and take a
blood pressure reading while gaining intravenous access (take bloods,
including a glucose measurement, and start an intravenous infusion of
Hartmann‟s solution).
 Disability: assess the patient‟s neurological function and calculate their
Glasgow Coma Scale (GCS) score.
 Exposure: with environmental control.
 Order a trauma series of x-rays (chest x-ray, pelvis and lateral cervical spine
views) before any further intervention.
Move on to the secondary survey,with examination from skull to toes for injuries.
Can you describe the specific management required for the femoral fracture,
chest burns and head injury?
Each of the injuries will have been appropriately stabilised at the time of the primary
survey.
 The head injury should be assess as mentioned and if there are signs of base of
skull fracture (decreased GCS, rhinorrhoea, otorrhoea, haemotympanum or
periobital haematomas) or indeed just a decrease in GCS with this history of
head trauma, then a CT scan should obtained once the patient has been
stabilised.
 The burns should be treated according to their extend and depth and the fluid
balance must be attended to. Fluid replacement can be calculated using a
number of formulae, such as the Parkland formula or the Muir and Barclay
formula. Consider an escharotomy if repiratory function is compromised.
Definitive care should be discussed with the regional burns unit.
 The femoral shaft fracture should be assessed, reduced and stabilized with in-
line fraction to reduce the possibility of the neurovascular compromise
distally, pain, and fat embolus.
 A patient with an open fracture will require intravenous antibiotics and a
Betadine ®-soaked dressing. X-ray should be taken to plan the orthopaedic
management.
What is the trimodal distribution of death in trauma?

There are three peaks in the incidence of death due to trauma:
 Immediate deaths: due to massive head and thoracic injuries.
 Secondary peak: after minutes to hours, due to subdural haematomas, hypoxia
and hypovolaemia.
 A late peak: after days to weeks, due to sepsis and multiple-organ failure.
Fracture of femur
Describe the blood supply to the femoral head?

There are three sources of supply:
1. Nutrient artery through the diaphysis (from the profunda femoris).
2. Artery to the head through the ligamentum tetres-important in children but of
little significance in adults.
3. Retinacular vessels within the joint capsule from the medial and lateral
circumflex arteries (branches of the profunda femoris), these vessels are
distrupted in an intracapsular fracture.
How are fractures of the femoral neck classified?

Fractures of the femoral neck can be categorized by the Garden classification.
This is based on the amount of fracture displacemet evident on the anteroposterior X-
ray of the hip alone. The grades are as follows:
 I = Incomplete or impact fracture
 II = Complet fracture with no displacement
 III = Complete fracture with partial displacement
 IV = Complete fracxure with full displacement
The grades correlate with the prognosis and the rates of avascular necrosis of non-
union.
Garden grades III and IV have a low likelihood of healing and a high risk of
steonecrosis
Fracures can also be classified in relation to the capsule of the hip iont-intracapsular
or extracapsular.
What are the treatment options of intracapsular fractures?

The aim of surgery is to preserve the femoral head if possible, as this causes lower
postoperartive morbidity.
An intracapsular fracture is likely to cause disruption to the blood supply, particularly
if displaced. There are two treatment options:
1. Femoral head replacement is used in most patients with displaced fractures or
pathological fracures.
This is performed with a haemiarthroplasty (cemented or uncemented) or total
hip replacement.
2. Internal fixation with cancellous screwes is used in undiplaced fractures and
displaced fractures in patients under 70 years of age.
Young patints benefit from preservation of femoral head, and if the diagnosis
is made less than 6 hours after injury an emergency internal fixation can be
attempted.
Which operation would you perform for an extracapsular neck of femur?

An internal fixation with insertion of a dynamic hip screw.
Briefly, describe how you would perform this operation.

Obtain informed consent from the patient if possible, mark the side of the fracture and
ensure that preoperatively anterior-posterior and lateral radiographs of the fractured
hip are displayed.
The procedure is performed with the patient supine on a fracture table. The most
important part of the operation is obtaining a satisfactory reduction of the fracture,
which can be confirmed with an image intensifier
 The skin is prepared with an appropriate antiseptic and the patient draped.
 A lateral incision is made 2 cm distal to the tip of the greater trochanter,
extending 15 cm distally and the fascia lata is incised in line with the skin
incision.
 The vastus lateralis is detached from the femur, which is tripped distally with a
periosteal elavetor, and adequate exposure is obtained.
 A guide-wire is then placed on the skin over the neck to ascertain aligment and
using an 135 guide on the drill, a guide-wire is drilled parallel to this into the
neck in the lateral plane, checking the placement with the image intensifier.
The tip of the wire should sit in the subchondral bone of the femoral head.
 The length of insertion should be measured and a cannulated reamerset to this
measurement (subtracting 5mm). then ream and insert a screw with an
introducer and confirm its position using the image intensifier.
 A four-hole plate is then applied to the femoral shaft, and four screws are
inserted. The image intensifier again confirms the plate's position.
 The fascia lata is closed with absorbable suture and clips are applied to the
skin.
Postoperatively, request a formal check X-ray and encourages full weight-bearing
mobilization.
What are the complications of femoral neck fractures?

1. Avascular necrosis: caused by a loss of blood supply to the femoral head.
Eventually the head will collapse, causing pain and loss of function.
2. Non-union.
3. Osteoarthritis: develops prematurely in the affected hip.
4. Loosening and peri-prosthetic fracures in replacement hips.
5. General complications:
 Chest infection.  DVT/pulmonary embolism.
 Urinary sepsis.  Pressure sores.
A fractures neck of femur can be a life threatening event in an elderly patient, and the
in-hospital moratlity rate is 10-15%, often due to complications and underlying
disease. Subsequent mortality at 1 year is 33%.
Compartment syndrome
You are called to the ward to sent a 16-year-old with a closed transverse tibial
fracture that was sustained 12 hours ago. He is complaining a painful leg. What
might be the cause?
In a patient with a traumatic injury to a limb and severe pain, one would wish to rule
out an acute compartment sundrome.
Other differential diagnosis to be excluded are as follows:
 Distal ischaemia due to vascular damage.
 Inadequate analgesia for the injury.
 Deep vein thrombosis.
What is compartment syndrome?

It is an increase in pressure in a closed fascial compartment, which causes a
comprised circulation and therefore a reduction in tissue perfusion.
It occurs when trauma causes muscular swelling within a closed (normally
osteofascial) compartment and increased interstitial pressure. As the pressure rises
above capillary perfusion pressure, there is a reductin in blood supply to muscular and
neaural tissue and subsequent ischaemic damage.
This causes further swelling and vascular compromise, leading eventually to muscular
necrosis.
What are the causes of the compartment syndrome?

Increase in volume of compartment contents:
1. Large haematoma.
2. Haemorrhage & oedema after a fracture and soft tissue injury.
3. Swelling of muscle tissue post-ischemic insult.
4. Limb compression.
Decrease in volume of compatment:
1. Overly constricting dreesing or cast.
2. Full-thickness burns.
3. Closure of facial defects at burns.
For what signs compartment syndrome would you examine the patient?
1. Pain worsened by passive stretching of the muscle of the involved compartment.
2. Pain out of proportion to the injury.
3. Paraesthesia.
4. Weakness.
5. Loss of pulses in a late sign and in the presence of trauma may indicate vascular
injury rather than compartment syndrome.
What testes could you perform to confirm the diagnosis?

In the presence of classic symptoms and history, no further investigations should
delay treatment.
If the diagnosis is unclear the compartment pressure can be measured using:
 An intra-compartmental cannula (attached to a pressure transducer). or
 The wick catheter technique.
The normal pressure of a lower leg compartment is 3-4 mmHg.
A pressure rise within 30mmHg of the diastolic blood pressure would require urgent
fasciotomy.
How would you perform a fasciotomy?

One would use the double incision technique, as it is safer and more effective than a
single incision. The aim of the operation is to decompress all four osteofascial
compartments of the lower leg.
 The patient should be anaesthetized and the affected leg prepared and draped
with the foot excluded but visible.
1. Make an antero-lateral incision between the fibula and the subcutaneous border
of the tibia. In an emergency procedure, make a 15-cm incision to allow adequate
visualization.
 From this skin incision, dissect through the subcutaneous tissue anteriorly to
release the anterior compartment using scissors to release it fully proximally
and distally in line with the tibialis anterior.
 Then fully release the lateral compartment that lies posterior to the skin
incision, first identifying and avoiding the superficial peroneal nerve, which
lies deep to the intermuscular septum.
2. The second skin incision is postero-medial, approximately 2 cm posterior to the
subcutaneous border of the tibia. It is important to identify the long saphenous
vein and nerve lying in the subcutaneous tissue and to retract them anteriorly.
 From this incision the superficial posterior compartment could be released,
and through this, the deep compartment.
 Perform any haemostasis that is required and dresss the wound with occlusive
antiseptic dressing. Then place the leg in backslab with the ankle held at 90.
How would you manage the wounds postoperatively?

 Daily dressings of the fasciotomy wounds.
 Prophylactic systemic antibiotics because of the open fracture and the
possibility of necrotic tissue.
 Re-examine at 24-48 hours to debride any necrotic tissue and cover the
wounds if possible. This can be done by split skin grafting or serial
suturing.
What are the complications of a missed compartment syndrome?

 Muscular necrosis leading to myoglobinuria subsequent renal failure.
 Infection in the limb leading to systemic sepsis or amputation.
 Foot drop due to peroneal injury.
 Volkmann's ischemic contracture from muscle death and fibrosis.
Where can compartment syndrome occur?

It can occur in any enclosed compartment of the body, but most commonly occur in
the lower leg and forearm. Around 45% of cases arise following tibial fractures.
Abdominal compartment syndrome
What do you understand by the term abdominal compaertment syndrome?

It is the adverse physiological effects of increased intraabdominal pressure (IAP).
Prolonged unrelieved increased IAP > 20 mmHg can produce pulmonary
compromise, renal impairment, cardiac failure, shock and death.
It can be categorized into ptrimary, secondary and crhonic.

It occur when the IAP is too high similar to compartment syndrome in an extremity.
The 3 types of ACS have different and sometimes overlapping causes.
Primary (i.e. acute with abdominal pathology):

 Penetrating trauma.
 GIT haemorrhage.
 Pancreatitis.
 External compressing forces, such as debris from a motor vehicle collision or
after explosion of a large structure.
 Pelvic fracture.
 Rupture of abdominal aortic aneurysm.
 Perforated peptic ulcer.
 Closure of abdominal fascia in gastroschitis and exomphalosneonatally.
Secondary:
Secondary ACS may occur in patients without an intraabdominal innjury, when fluid
accumulates in volumes sufficient to cause a rise in IAP.
 Sepsis.
 Large areas of full-thickness burns.
 Penetrating or blunt trauma without identifiable injury.
 Postoprative.
 Packing and primary fascial closure after emergency laparotomy.
 Large-volume resuscitation.
Chronic:
 Peritoneal dialysis.
 Morbid obesity.
 Cirrhosis.
 Meig's syndrome (ovarian fibroma associated with ascitis/pleural effusion).
Pathophysiology of abdominal compartment syndrome:

Direct effects of compression on intra-abdominal and other viscera:
o Gut: compression of vasculature and portal system leads to thrombosis and
mucosal oedema, ultimately resulting in translocation of bacteria across
mucosal wall and systemic sepsis; this causes more fluid secretion in the
inttra-abdominal compartment and a further rise in pressure.
o Kidneys: renal perfusion is impaired and urine output drops.
o Liver: portal vein collapses along with the IVC, causing congestion.
o Respiratory: increased IAP makes it harder to breath and ventillation becomes
more difficult.
o Cardiac: rise in IAP causes CVP & PAOP to rise despite a hypovolaemic state,
leading to possibility to inadequate fluid resuscitation.
History:
 Pancreatitis and/or alcohol abuse.
 Emergency laparotomy.
 NSAID use.
 Melaena.syncope.
Signs & symptoms:

1. Abdominal pain: not always useful (particulary in sedated and ventilated
obtunded patients in the ITU).
2. Decreased urine output: a frequent & early sign of abdomial compartment
syndrome.
3. Melaena.
4. Progressively difficult ventillation.
5. Increased abdominal girth (not always easy to use).
Investigations:
1. Measurment of IAP:
It is by the use of a foley catheter introduced into the bladder; 50 ml saline is
injected into it and then it is connected to a manometer to measure intracystic
pressure which is thought to be a reflection of IAP.
2. Abdominal CT:
It can be useful to look for radiological signs of raised pressure such as
collapsed IVC, bilateral inguinal hernias and enhanced and thickened gut wall.
Management:
The best management of abdominal compartment syndrome is pervention & early
detection of any intra-abdominal hypertension.
 Consider avoiding primary closure in emergency laparotomies, which are at
high risk from abdominal compartment syndrome (extensive dead bowel, liver
laceration and packing, necrosectomy for pancreatitis).
 Percutaneous drainage of fluid collections.
 Laparoscopic decompression may be used in abdominal blunt trauma.
 Laparostomy remains the mainstay of treatment in the UK.
Complication:
These can be split into complications from the compartment syndrome and
complicatins from immediate decompression.
Direct complications from compartment syndrome:

 Respiratory failure (increased airway pressure and decreasing tidal volumes in
ventilated patients).
 Renal failure.
 Bowel ischaemia and infarction.
 Increased ICP.
 Decreased cardiac output and refractory shock.
Complication from immediate fall in blood pressure:

Massive and precipitous fall in blood pressure:
 Caused partly by reperfusion syndrome with a fall in systemic vascular
resistance and partly by inadequate fluid resuscitation as a result of a falsely
elevated CVP.
 Extensive fluid resuscitation preceeding decompression reduces the incidence
of refractory hypotension.
Spinal injuries
What is a Jefferson fracture?

This is a burst fracture of C-1.
It results in disruption of the anterior and posterior rings of C-1 and displacement of
the lateral masses away from the spinal cord.
Because of this, patients are normally neurologically intact.
It is a result of axial loading on the spine, normally when object lands on the head or
when the patient falls in such a way that they land on the top of their head. It is best
on the open-mouth X-ray view.
How would you classify odontoid fractures?

 Type I: avulsion fracture involving the tip of the odontoid peg. It is stable and
is treated with a cervical collar.
 Type II: a fracture through the base of the dens that may require fixation if
displaced
 Type III: a fracture through the base extending into the body of C-2. it will
heal in a collar alone.
Where else do injuries of the spinal column frequently occur?

Fractures most frequently occur at the junction between mobile and relatively fixed
parts of the spinal column.
 Hangman's fracture:
It involves the posterior elements of C-2, and represents 5-10 % of all cervical
spine injuries.
It results from hyperextension of the neck.
 C-5/C-6 subluxation with facet dislocation: is a shear forces injury.
 Chance fracture (L-1):
It is a compression fracture resulting from hyper flexion.
It is normally seen in restained drives, and is associated with abdominal
injuries.
 L-1 compression fracture: from a fall from a height on both feet or the sacrum.
Axial force is transmitted up to the junction between the mobile lumbar spine
and fixed thoracic spine.
What injures to the spinal cord can occur as a result of these bony injuries?
Spinal cord injuries may be completed or incomplete.
A. Complete spinal cord injury
There is flaccid paralysis with loss of deep tendon and loss of sensation below
the level of injury.
The presence of the bulbocarvenosus reflex (pulling on the urinary catheter
results in anal contractions) is a poor prognostic sign, as it is usually absent in
higher cortical control.
B. Incomplete spinal cord injury
The presence of some motor or sensory function below the level of injury.
It may be indicated by the presence of "sacral sparing" alone. Specific
syndromes include the following:
o Brown-sequard syndrome:
Loss of power, proprioception and light touch on the ipsilateral side.
Loss of temperature and pain on the contralateral side due to the
decussation of fibres.
o Anterior cord syndrome:
Loss of motor function, pain and temperature on the ipsilateral side,
with a sparing of the dorsal columns (vibration and position sense).
o Central cord syndrome:
Decreased motor function found in the arms compared with that in the
legs.
o Cauda equina syndrome:
Saddle anaesthesia, loss of bladder and bowel control and possible foot
drop, resulting from lumbar and sacral nerve root injury.
What systemic findings may raise the suspicion of a spinal cord injury in an
unconscious patient?
 Hypotension due to vasodilatation.
 Bradycardia due to unopposed vagal stimulation.
 Paradoxical breathing.
 Hypothermia.
 Priapism.
 urinary retention with overflow incontinence.
 Lax anal sphincter tone.
How would you examine an immobilized patient in order to exclude a cervical

spine injury?
o Treat the patient using the ATLS principles, ensuring that airway, breathing
and circulation are adequate before further examination.
o If the patient is a wake, examine them for head injury, neck pain or stiffness,
focal neurological deficit, and any parathesia or altered sensation in their
limbs.
o If any symptoms or signs are present, the patient should have AP and lateral
cervical spine and open mouth X-rays, the collar can be removed.
o The patient should then be examined for further neck pain, and asked to move
their head from side to side and to flex and extend it. If these movements
cause neither significant pain nor any alteration in sensation, the cervical spine
can be cleared.
When is a CT scan of the cervical spine indicated?

Current NICE guidelines suggest that a CT scan of the cervical spine shoud be
performed when it is no possible to obtain adequate X-rays.
How would you manage a patient with a spinal cord injury?

1. During the primary survey, ensure that the patient has a adequate inline
cervical spine immobilization, and continue to ensure that all life-threatening
injuries are managed first.
2. The patient may be in neurogenic shock with peripheral vasodilatation:
 Obtain adequate intravenous access, using A CVP line for monitoring
if necessary.
 A urinary catheter should be inserted to monitor output, as loss of
cardiac sympathetic tone prevents heart rate from reflecting adequate
resuscitation.
 A nasogastric tube should be inserted to prevent aspiration.
3. If presentation is within 8 hours of treatment:
 Intravenous steroids can be administered (methylprednisolone 30
mg/kg immediately, then 5.4 mg/kg/hour over 23 hours).
 Gastric protection (a proton-pump inhibitor) can also be given to
prevent stress ulceration.
4. The patient should be moved from the backboard as soon as possible, and in
the mean time they should be turned regularly to prevent pressure sores.
5. Obtain X-rays and a CT scan of the spine, and discuss the patient with a
neurosurgeon or spinal surgeon at an early stage treatment in order to arrange
transfer to specialist unit.
Emergency
Burns
What are the cuases of burn injury?

Burns are defined as coagulative necrosis of the skin resulting from thermal, electrical
or chemical injury. Radiation can also cause burns.
How would you classify them?

They are classified according to the depth of injury as follow:
 Superficial (1st degree):
 Involve only epidermis.
 Local pain and erythema with no blistering.
 Heal spontaneously within 2-5 days without scarring (heals from basal cells).
 Not included when calculating percentage of total body surface area (TBSA).
 Partial thickness (2nd degree):
 Involve epidermis and dermis.
 Superficial partial-thickens burns are red,painful and blistered.
 Deep partial-thickness (deep dermal) burns are pale, mottled and very painful.
 Its healing depends on re-epithelialisation from hair follicles, sweat and
sebaceous glands.
 Infection may result in partial-thickness burns devolping into full-thickness
ones.
 Full thickness:
 Involve epidermis, dermis and subcutaneous tissue.
 White and waxy or red/brown and leathery dry and painless
 May involve underlying muscle and bone.
How wold you classify burns in terms of mechanism?

 Thermal.
 Chemical (alkali worse than acid).
 Electrical.
 Radiation.
How can you assess the area of burn?

1. Wallac's rule of 9s:
Rule of nines" that is, dividing the body into separate areas each representing
9% of TBSA:
 The head and upper limbs are 9% each.
 The anterior and posterior torso and each lower limb are 18%.
 The perineum is 1% of TBSA.
2. Patient's hand: a quick & easy method of calculating relatively small burns.
The area of closed palm is approximately 1% of the total body surface area.
3. Lund & Browder charts: these charts give the most accurate estimations of
burn area. They also have the advantages of being able to correct for different
age groups and they provide documentation of the burn for the patient's notes.
What are the physiolical consequences of major burns?

 Hypovolaemic shock: causing reduced cardiac output and increased peripheral
vascular resistance.
 Raised metabolic rate.
 Increased haematocrit: plasma lost through the burnt tissue effectively
concentrates the blood constituents.
 Cortisol increase: stress response causing catabolism and gluconeogenesis.
What are the pathophysiological features of a burn?

 Increased capillary permeability: this leads to fluid loss, which is proportional
to the size and depth of the burn (with large burns, increased plama loss can
lead to hypovolaemic shock).
 Heat loss: loss of normal skin leads to increased evaporation.
 Altered cell metabolism.
What metabolic changes occur with burns?

 Increased meatobolic rate.
 Increase in anaerobic metabolism.
 Increased catabolic catabolism of proteins.
 Lipolysis.
 Gluconeogenesis: increase in plasma cortisol and catecholamines.
 Impaired insulin release.
A 30-year old man is brought into accident and emergency following a haouse
fire. He appears to have extensive burns to his chest, upper arms and face. How
would you determine the extent of this burn injury?
Each of the follwing would need to be established:
 Total body surface area (TBSA) involved in the burns.
 Depth of the burn-including all patial and deep thickness in TBSA involved.
 Presence of an inhaltional injury.
How would you calculate how much fluid needs to be given?

Any burn > 15% in adults or > 10% in children requires I.V. fluid resuscitation.
Several formulae are available.
A. Parkland's formula:
Volume of crytalloid required (ml) = 4  % burn  patient's weight (kg)
This volume is needed witin the first 24 hours:
 Half is given in the first 8 hours.
 Half in the subsequent 16 hours.
B. Muir and Barclay formula.
This calculates the amount of fluid to be given over the first 36 hours.
V = Body weight (kg) x Body surface area(%)
2
V is the amount to be given:
 4 hourly for the first 12 hours.
 6 hourly for the next 12 hours.
 Then 12 hourly.
This is in addition to the patient‟s normal fluid requirements.
What is the fluid replacement regimen for a 70kg man with 30% burns?
 Crystalliods containing salt and water are ideal (e.g. normal saline containing
0.5 mmol sodium /kg/% burn).
 The total additional fluid volume is:
Between 2 and 5 ml/kg/body surface area of burn (%) given over a 36-48 hour.
Salt containing fluid (e.g. Dioralyte) (50 ml/kg per 24hrs) is given orally if
possible .
For above patient give:
 3500 ml of water orally per 24hrs.
 IV 0.95 Normal Saline volume of 70 kg x 30% x 3 ml = 6300 ml over 36 hrs
(Give 3150 ml over the first 12 hrs).
Can you describe the important principles of burns management ?

It is important to know the history, time of injury and the cause ob burn.
 ATLS (consider inhalational injury and concomitant trauma).
 ABC should be evaluated and established, particularly if an inhalational
injury may be present.
 Ensure that there is large-bore venous access and begin fliud resuscitation.
 Any residual burning should be stopped by ensuring that all burnt fabric is
removed. (in the case of chemical burns, also begin copious irrigation to
prevent further injury).
 Then assess the wounds, estimate the TBSA involved and tailor fluid
resuscitation to the extent of the injury.
 Fluid resuscitation would be with isotonic crystalloid such as Ringer's
lactate or normal saline.
 Assess the size, depth and location of the burn („ rule of nines‟ or Lund and
Bowder chart).
 Cold water irrigation to control pain and prevent further tissue injury.
 Decied between open- and closed-dressing management.
 Calculate fluid requirements using a fixed protocol
 Beware of circumferential burns and circulatory compromise needing
escharotomy.
 Note that > 10% total surface area burns in adults will require patient transfer
toa regional burns unit.
 Early nutritional supplementation (enteral> parenteral).
 Escharoromies /fasciotomies: relief of the constricting effect of full thickness
burns where tissue ischaemai and necrosis may occur due to tissue damage
and swelling negating an already diminished peripheral circulation 9 due to
central hypovolaemic failure).
 The eyes of exposed joints amy require early surgery to prevent further
damage.
National burns care review guidleine recommend that the followinf paatients be
transferred to a burns center or burn unit:
 Adults with burns > 15% or 10% with dermal loss.
 Children with burns > 5% (note that not 10% as required for fluid
resuscitation).
 Burns at extreme of age.
 Airway burns or patients at risk of airway obstruction.
 Facial burns.
 Perineal burns.
 Hand or feet burns.
 Burns requireing escharotomy.
 Other complex burns:
1. Burns in patients with significant associated injuries.
2. Burns in patients with pre-existing medical conditions, chemical, radiatin,
high pressure or high tension electrical burns of felxures, especially the
neck.
 When non-accidental burn injuries are suspected.
 Except when specialist management of the burn is redundant )moving a
aptient who will die from urn away form friends and family causes
unnecessary additional distress).
How do you monitor the fliud replacement?

The fliud replacement is monitored through clinical and haematological assessment.
 Peripheral circulation.
 Skin colour.
 Pulse rate.
 Blood pressure.
 Hourly urine output measurement.
 Regular haematocrit levels.
What are the complications of burns?

Local:
 Infection.
 Inhalational injury.
 Ischaemia.
Systemic:
 Hypovolaemic shock.
 Septicaemia.
 Respiratory insufficiency.
 Renal failure (due to hupovolemia, haemoglobinurea and high K load).
 Ileus.
 Haemoglobinuria.
 Curling‟s ulcer.
 Disseminated intravascular coagulation (DIC).
 Scarring and contractures.
What are the indications of an inhalational injury?

1. History of burn injury occurring in an enclosed space.
2. Presence of fascial burns.
3. Evidence of soot in the nose or mouth.
4. Singed fascial hair.
5. Hoarseness or wheezing.
6. Difficulty in breathing or low oxygen saturation.
What are the indications for transfer to burn unit?

1. Adult parietal or full-thickness burns greater than 15% TBSA.
2. All paediatric burns with more than 10% partial thickness, or that may require
surgery.
3. All partial-and full thickness burns at the extremities of age.
4. Burns involving the hands, feet or perineum.
5. Circumferential extremity burns.
6. Any electrical burns.
Which burns will require graffing?

Deep or full thickness burns will not regenerate and therefore are treated by excision
and skin graffing.
Deep dermal burns may be grafted on the 3rd or 4th post burn day.
A less aggressive approach is to assess after 2 weeks and shave and skin graft
unhealed areas.
 Superficial burns re-epitheliase rapidly from the remaining basal cells usually
with minimal scarring
 Superficial dermal burns also heal by regeneration fron undamaged
keratonocytes within 10-14 days with little or no scarring. They do not require
skin grafting.
You are called to A&E to manage a 64-year- old lady who was trapped in her
room in a housed fire and has suffered obvious burns including the face .
Describe the first steps in your management.
In a severely injured person such as this, a methodical approach is used and given the
history of entrapment and facial burns the first priority is ensuring a secure airway.
There should be a low threshold for intubating the patient electively as there is likely
to be an inhalational component to the burn and laryngeal oedema can make
emergency intubation later on very hazardous.
Features that indicate likely inhalational injury are the history of fire in an enclosed
space, cough, sooty sputum, fascial burns, signed nasal hairs and chest signs.
Ventilation is maintained and secure intravenous access is obtained, which is needed
for both fliud resuscitation and administration of opiate analgesia.
An estimate of the patient‟s weight is needed and an estimation of the depth and
severity of burn injury.
The 64-years-old lady has 45 percent full-thickness burns, including her entire
anterior chest wall and encircling her right arm. She is tachycardiac,
tachypnoeic and hypotensive. What will you do now?
In view of the inhalational injury and the widespresd burns, blood is withdrawn for
FBC including PCV, urea and electrolytes, clotting group and save calcium, glucose
and liver function tests.
An arterial catheter is palced for invasive blood pressure monitoring and repeated
arterial blood gas estimation.
Similarly, at some stage in the initial resosciation phase, a central venous catherter is
inserted to allow monitoring of progressive fluid resuscitation.The patient is discussed
at an early stage with the regional burns unit and transfer arranged, when appropriate,
which is as soon as the patient is stable enough for transport.
There are no immediately available burns ITU beds in the region and your
anaesthetist is becoming concerned about the increasing difficulty in ventilating
her. What else would you consider?
Probable causes of the decreasing chest comphance are the effect of the inhalational
injury itself causing pulmonary oedema and the constricting effect of the chest wall
burns.
This lady needs urgent escharotomy and, if urgent transfere to a burns unit is not
feasible, then it should be performed in location – also paying attension to her arm,
which will also need releasing escharotomies to prevent limb ischemia.
The plan should be discussed with the local burns centre to confirm that they agree
that escharotomy should be performed rather than waiting for transfer.
What are the principles regarding urgent escharotomy of this patient’s chest and
arm?
If possible, escharotomies are performed in a proper operating theatre rather than in
A& E.
A supply of scalpel blades, a diathermy machine , a large supply of sterile swabs and
crepe bandages, and a dilute solution of adrenaline are organized.
Full-thickness burns requiring escharotomy are insensate and no further anaesthetic is
needed.
 The chest wall burns are incised lateral to the nipples on both sides and
transversely to release a „ breastplate‟ of burnt tissue to relieve the
constriction. Chequerboard escharotomy gives a worse cosmotic result and is
no longer in vogue.
 The arm is incised along the pre-axial borders and continued on the ulnar
border of the fingers, taking care to avoid the position of the digital nerves just
volar to the axial plane.
Liberal use of dithermy to provide haemostasis and wrapping the limbs in adrenaline-
soaked swabs with firm crepe bandaging helps to decrease blood loss , which can be
considerable.
What is this patient’s prognosis?

Poor.A chart (Bull 1971) is available relating chances of survival to age and area of
burn. For this lady, there is only a 20 % survival chance. As a general rule, if the age
and the percentage burn added together are greater than 100, then the chance of
survival is poor.
Gastrointestinal failure
Define gastrointestinal failure. List the causes

Gastrointestinal failure occurs when there is insufficient nutrient absorption to
maintain health and physiological function.
The causes can be broadly grouped as a decrease in area, decrease in transit time,
enzymatic failure, infection or one of a group of specific absorption defects.
1. A decrease in absorptive area, may be the result of:
1. Multiple surgical resections in diseases such as Crohn‟s disease or
mesenteric thrombosis. Sometimes these patients require long-term
TPN at home to survive.
2. Resection of the terminal ileum will produce a specific defect in that
vitamin B12 will no longer be absorbed.
3. Coeliac disease is an autoimmune condition in which the patient is
sensitive to the α-gliadin fraction of wheat gluten and villous atropy
results, which massively decrease the gut surface area.
4. Similar histological appearances may be seen in tropical sprue, but the
patient does not respond to a gluten-free diet.
5. Inflammation of the gut wall by conditions such as Whipple„s or
Crohn‟s disease or lymphoma can also have the effect of reducing
surface area.
2. Rise in transit speed: After a gastrectomy, there may be a significant rise in
transit speed that reduces enzyme mixing and decreases absorption. Similarly,
 In carcinoid syndrome the excess levels of 5-hydroxytryptamine and
simultaneously secreted substance P cause rapid gut transit. This,
however, is very rare.
3. Decreases the amount of enzyme secretion:
 Chronic pancreatitis is a common cause in this country of
malabsorption, as destruction of the gland decreases the amount of
enzyme secretion, although steatorrhoea only occurs when > 75 % of
lipase activity is lost.
 Cystic fibrosis is another chronic condition that may cause pancreatic
malabsorption, as the chloride transport defect at the heart of the
disease makes the secretions of the pnacrease and other organs-too
viscid. The raised {H+} accured in Zollinger-Ellison syndrome can,
rarely inactivate pancreatic lipase and decrease absorption.
4. Gut infestation with protozoa Gardia lambia may cause malabsorptive
diarrhoae.
5. Blind loop syndrome occurs with stagnation of bowel contents, which leas to
an overgrowth of bacteria that has two effects:
 Firstly, there is increased competition for vitamin B12 and there is a
decreased absorption of this.
 Secondaly, there is catalysis of bile salt deconjucation impairing fat
absorption.
A similar effect is seen after alteration of the gut bacterial flora by broad-
spectrum antiobiotics.
6. Bilary obstruction affects fat absorption by interruption of the enterohepatic
circulation of bile salts.
7. Pernicious anemia results in a deficiency of intrinsic factor, thus affecting
vitamin B12 again.
8. Disacchrides deficiency results in an osmotic diarrhoae and electrolyte

deficiency.
9. Protein-losing enteropathy is a gut condition akin to nephrotic syndrome in
which large amount of protein are lost through an abnormally permeable
intestinal wall; hypoalbuminaemia results.
What are the treatment options?

Many of these conditions have specific causes and treatment should be directed
towards those, for instance,
 A patient diagnosed with coelic disease should be instructed on the benefits of
a gluten-free diet.
 Short bowel syndromes may have to be treated with permanent TPN.
Insertion of an anti-peristaltic segment of gut to slow transit may be beneficial
although gambling with a length of gut in patient with short bowel problems is
a risky business and remains controversial.
 Sprue often responds to antibiotic therapy as will giardiasis.
 In cases of pancreatic enzyme deficiency of whatever cause replacement
therapy can be instituted using commercially available preparations.
If the failure is pancreatic, what may the patient describe for you?
Classically, they will describe:
 Weight loss.
 Steatorrhoea- pale bulky stive stools, which float and are difficult to flush
away. They leave an oily sheen in the toilet pan.
Steatotorrhoea is defined as a daily faecal fat excretion of >5 g.
Stomas
Definition:
It is an artificial opening which allows a connection between two surfaces.
What are the uses of a stoma?

A. Input:
 Allowing enteral feeding in cases where surgery or neurological disease
prevents oral intake (eg, gastrostomy or {PEG}, jenjunostomy).
 Bypass pf proximal blockage (e,g, trachestomy in airway obstruction).
B. Output :
 Where the lower gastrointestinal tract has been removed due to disease
(eg, end ileostomy in panprotocolectomy, end colostomy in AP resection).
C. Diversion:
 Temporary protection of an anstomosis or dioversion from a diseased part
of the bowel (eg, ileostomy, loop colostomy).
 Protection of distal organs (eg, pharyngostomy in neonatal tracheo-
oesophageal fistula).
D. Decomposition:
 In decomposition of the thorax (tube thoracostomy). Or
 Uncommonly used for decomposition in large bowel obstruction
(caecostomy).
What are the indications for performing a transverse (loop) colostomy?

 Distal colonic obstruction:
 If the patient is unfit for urgent resection or the cause of the obstruction is
inoerable.
 Defunctioning of the distal colon:
 Biventricular disease of the distal colon with abscess formation.
 Colovesical fistula with sever urinary tract infection.
 Anal carcinoma prior to radiotherapy.
Describe the procedure of the transverse colostomy?

1. The stroma is marked preoperatively in discussion with the patient and
informed consent is obtained.
2. A transverse incision is made, centred on the upper right rectus muscle
between the costal margin and the umbilicus, and a 2-cm disc of tissue is
excised from skin to rectuc sheath. A crucuate incision is made in the rectus
sheath and the rectus muscle is blunty divided to the periteinium.
3. A loop of the proximal transverse colon is identified in the wound and a
window is made through the mesentry close to the bowel. A length of soft
rubber tubing or a colostomy rod is passed through the mesentry and the colon
is delivered through the wound.
4. A longitudinal incision made through the colon along one taenia coli. The
edges of the opend colon are turned back and sutured to edges of the skin
incision with interrupted Vicryl sutures. A stoma appliance is fitted.
What is the colostomy rod usually removed?

Approximately 10 days after the operation
When should a temporary colostomy be closed?

Closure is safest when the stoma matured, at least 2-3 months following formation of
the colostomy.
The patient should also have recovered from the primary pathological process that
necessitated the stroma.
Closure should be performed using an intraperitoneal technique, as it has fewer
complications inlvolving faecal fistulae.
Classification:
I. Temporary:
PEG tube, pharyngostomy, oesophagostomy, caecostomy, loop ileostomy or
transverse colostomy.
II. Permanent:
End-colostomy after an abdominoperineal resection (APER), or end-ileostomy
after a panproctocolectomy.
Preoperative preparation:
 Psychosocial physical preparation.
 Informed consent with risk and benefits explained.
 Use of a clinical nurse specialist in stoma care – who would also mark the site.
Stoma site:
Generally:
 5 cm away from umbilicus ( not for PEG).
 A way from scars or skin creases.
 Away from bony prominences or waistline of clothes.
 Site that is easily accessible to the patient – not under a large fold of fat.
 Stoma must be within the rectus abdominis , otherwise parastomal herniastion
will occur and obstraction and pain will ensue (not for PEG).
 Need to consider patient's mobility and eyelight.
What complications can occur in association with a gastrointestinal stoma?

Complications:
 General versus specific.
 Technical versus general versus practical.
 Immediate ( < 24 hours), early (< 1 month) or late (> 1 month).
General
This is related to the underlying diasease:
 Stoma diarrheoa : water and electrolyte imbalance, hypokalemia.
 Nutritional disorders: vitamin B deficiency, chronic microcytic /normochronic
anemia.
 Stones: both gallstones and renal stones are more common after an ileostomy
 Psychosexual.
 Residual disease , e.g. Crohn's disease and parastomal fistula , metastases.
Specific
 Ischaemias and gangarene.
 Haemorrhage.
 Retraction.
 Prolapsed / intusussception.
 Parastomal hernia.
 Stenosis – leads to constipation.
 Skin excoriation.
Practical problems:
 Odour: advice on hygiene, diet and deodorant sprays.
 Flatus: improved with diet and special filters.
 Skin problems.
 Leakage: especially transverse loop colostomies.
Local complications:
 Skin irritation by stoma contents.
 Leakage and odour.
 Parastomal hernia.
 Prolapse.
Surgical complications:
 Strangulation and isaemia where abdominal wall is too tight.
 Inadequate diversion and spillage of contents into the distal bowel.
 Stomal stenosis due to poor siting or recurrent disease.
 Retraction.
 Stomal ulceration.
What are the differences between an ileostomy and a colostomy?

Ileostomy colostomy
Site Right iliac fossa ( RIF) Left iliac fossa ( LIF)
Surface Spout ( prevents irritation of underlying skin) No spout
Contents Watery –small bowel Faeculent
Effluent Continous Intermittent
Permanent Panproctocolectomy APER
Temporary Loop ileostomy after low anterior resection Hartmann's procedure
Mucous fistula:
Used in similar cirmumstances to Hartmann's procedure but, instead of dropping the
rectal stump back into the abdomen, it is brought out as a separate stoma, which being
an efferent limb procedures only mucous. This makes the distal the distal limb more
accessible when the bowel is later rejoined. Also performed in inflammatory bowel
surgery because of fear of rectal stump blow-out.
Rehabilitation:
 Diet should be normal.
 Bag should be changed once or twise a day (need to be emptied more
frequently if urine or watery small bowel contents).
 Ileotomies should have a base plate under the bag changed every 5 days and
the bag changed daily.
 Psychological and psychosexual support.
Systemic inflammatory response syndrome
What is the difference between systemic inflammatory response syndrome

(SIRS), sepsis and septic shock?
SIRS is defined by the presence of two of the following criteria:
 Temperature > 38.4 oC or < 35.6 oC.
 Heart rate > 90 bpm.
 Respiratory rate > 40 breaths/minute or PCO2 <32 mmHg (< 4.2 kpa).
 White cell count > 12.000/ml, < 4.000/ml or 10% immature forms.
Sepsis is SIRS with documented infection.
Sever sepsis: sepsis with organ dysfunction, hypoperfusion or hypotension.
Septic shoch: sepsis with hypotension despite adequate fliud resuscitation plus
perfusion abnotmalities suggested by oliguria, metabolic acidosis or mental state
changes.
MODS: the presence of altered organ function in an acutely ill patient such that
homeostaisis cannot be maintained without intervention, eg, renal failure, respiratory
failure or disseminated intervascular coagulation.
What are the common causes of SIRS?

Non-infectious cuases:
 Pancreatitis.
 Burns.
 Aspiration pneumonitis.
 Polytrauma
 Haemorrhagic shock.
Infective causes:
Although infection is a common cause.
Staphylococci and enterococci are pneuminant; gram-negative endotoxin is another
potent initiator.
What mediators are involved in SIRS?

There are bacterial factors and host factors
Bacterial cell walls (endotoxin) and various exotoxins, such as toxic shock syndrome
toxin-1, act directly on immune cells to activate the inflammatory response
In response to the inflammatory stimulus host cells release pro-inflammatory
cytokines such as interleukin 1 (IL-1), (IL-6) and (TNF∞). These are kept in check by
inflammatory cytokines such as (IL-10) and (TNFв)
The balance of the pro-inflammatory and anti-inflammatory factors determines the
response.
What is MODS and what the mortality rate?

A MODS is defined as multiorgan dysfunction syndrome.
As the number of failing system increases, so the associated mortality rises.
 Single-system failure has a mortality rate of 40 %.
 2 systems failure has 60 %.
 3 systems failures are associated with 98 % mortality rate.
Define shock and give a simple classification

It is an circulatory disturbance resulting in adequate organ perfusion and tissue
hypoxia.
It may be classified as one of four general types: hypovolaemic, septic, cardiogenic
and neurogenic.
Hypovolaemic shock:
It is due to decreased circulating volume as in:
 Haemorrhage.  Gastro-intestinal fluid loss.
 Burns.  Third-space sequestration.
It is the clinical picture typically presenting after significant haemorrhage.
The patient is:
 Pale.  Peripherally shut down.
 Tachycardic.  Hypotensuve with a reduced pulse pressure.
 Tachypnoeic.  Oliguric.
Although the presence of some or all of these is dependent on the degree of
hypovolemia.
It is the picture after sever burns owing to loss of plasma, intestinal obstruction
because of fluid sequestration, and excessive vomiting or diarrhoea in cholera, for
examples.
Septic shock:
Circulatory collapse as a result of overwhelming infectionn.
Gram –ve bacilli and their endotoxins are particularly implicated.
 The endotoxin acts on capillaries to render them "leaky" and this together with
vasodilatation can result in profound hypovolaemia.
 Endotoxins are also negatively inotropic.
The typical response is a hyperdynamic circulation.
The patient is:
 Pink warm peripheries.  Bounding pulses.
 Gereatly raised cardiac output.  But oxygen extraction is diminshed.
If, however, the septic shock has poor cardiac reserve or is hypovolemic, then they
will not be able to enter this hyperdynamic phase and will develop "low-flow" septic
shock, similar in most respects to hypovolaemic shock with cool pale, mottled
extremities
Cardiogenic shock:
It implies that the heart is faling in its role as a pump to maintain adequate perfusion
pressure.
This may be due to:
A. Primary myocardial failure from:
 Ischaemia.  Arrythmias.
 Cardiomypathy.  Cardiac tamponade.
 Tension pneumothorax.
B. Secondary to:
 Peripheral perfusion depression from SIRS or sepsis.
The kidneys interprets decreased peripheral perfusion as hypovolaemia and the initial
peripheral response is the same with cool extremities.
Increased activation of the rennin-aldosterone raised venous pressure and peripheral
oedema. This is usually obvious in the normovolaemic cardiogenic shock-in the
hypovolaemic able and pulmonary artery floatation catheter placement may be

necessary to determine myocardial function.
Neurogenic shock:
It results from an acute central neurological injury, which results in a complete loss of
peripheral vasomotor tone and consequent circulatory collapse.
It may in this context be viewed as a form of relative hypovolaemic shock.
What are the signs that may distinguish septic from haemorrhagic shock?
The septic patient is often pyrexial, with warm periphery and may have a high CO.
In haemorrhagic hock the patient is cold and clammy, peripherally shunt down and is
likely to have a low CO.
What is the difference between the systemic inflammatory response syndrome

and septic shock?
The systemic inflammatory response syndrome is a systemic response to endothelial
inflammation and is defined by the presense of two or more of the clinical signs of:
 Temperatue > 38˚C or less than < 36˚C.
 Heart rate > 90 bpm.
 Tachypnoea.
 White cell count > 12 x109/l or < 4 x109/l. (or presence of more than 10%
immature neutrophils).
In contrast, septic shck is sepsis induced hypotension despite adequate fluid
resuscitation. Hence, it is a haemodynamic disturbance characterized by raised cardiac
output and reduced systemic vascular resistance.
How do you assess volume status in a patient with suspected shock?

 Examine the patient for signs of hypovolaemia or fluid overload:
 Pulse and blood pressure (especially postural drop), JVP, basal crackles
(interstitial compartment), peripheral perfusion (e.g. capillary refill) and
oedema (interstitial compartment).
 The charts should be checked for serial weights and fluid balance
(input/output). Additional tools
How can a Swan-Ganz catheter help in the diagnosis of shock?

The calculation of PAWP, CO and SVR is used to diagnosis shock.
 A high PAWP, low CO and high SVR is consistent with cardiogenic shock.
 A low PAWP, high CO and low SVR is characteristic of septic shock.
However, these are not absolute. For example in profound sepsis, myocardial
depression also occurs due to circulating cytokines such as tumour necrosis factors
(TNF) include chest X-rays (signs of pulmonary oedema or cardiomegally), a CVP
line (used dynamically) and Swan-Ganz catheter.
Which inotrope is commonly used to treat septic shock?

Noradrenaline.
This agent predominantly acts on α1 receptors to cause casoconstriction and raise total
peripheral resistance thus increasing systolic and diastolic blood pressure (SBP and
DBP).
What is the initial treatment of hypovolaemic shock?

 Airway: oxygen via face mask.
 Breathing.
 Circulation (with haemorrhagic control) 2 large-bore cannulae for intravenous
access (antecubital fossa).
 Crystalloid /colloid, blood, clotting products (if large transfusion required).
 Patient positioning (head down).
 Crossmatch as necessary.
 Investigations (FBC, U&Es, clotting screen).
How do you assess adequate resuscitation ?

Assess:
 Blood pressure.
 Heart rate.
 Capillary refill (peripheral perfusion).
 Temperature (peripheral perfusion).
 Urine ouput.
 Blood gases:
 Lactate.
 Base excess.
If available
 Central venous pressure monitoring.
 Pulmonary capillary wedge pressure (PCWP).
Priciples of treatment of MODS, SIRS & SEPSIS.

1. Removal of any precipitating cause & treatment of any underlying infection.
Antibiotic treatment is initially broad spectrum and empirical. This will be
changed depending on culture results and microbiological advice.
2. Airway and breathing: ventillaory support for ARDS and respiratory failure.
3. Circulation: intravenous fluids, invasive monitoring (arterial line, CVP ±
PAFC) and inotropic support to maintain cardiac index, noreadrenaline tp
increase SVR, MAP and organ perfusion, thereby maximizing oxygen
delivery to the tissues.
4. Renal support: maintain urine output and renal perfusion. Dopamine &
frusemide have been used to maintain renal perfusion but there is no evidence
that either of these improves outcome. Renal replacement is the mainstay of
renal support (haemofilteration, haemodialysis, haemofilteration).
5. Nutritional support: in the presence of gut failure, parenteral feeding may be
necessary to account for the body's massive calorific demands in MODS and
SIRS.
What is activated protein C? who should receive it?

Activated protein C modulates both inflammmation and coagulation in sever sepsis,
and reduce mortality.
Activated protein C is an endogenous protein that promotes finrinolysus and inhibits
thrombosis and inflammation. It is an important modulator of the coagulation and
inflammation associated with sever sepsis.
It is converted from its inactive precursors, protein C, by thrombin coupled to
thrombomodulin. The conversion of protein C to activated protein C may be impaired
during sepsis as a result of the downregulation of thrombomodulin by inflammatory
cytokines. (reduced levels of protein C are found in most patients with sepsis and are
associated with an increase mortality).
A large randomized controlled trail has confirmed the efficacy of activated protein C.
in patients with sever sepsis, an intravenous infusion for 96 hours is associated with a
significant reduction in mortality. The use of this drug is indicated if the patient has a
systemic inflammatory response at least one organ dysfunction and known or
suspected infection.
When using an infusion of activated protein C, it is important to monitor for signs of
bleeding, an important side effect of therapy with this compound. The value of this
agent in patients with multiorgan failure or outside the first 24 hours of injury, is
unknown.
Terminology
What is an infection?
The invasion of a host by micro-organisms resulting in inflammatory response.
What is the difference between bacteraemia and septicaemia?

Both bacteraemia and septicemia are characterized by the presence of viable bacteria
in the blood. However septicaemia is associated with a systemic response.
What are the criteria which define sepsis?

Sepsis is a systemic response to infection characterized by at least two of the
following criteria:
 Temperature >38C.
 Heart rate> 90 /minute.
 Respiratory rate >20 breaths/minute (or PaCo2< 32 mmHg).
 White cell count >12.000 cells/mm3, (or >10% immature forms).
What is the difference between sepsis and septic shock?

Septic shock is the state sepsis but with associated hypotension despite adequate fliud
resuscitation.
Consequences of sepsis
Gram-negative septicaemia have life-threating consequences. How do these

organisms cause such sever pathology?
Gram-negative rods have a lipopolysacchrides (LPS) in their cell wall, which is a
powerful endotoxin. LPS activates a wide range of inflammatory cascades.
Name some of inflammatory mediators involved?

 Tumor necrosis factor.
 Interleukins.
 Postglandins leucotriens.
 Nitric oxide.
 Bradykinnin.
 Complement.
How do these mediators lead to septic shock?

The effect of these inflammatory cascades is to increase the body's metabolic needs
and cause massive vasodilatation.
The systemic vascular resistance (SVR) falls precipitously and hypotension results
despite increased cardiac output.
This result in the classic appearance of septic shock of unwell, hypertensive patient
with flushed cheeks, warm peripheral and bounding pulses.
What other organ systems are affected by these inflammatory cascades?

 Haematological clotting cascade activated, microclots and bleeding as factors
consumed. This is disseminated intravascular coagulopathy (DIC).
 Respiratory: inflammatory mediators lead to leaky capillaries and adult
respiratory distress syndrome (ARDS).
 Neurological: poor perfusion leads to confusion, drowsiness and coma.
 Cardiac: increased work can result in ischaemia and failure in stage shock.
 Renal mediators and poor perfusion lead to acute tubular necrosis (ATN).
 Hepatic: liver failure can result from hypotension.
 Intestinal ischemic bowel becomes permeable to bacteria leading to
translocation and further septic insult.
How is this clinical picture labeled?

This is poor as multi-organ dysfunction syndrome (MODS).
What is the prognosis?

Prognosis is poor; mortality approaches 95% with established three organ failure.
Principles of sepsis management
What are the principles of treating sepsis?

 Resuscitate/supportive therapy with appropriate monitoring.
 Remove source of sepsis/drain pus.
 Appropriate antibiotics, as narrow spectrum as is safe.
What needs to be considered before starting antibiotics?

Have appropriate cultures been sent.
Will the antibiotic cover the most likely organisms (local policy useful) broad
spectrum antibiotics can be used if there is no time to wait for cultures.
What is the mainstay of supportive therapy sepsis?

 Fluid resuscitation.
 Vasopressors.
 Organ support as required.
 Monitoring.
By what means can the source of sepsis be removed/drained?

 Incise and drain abscess.
 Debride infected tissue (trauma/necrotizing fasctitis).
 Percutaneous/ open drainage of collection.
Do you know of any specific treatment that is acquiring an evidence base?

Anti-protein C, an exciting development as previous immune modulators have failed
in trials.
Sources of sepsis
List some categories of infection in surgical patient?

 Wound infection.
 Pneumonia.
 Urinary tract infection (UTI).
 Bacteraemia from intravascular devices.
What are the broad sources of bacterial infection? Where can it arise?
Endogenous infections arise from the pateint's own flora.
Can you explain these terms?

 Endogenous infections arise from the patient's own flora.
 Exogenous micro-organisms come from elsewhere: the air, medical
equipment, the surgeon or other health are workers.
In broad terms, what factors predispose to an endogenous wound infection?

These can be summarized by remembering that:
Risk of infection =
(dose of bacteria X virulence) / patient resistance
What effects patient resistance?

 Age.  Nutrition.
 Obesity.  Diabetes.
 Smoking.  Immunosuppression.
 Malignancy.  Renal failure.
 Anaemia.  Jaundice.
What factors during the operation increases the risk of surgical site infection?
 Inadequate skin prepration.
 Pre-operative shaving.
 Long procedure.
 Foreign material.
 Drains.
 Poor haemostasis.
 Tissue trauma.
 Poor sterile technique.
Multi-organ dysfunction syndrome

What is multiple organ dysfunction syndrome?
This refers to altered organ function in an acutely ill patient such that homoestasis
can't be maintained without intervention .
It usually follows a predictable course starting with the lungs progressing to heart
liver, gastro-intestinal tract and kidney's.
What is the mechanism leading to multi-organ dysfunction syndrome (MODS)?

The main causes of MODS are:
 Infection.
 Inflammation, eg.acute pancreatitis.
 Injury e.g., trauma and burns.
 Ischaemia.
 Immune.
 Idiopathic.
These triggeres initiate an inflammatory response which progresses to multiple organ
dysfunction and can lead to death.
Do you know the difference between primary and secondary MODS?

In primary MODS:
 A well defined insult leads directly to organ dysfunction.
 This injury is sever enough to provoke the systemic inflammatory response
syndrome which leads to MODS.
Secondary MODS:
 It develops as a consequence of host response to inflammatory response
syndrome.
 "Two hits" are required:
 The first insult primes the host.
 The second insult brings about a greatly amplified sysremic
inflammatory response.
How would you manage a surgical patient at risk of developing MODS?

It is primary prior to surgery to predict and anticipate complications to try and prevent
a patient going into multi-organ failure.
The aims of treatment are to restore and maintain optimal oxygenation and tissue
perfusion.
 The patient should be treated with high flow oxygen and fluids (colloid or
crystalloid).
 A careful history and examination is required with review of the patient's
medical notes.
 Appropriate investigations to identify the cause should be carriedout. This
would include
 A full blood count and clotting.
 Renal and liver function testes.
 Septic screen.
 Chest X-ray and electrocardiography (ECG). Other modalities of
imaging may also be required.
 Empirical broad-spectrum antibiotics may be started.
 Operative intervention may be carried out if appropriate.
How would you proceed if the patient develops MODS?

This patient would require management in an intensive care unit (ICU).
He may develop adults respiratory distress syndrome and may require ventillatory
support.
Adequate renal support and antibiotics should be given.
It is also important to maintain adequate nutritional support.
Why is it preferable to have enteral feeding in these patients?

Enteral feeding helps to prevent colonization by pathogenic flora and maintain a
mechanical gastro-intestinal mucosal barrier.
In addition, enteral feeding maintains gut-associated immunity and blunts the
catabolic stress response.
Do you know of any experimental therapies that have been tried to improve
outcome in MODS?
Antibodies to tumor necrosis factor (TNF∞), (IL-8) and endotoxins have been tried
with little success.
Brainstem death
What are structures in the brainstem?

 Midbrain.
 Pons.
 Medulla oblongata.
These contain:
 Respiratory and cardiovascular centres.
 Reticular activating system (a diffuse area of the upper brainstem, necessary
for consciousness).
 Areas for integration of sensory and motor traffic from the cranial nerves.
What are the preconditions for diagnosing brain stem death?

The patient is in an apnoeic coma (the patient maintained on a ventilator because
spontaneous respiration has previously become inadequate or ceased).
There is demonstrable, structural and irreversible brain damage due to a disorder that
can cause brain stem death which has been diagnosed with certainty.
What conditions must be met before a diagnosis of brainstem death can be

made?
General:
 Irremediable brain damage.
 Exclusion of reversible causes for absent brainstem function.
 Comatose patient/ ventilated.
 Known aetiology for the coma.
Exclusion of:
 Hypothermia.
 Metabolic/ endocrine disturbance.
 Depression of central nervous system due to drugs.
 Recent circulatory arrest.
What conditions may mimic brain stem death and therefore should be excluded
before making such a diagnosis?
 Sedative drugs, alcohol, poisons or neuromuscular blocking agents.
 Primary hypothermia.
 Metabolic or endocrine disturbances.
Who should undertake brainstem function testing?

Two doctors who have been qualified for at least 5 years.
Is there a role for EEG?

In the UK, it is not necessary to perform EEG as a confirmatory test as it though to be
misleading.
When should the test be carried out?

The test should only be performed a minimum of 6 hours after the onset of the coma
or 24 hours post cardiac arrest.
What are the criteria for brainstem death?

1. Absence of anaesthesia (sedative or paralyzing agents).
2. Normothermia.
3. Normal blood biochemistry.
4. No motor response to painful stimuli.
5. No papillary light reflex.
6. No corneal reflex.
7. Absent Doll's eye reflex.
8. Negative caloric testing.
9. No gag reflex.
10. Absence of respiratory effort.
Are there any conditions that must be satisfied before brainstem testing can be
undertaken?
Yes, the patient must have a diagnosis compatible with brainstem death and have been
in a coma for at least 6 hours.
Are there any investigations that might be used to help confirm brainstem
death?
Electroencephalogram (EEG) testing may be used.
Other ITU issues

Diabetic ketoacidosis
What is diabetic ketoacidosis ?

Diabetic ketoacidosis is defiened as a metabolic acidosis (arterial Ph< 7.3) associated
with ketonaemia and a blood glucose >11 mmol/l.
What are the predisposing factors to diabetic ketoacidosis ?

 Surgery.
 Infection.
 Inappropriate reduction of insulin.
 Myocardial infarction.
 Stress.
Can you explain why blood sugar rises in response to surgery?

This occur as part of the metabolic response to injury. A rise in growth hormone
levels decreases glucose uptake in tissues. Increased cortisol levels stimulate
gluconeogenesis. Increased levels of catecholamines stimulate gluconeogenesis and
increased glucagons levels stimulate glucoconeogenesis and glycogenolysis. Insulin
levels do increase, but this countred by a degree of insulin resistance helping maintain
a hyperglycaemia state.
What are the clinical features of diabetic ketoacidosis?

 Polyuria.
 Thirst.
 Abdominal pain.
 Vomiting.
 Hyperventilation.
 Hypotension and tachycardia.
 Drowsiness and coma.
What are the principles of management ?

Diabetic ketoacidosis is a medical emergency. The main principles of management
are to replace lost fluid and minerals and administer insulin to counteract the
metabolic disturbance. Fluids in the form of normal saline should be given rapidly to
try to overcome the fluid deficit. Over the first few hours of treatment, this can then
be adjusted according to the pateint's clinical condition. Insulin is given as a continous
sliding scale infusion depending on the blood glucose of the patient. Potassium
supplements need to be administered as insulin leads to potassium uptake by cells,
further supportive measures such as nasogastric drainage and bladder catheterization
may be required. It may be necessary to transfer the patient to a high-dependency unit
(HDU).
Jaundice
What is bilirubin and how is it metabolism?

 Bilirubin is a pigment and metabolic end-product of haem degradation. Most
bilirubin is derived from the breakdown of senescent red blood cells, with
approximately 20% from other haem-containing proteins, such as myoglobin
and the cytochrome complexes.
 Haem is degraded by haem oxygenase to biliverdin which is reduced to
bilirubin
 Bilirubin is insoluble and is strongly bound to albumin in plasma, where it is
transported to the liver. Here it is taken up by active transport into the
hepatocytes and conjugated to glucuronic acid, rendering it water-soluble.
 The conjugated bilirubins are secreted into bile and enter the gut.
 Some of the conjugated bilirubins are broken down into urobilirubin by gut
bacteria, which is freely permeable through the bowel wall, and enters the
circulation to be excreted in the urine
 The rest of the bilirubin enters the colon where it is converted to
stercobilinogens by the gut bacteria and excreted in faeces
 A fraction of the sterocobilinogen and urobilinogens are reabsorbed into the
enterohepatic circulation.
How would you classify jaundice?

Jaundice may be classified according to the mechanism of occurrence or by the type
of product that accumulates. It is the visible manifestation of hyperbilirubinaemia.
The upper limit of normal for bilirubin is a bout 19 µmol/L (depending on laboratory
references), and it becomes visible in the skin, scelera and mucous membranes at
concentrations of greater than about 35 – 40 µmol/L
How is jaundice classified?

 Prehepatic:
Due to increased production of bilirubin beyond the capacity of hepatic
conjugation, eg. Haemolytic anaemia.
 Hepatic:
Due to impaired uptake or conjugation of bilirubin as a result of hepatocellular
dysfunction, eg. Hepatitis, Gilbert's syndrome.
 Post-hepatic:
Due to obstruction of the bilary tree, preventing the elimination of conjugated
bilirubin, eg. Gallstones and carcinoma of the head of pancreas.
What are the important aspects of perioperative care in the jaundiced patient?
 Coagulopathy due to impaired vitamin K absorption.
 Development of hepatorenal syndrome-keep patients adequately hydrated.
 Development of drug toxicity due to impaired hepatic metabolism.
How would you investigate a jaundiced patient?

After history taking and examination, blood should be taken for a range of laboratory
tests:
 Haemoglobin estimation: anaemia may be an indictor of chronic disease or a
bleeding ampullary carcinoma.
 White cell account: if elavated, then cholangitis should be considered.
 Clotting screen: hepatic dysfunction disrupts clotting factor synthesis. A
normal clotting screen is essential before embarking on invasive procedures
 Urea and electrolytes: used to assess hydration and renal function as patients
are at risk of hepatorenal syndrome.
 Liver function tests:
 Bilirubin-diffrential assays will detail conjugated and unconjugated
levels.
 Alkaline phosphatase- this rises massively in obstructive jaundice.
 ALT/AST-these tend to rise more in hepatic disease.
 Albumin- decreased in chronic disease states.
 Blood cultures :cholangitis can cause severe sepsis and cultures are essential if
this diagnosis is considered.
 Hepatic serology.
How would you treat a jaundiced patient?

 The initial aim of management is confirmation of diagnosis, elucidation of
cause and maintenance of good hydration and urine output.
 The baseline imaging investigation:
 Abdominal ultrasound, This may reveal the presence of:
1. Gallstones and outline and position of any stones.
2. Intrahepatic or extrahepatic duct dilation.
3. The level of obstruction are usually clearly seen.
 Ultrasound vein flow and porta hepatic lymphadenopathy, and may
even demonstrate:
1. Pancreatic masses.
2. Extrahepatic duct dilatation.
3. The level of obstruction are usually clearly see.
Ultrasound is also very good for examining the liver parenchyma for tumor, portal
vein flow and porta hepatic lymphadenopathy, and may even demonstrate
pancreatic masses, if overlying bowel gas permits. The septic cholangitis will
need appropriate antibiotic treatment.
If it becomes clear from the ultrasound that a patient has obstructive jaundice,
what is your next investigate procedure of choice?
In a case of demonstrate common bile duct obstruction, with no cause seen on the
ultrasound, an urgent pancreatic CT scan is mandatory. This is to look for pancreatic
lesions that would be amenable to resection.
Endoscopic retrograde cholsngiopancreatiography should not be performed until after
the pancreatic lesion is assessed. ERCP causes pancreatic inflammation, which makes
subsequent imaging difficult to interpret and may occasionally make operative
intervention impossible.
What are the advantages and complications of ERCP?

Advantages:
1. ERCP allows excellent demonstration of the ductal anatomy including
congenital abnormalities and the level of obstruction.
2. It may allow brush cytology of intraluminal tumors.
3. It can be therapeutic via sphincterotomy and stone extraction, balloon
dilatation or stenting.
Prior to the procedure, a cloting screen should be taken and corrected, if
deranged and prophylactic antibiotic are essential.
Complications:
1. ERCP-induced acute pancreatitis that occurs in up to 3 percent of cases,
although the incidence of acute sever, life threatening pancreatitis following
the investigation is about 0.1 percent. Despite being performed with antibiotic
prophylaxis, there is an incidence cannot be relieved once contrast has been
injected.
2. If therapeutic sphinctreromy is undertaken, hemorrhage may result, which can
be life threatening.
3. A small number of people may have contrast reactions.
4. A further limitation of ERCP is necessity of having specialist equipment and
skilled endoscopists, which mean it may not be universally available.
What is this investigation, and what are the advantages and disadvantages of this
test?
A magnetic resonance chalangiopancreatogram (MRCP).

The main advantage of MRCP is:
It is non-invasive. Provided the patient is not claustrophobic and can undergo MRCP,
then there are no known side effects.
The disadvantage of MRCP is:
It is only diagnostic and no therapeutic intervention can be performed.
Drug toxicity
Gentamicin is a commonly used drug in the septic surgical patient. How does it
work and what are its common side effects?
Gentamicin is an aminoglycoside antibiotic.
It inhibits protein synthesis in the bacterial ribosomes and RNA to DNA translation.
This is bacteriostatic, yet the aminoglycosides are also bactericidal although the
mechanism is obscure.
Important adverse effects include:
Hypersensitivity reactions with 5 % of patients developing:
 Skin rash.
 Auditory and vestibular dysfunction leading to dizziness and acute
renal impairment due to tubular damage, especially in patients with
pre-existing renal disease.
A poor renal function is common in the elderly surgical patient as is the use of
non-steroidal anti-inflammatory drugs and ACE inhibitors. Why is it wise to
avoid NSAIDs in renal impairment?
Non-steroidal anti-inflammatory drugs should be avoided because of their effect on
prostacyclin synthesis.
By inhibiting the cyclo-oxygenase pathways, prostacyclin production isdecreased and
prostacyclin- dependent rennin release is inhibited.
The resultant hyporeninaemic hypoaldosteronism, coupled with decreased glomerular
perfucsion pressure will worsen renal impairment. There is also a risk of acut tubulo-
interstitial nephritis, which occurs as a cell-mediated hypersensitivity to some
NSAIDs and results in interstitial oedema, inflammatory cell infilterates and a further
worsening of renal function.
Why is it wise to avoid ACE inhibitors in renal impairment?

ACE inhibitors have a significant risk of first-dose hypotension.
Serious hyporension can result in renal failure, especially if there is already a degree
of renal impairment.
Angiotensin II is a potent vasoconstrictor, which tends to act to a greater degree on
the efferent than the afferent glomerular arterioles; this serves to increase glomerular
perfusion pressure and maintain renal function. Inhibition of angiotensin II
production, therefore, has obvious consequences.
What is the difference between cyclo-oxygenese inhibitors and NSAIDs?

The recent discovery of two isoenzyme forms of cyclo-oxygenase (COX), and the
differentiation of the function and deposition of each led to the synthesis of specific
COX-2 inhibitors.
COX-1:
 Alone is found in the gastric mucosal cells and its prostaglandin products are
protective for the mucosa.
 NSAIDs inhibit both COX-1 and 2, reducing inflammatory products but also
reducing gastroprotective prostaglandin synthesis and predisposing to gastric
ulceration.
COX-2:
 Specific COX-2 inhibitors maintain the anti-inflammatory and analgesic effect
of NSAIDs, but also reatain a gastric protective action.
The incidence of major gastrointestinal bleeding, which is estimated at between 2 and
4 % year, has limited the use of NSAIDs.
The new COX2-specific drugs have enabled analgesia and an anti-inflammatory
effect with decreased gastrointestinal risk..
How does warfarine work as an anticoagulant and how is it monitored?

The synthesis of clotting factors II,VII,IX and X as well as the anticoagulant factors
protein C and S occur within the liver and is vitamin K dependent.
Warfarin acts by:
 Preventing the γ-carboxylation of the glutamic acid residues necessary for
calcium binding.
 Without these residues, they cannot bind to anionic phospholipid surfaces and
the coagulation complexes cannot be assembled.
It is monitored by using the international normalized ratio (INR), which compares the
patient's prothrombin time with a control sample, e.g. If the patient sample has a
prothrombin time twice that of the control, the INR is 2 .
How does heparin work as anticoagulant and how is it monitored?

Heparin is a mucopolysacchride.
Heparin that works by:
 Enhancing the activity of antithrombin on both thrombin and other coagulant
proteins of the intrinsic pathway, particularly factor Xa to antitghrombin
activity ratio and give rise to mopre predictable anticoagulation.
It can be monitored by measuring the activated partial thromboplastin time (APTT).
Draw the clotting cascade?

Pressure sores
What is a pressure sore ?

 A term used to describe a range of destructive lesions ofskin and subcutaneous
tissue which are of varied pathogenesis.
 Also referred to as "bed sores" decubitus- ulcer", " pressure ulcers" and "brush
burns".
 Range in severity from erythromatous soft-tissue lesions" to open wounds
which extend deep into the tissue.
Which patients are at risk from pressure sores?

Waterlow pressure sore risk factors:
 High BMI.
 Incontinence.
 Frail skin.
 Immobility (sedated, bed-bound, neurological deficit).
 Poor tissue nutrition (cachexia, cardiac failure, peripheral vascular disease,
anaemia, smoking).
 Major surgery/ trauma.
 Poor appetite.
 Elderly.
 Immunosuppressant medication (cytotoxics, high –dose steroids, antii-
inflammatories).
How can pressure sores be prevented?

 Identify at-risk individuals (on admission).
 Have a policy for nursing staff for pressure care nursing (turning, padding,
mattresses).
 Skin condition should be inspected daily (especially bony promineneces) with
reassessment of risk.
 Frequent repositioning eg. Avoid sitting in chair for more than 2 hours.
 Find and eliminate any sources of excess moisture, eg. Due to incontinence,
perspiration or wound drainage.
 Nutritional support
 Early mobilization.
Infection in ITU
What clinical findings on ITU would lead you to suspect that a patient is
harbouring an infection?
 Pyrexia.
 Elevated white cell count.
 Altered neurological state.
 Cardiovascular instability
 Productive cough (or increased secretions on suction).
 Changes on chest X-ray.
 Rising platelet count.
 Persistently low albumin.
What factors increase the risk of infection?

Pre-hospital factors:
 Extremes of age.
 Underlying disease, eg. Diabetes.
 Malnutrition.
 Immunosupreesion lifestyle, eg. Smoking.
Intra-hospital factors:
 Underlying disease on admission to ITU, eg. Aspiration
 Organ failure, e.g. Renal failure.
 Damage to skin/ mucosal surfaces.
 Surgery.
 Prolonged hospitalization.
ITU factors:
 Poor adherence to hygiene protocols.
 Reduced bed space.
 Reduced staffing levels.
 Contaminated airflow/ equipment.
 Invasive procedures.
 Mechanical ventilation.
 Catheterization.
 Antibiotic.
How would you attempt to control infection on ITU?

 Use of plastic aprons when approaching patients.
 Hand-washing technique.
 Single-pateint equipment.
 Isolation of infected patient (cubicles).
 Staff education.
 Use of aseptic technique for invasive procedures.
 Early identification of infections and targeted antimicrobial therapy.
 Minimization of potential infarction routes (e.g., removal of arterial or venous
lines that are no longer needed).
Closed head injury
In a closed head injury, what are primary and secondary brain injuries?
 A primary brain injury is one that is caused at the time of injury. A number of
mechanisms may be involved.
The cortex may be injured directly as it impacts against the skull vault or
projecting areas of the skull base, such as the wing of the sphenoid, shearing
forces during acceleration may sever axonal connections causing diffuse
axonal injury or laceration of subdural veins giving rise to haematoma; if
smaller vessels are injured, cerebral petechial haemorrhage result .
 A secondary brain injury results from subsequent hypoxia or infection after
the initial injury. This may be due to:
 Pressure from haematoma or brain herniation.
 Regional ischemia from major vessel compression.
 Global ischaemia as a result of reduction in cerebral perfusion owing to the
rise in intracranial pressure.
 Hypoxia due to associated airway or chest problems.
 Anaemic hypoxia owing to blood los from associated injuries.
How do you assess the severity of a head injury ?

 Glasgow coma scale (GCS):
 13-15 minor.
 9-12 moderate.
 3-8 sever.
 Observation of pupil size (unequal pupils).
 Bradycardia and hypertension- may suggest raised intracranial pressure
(although this may be masked in trauma).
 Unequal motor response.
 Imaging-skull and cervical spine X ray, CT scan of head.
How may conscious level be graded?

The Glasgow coma scale (GCS) allows a rapid and objective assessment of conscious
level that is universally accepted.
It assess the parameters: verbal response, eye opening and motor response.
It gives a score out of 15 and is broken down as follows:
 Eye opening:
 4 spontaeously.  3 to speech.
 2 to pain.  1 not at all.
 Motor response:
 6 obeys commands.  5 localises pain.
 4 withdraws from pain.  3 abdominal flexion to pain.
 2 extension to pain.  1 no response.
 Verbal response:
 5 orientated.  4 confused conversation.
 3 inappropiate words.  2 incomrehensible sounds.
 1 noveralization.
A GCS of 8 or below is an indication for intubation for airway protection.
Coma is defined as not obeving commands not uttering intelligible words and not
opening the eves.
What are the immediate priorities manging a patient who is comatose due to a
head injury?
The priorities are those outlined in the advanced trauma life support (ATLS)
guidelines.
Attention should be given to support of airway (and cervical spine protection),
breathing and circulation.
Consider a patient who is comatose after head injury. After adequate

resuscitation a computed tomography head scan is performed and the patient is
found to have not to have any intracranial haematomas or focal contusions.
What is the likely reason for the coma?
Yes. The contusions may blossom over the next 72 hours resulting in deterioration in
the pateint's condition. Supportive care and or/an operation may then be required.
What are the aims of management of the head-injured patient?

The first aim is to protect the brain from further damage as secondary brain may result
from ischaemia due to fluctuation is blood pressure or due to further development of
the primary lesion, eg. Further swelling around areas of contusion.
In addition, head-injured patients often have associated injuries, eg, cervical spine and
limb injuries which need to be investigated and treated.
What metabolic abnormality common in head injuries is associated with a poor

prognosis?
Diabetes insipidus.
Should steroids be used routinely in the management of head-injured patients?

No, there is no evidence that outcome from head injury is improved by the use of high
dose steroids. However, this situation may change depending on the result of on-going
trails.
How would you mange a sever head injury?

 Advanced trauma life support (ATLS) guidelines (ABCDE).
 GCS score less than 9 warrants consideration of intubation/ ventilation.
 Also consider transfer to specialist centre.
How would you mange a sever head injury on ITU?

 General-avoid hypoxia, hypotension, hypoperfusion (with supportive
treatment, eg, ventilation, inotropes).
 Reduce raised intracranial pressure if feasible-hyperventilation (only short-
term), diuretics (mannotol), sedation, mild hypothermia.
 Suspect cervical spine injury.
 Keep blood sugar within normal limits.
 Keep plasma osmolarity between 310 mosmol/kg and 320 mosmol/kg.
 Use anticonvulsants if seizure activity is likely.
 Other measures:
 Nutrition.
 Antibiotics.
Control of intracranial pressure

What is the Munro-kelly hypothesis?
The Munro-Kelly hypothesis (1852) postulated that the intracranial contents (blood,
cerebrospinal fliud (CSF) and brain tissue) are not compressible and thus an increase
in volume of any part causes a rapid increase inpressure.
Can you give the normal range of intracranial pressure (ICP) values for a
healthy individuals ?
The range is 0-10 mmHg.
Why should we concentrate about an elevated ICP?

Raised ICP will reduce cerebral perfusion with a resulting risk of ischaemic damage
to brain cells.
What values of ICP should we be concerned about?

An ICP of > 15 mmHg over a sustained period is trmed '' intracranial hypertension"
although cerebral ischaemia is unlikely to oocur in this range.
An ICP of >20 mmHg is associated with areas offocal ischaemia and ICP > 50 mmHg
will result in global ischaemia.
How is eaised ICP measures?

1. Clinical assessment:
Headache.
Nausea.
Vomiting.
Paplliodema on fundoscpe.
2. Lumbar puncture:
Although CSF pressure can be measured during this rocedure, this isn't
routinely used because diagnostic lumbar puncture is contraindicated in raised
ICP.
3. Ventricular catheter:
It is inserted into the anterior horn of the lateral ventricle via a frontal burr
hole to measure pressure directly.
 A pressure > 20 mmHg is moderately elevated.
 A pressure > 40 mmHg is severly elevated.
It is used postoperatively and during treatment aimed at reducing the ICP,
where the CSF can be aspirated to reduce the overall ICP.
Why is limiting the ICP so important?

Cerebral perfusion pressure (CPP)
= Mean arterial pressure - (ICP+CVP)
Cerebral perfusion pressure is the driving pressure that pushes blood around the
cerebral circulation.
The intracranial compliance curve shows that:
 Up to a given point, arise in intracranial volume is compensated for and a
constant ICP and the compensatorty mechanisms are saturated a small increase
in volume results in large rises in pressure.
 Thus a rise in ICP will in general mean a fall in CPP, which will cause global
hypoxia to an already injured brain. One of the basic tenets of manging a
closed head injury is to control ICP, so that CPP is maintained at adequate
levels to prevent secondary injury.
What is the relation between cerebral perfusion pressure (CPP)and ICP and
what are the implications of this relationship for the management of ICP?
CPP is the difference between the mean arterial pressure (MAP) and ICP, i.e.
CPP = MAP - ICP
In practice a CPP of 70 mmHG is aimed for so that if there is a raised ICP the MAP
can be increased accordingly, e.g., with intropes.
However, if there is impairment of the normal autoregulatory mechanisms,
maintaining an adequate CPP will not necessarily prevent focal or global ischaemia.
In an unconscious patient, how is ICP measure?

ICP is usually measure through an extracranial transducer connected toventricular
catheter or subdural bolt.
If the ICP was not being measured, what features would pont towards a raised
ICP in an unconscious patient?
The presence of the Cushing reflex (rising blood pressure with associated
bradycardia) or evidence of conning (dialted pupil or pupils and / or posturing).
What factors may contribute to a raised ICP?

 Intracranial lesions, eg, tumor and blood clot (traumic or spontaneous bleed
from an aneurysm).
 Brain swelling secondary to primary lesion ( this may be delayed, eg,
blossoming of a traumatic contusion or edema around a tumor).
 Hyperthermia.
 Hyperglycemia.
 Hypercarbia.
 Raised venous pressure.
 Hypermetabolsim.
Can you briefly describe ways in which an ICP of > 40 mmHg might be treated
inpatient with a diffuse head injury with no intracranial blood clots?
1. Diuresis with mannitol.
2. Maintain PCO2 in the 4.5-5 Kpa range : an overly raised PCO2 produces
vasodilation and increses ICP and reduced PCO2 reduces ICP by producing
vasoconstriction ( this is the Munro-Kelly hypothesis). However, too low a
PCO2 may produce ischaemia due to too much vasoconstriction.
3. Control any seizures to help reduce metabolic rate (may need to paralysis
patient pharmacologicaly.
4. Reduce the temperature of the patient to normothermic or slightly hypothermic
5. Thiopentone can be considered but is controversial.
6. Consider decompresssive craniectomy.
What types of coning do you know about?

There are essentially two types of coning: transtentorial and central
 Transtentorail coning:
It can be in a downward direction due to the temporal lobe uncus pressing on
the brainstem resulting:
 Ipsilteral 3rd nerve palsy.
 Cushing reflex.
 Decerebrate dignity.
It can also occur in an upward direction is there is a posterior fossa mass or
bleed occur in an upward direction is there is a posterior fossa mass or bleed
pushing cerebellar tissue up through the tentorail incisura.
 Central conig:
It occurs when there is herniation of the cereblum and medulla down through
the foramen magnum resulting in Chyne-Stokes breathing sudden apnoea and
neck stiffness.
What measures may be insituated to control ICP?

There aree only three variables, brain, CSF and blood that can be manipulated.
The volume of the brain itself is difficult to alter, although:
1. Some of the cerebral oedema can be minimized by the use of osmotic diuretics,
such as mannitol in a dose of 1 g/kg as an intravenous infusion over 30 minutes.
2. Carbon dioxide is apotent vasodilator and will increase the volume of the
vascular compartment:
 Superficially it may appear to be beneficial to increase cerebral blood flow.
But;
 The increased blood volume actually raises ICP and therefore, lowers CPP.
Whilst studies have not shown any benefit from hyperventilating head
injured patients to subnormal PaCO2 levels, possibly due to altered vascular
reactivityin injured brain tissue, hypercapnia should definitly be avoided;
aiming for PaCO2 levels of low normal is appropriaate. Increased cerebral
metabolic activity demands increased oxygen delivery and will therefore,
raise ICP; thus, sedation avoidance of fitting by prophylactic anticonvulsants,
avoidance of hyperglycemia with its concomitant accumulation of lactic acid
in this anaerobic environment, are all beneficial in controlling ICP and
maintaining cerebral perfusion.
ICP may be measured directly by placement of an intraventricular catheter,

which has the added advantage that CSF can be withdrawn therapeutically.
`
Antibiotic in surgery
Routes, timing & duration of adminstration:

 Parental administration.
 Before surgery to ensure effective tissue levels.
 Postoperative antibiotics on their own do not prevent infection.
 During along operation, top-up doses may be given to maintain tissue levels of
the antibiotic.
 Gentamicin in the wash for colonic on-table lavage, as well as in orthopaedic
cement, has proved useful.
 Intrathecal vanomycin during cerebrospinal fliud (CSF)diversion procedures
has been shown to reduce the risk of postoperative shunt infection.
What are the aims of antibiotic prophylaxis?

Antibiotic prophylaxis is intended to reduce the risk of postoperative infection
without alteration of the normal flora.
It is require:
 When contamination is expected (eg, colorectal surgery).

 When operation of a contaminated site might lead to bacteraemia (eg, incision
and drainge of perianal abcess).
It is not required for "clean" operations except :
 Where a vascular graft or prosthetic implant (eg, total hip or knee
replacement) is used.
 In patients with pre-existing valvular heart disease to decrease the risk of
infective endocarditis.
 On an in-patient with pre-existing source of infection.
 If an infection would have devasting or life-altering consequences (eg, all
neurosurgical procedures).
Define bactericidal and bacteriostatic, giving examples of antibiotics from each

class of agent?
Bactericidal: an antibiotic capable of lysing and killing bacteria (eg, B-lactrams,
vancomycin, aminoglycosides).
Bacteriostatic: an antibiotic capable of slowing or stopping the multiplication of

bacteria. Final elimination of pathogens depends on host cellular defence mechanisms
having an effective phagocytotic response (eg, erythromycin).
Mechanisms of action of anribiotics:

Inhibition of cell wall synthesis:
 Leads to bacterial lysis as a result of defective peptidoglycan molecules in the
cell wall.
 Examples: B-lactams (eg, penicillin, ampicillin, cephalosporins), vancomycin,
monobactams.
Inhibition of protein synthesis within the bacteria:
 Transfer RNA (tRNA) via attachment of amino acids (tetracyclins,
bacteriostatic agents).
 Nuclear translocation (erythromycin {bacteriostatic at low concentrations},
chloramphinicol, fusidic acid {bactericidal at high concentration}).
 Meesenger RNA (mRNA) attachment to ribosomes (aminoglycosides-
bactericidal).
Inhibition of nulcleic acid synthesis:
 Decreased mRNA (eg, rifampicin).
 Decreased replication (eg, quinolones, suphonamides, metronidazole).
Alteration of membrane function:
 Polymyxin:bactericidal action against Gram-negative bacteria.
Broad spectrum versus narrow spectrum antibiotic:

Broad spectrum:
 Often covers wide range of bacteria.
 Useful for prophylaxis.
 Tends to alter normal gut flora of the patient.
 Can lead to complications such as clostridium difficle enterocolitis.
Narrow spectrum:
 Covers many fewer types of bacteria.
 Useful for prophylaxis if common infecting organisms are known but,
otherwise, better for use when treating a known infective organism.
 Less likely to alter the normal gut flora of the patient.
 Fewer complications such as C.difficle enterocolitis.
What precautions and practices can be put into place to prevent the transmission
of MRSA?
 Handwashing between patients is the single most important measure that can
be taken to curb the incidence of MRSA (meticillin-resistant S.aures)
colonization in hospitals.
 Many hospitals have instituted MRSA-only bays in wards and MRSA side
rooms.
 Before examing a patient with MRSA, examination gloves and an apron
should be worm.
 Stethoscopes should be disinfected between patients.
 MRSA cases should be left for the end of a list or ensure that a through
cleaning of theatre occurs afterwards.
 Barrier nursing.
 Make it clear to theatre that the patient is MRSA.

 The problem of resistant organisms has arisen, however, as a result of
continued overuse of antibiotics, arguably particularly prophylactic antibiotics.
A clinician can minimize this effect by ensuring appropriate use of prophylactic
antibiotics and compliance when a patient is prescribed a full treatment dose of
antibiotics- the patient is prescribed a full treatment dose of antibiotics-the patient
must finish the course to limit the risk of the formation of resisitant organisms.
Risk of antibiotics:
One of the most feared risks of antibiotic prescription, particularly in elderly people is
that of C difficle enterocolitis.
This occurs particularly after the intravenous adminsteration of a very broad-spectrum
antibiotic such as a second-or third generation cephalosporin or classically co-
omxiclav (augmentin). These antibiotics damage and kill the natural protective
bacterial flora of the patients gut, allowing an overgrowhth of pathogenic bacteria.
Indeed, some centres will not allow a cephalosporin to be administered to someone
aged over 65 unless the infection is very severe (e.g, central nervous system or CNS
infection/ overwhelming sepsis).
Presentation of antibiotic-associated enterocolitis:

 Usually occurs in the first postoperative week.
 Sever watery diarrhea (can be bloody).
 Colonscopy raveals mucosal inflammation and speuodomembranes.
 Abdominal distension.
 Shock secondary to profound fliud loss.
 Treatment is usually a course of oral metronidazole, although some strains that
are resistant will require oral vanomycin.
 C. difficle toxin positive.
What would be the antibiotic of the choice for a S.aures infection?

Venomycin is an excellent choice for an MRSA; indeed it is one of a very few
antibiotics that would be appropriate, although it is easy to forget that not all S.aures
infectiosn are MRSA.
For MSSA (meticillin-sensitive S.aures) infection, flucoxalline is a much better option
because its tissue penetration is better. Furthermore,the appropriate use of vanomycin
where it is not needed only inclreases the chance of developing further strains of a
vanomycin-resistant MRSA.
Antibiotic regimens- examples:

 Clean procedure (e,g. varicose veins)-no prophylaxis,
 Abdominal surgery with no expected contamination (e,g. cholecystectomy)
requires single-dose prophylaxis on induction only.
 Procedures with a contaminated field (e,g, anterior resection, appendectomy):
dose on induction and two further podtoperative doses.
 Wounds contaminated with skin flora need prophylaxis against staphylococcal
infection with 500mg-1g fluxacillin intravenously.
 Bowel procedures need braod-spectrum cover for Gram-positive, Gram-
negative organisms and anaerobes (an example regimen would be co-
amoxiclav or a second or third-generation cephalosporin with metronidazole
(for anaerobic cover).
 Biliary tract operations rarly involve a flora of anaerobes and , in this case, a
cephalosporin alonje would be adequate prophylaxis.
 Despite being clean, othropaedic implants and heart valve surgry require
prophylaxis because infection in either case is disastrous and potentially life
threatening (cefuroxime and gentamicin in the case of heart valves and
flucloxacillin and gentamicin in the case of othopaedic implants).

Surgical Critical Care For MRCS 3

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Surgical Critical Care For MRCS 3

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Surgical Critical Care

For MRCS part 3

ITU versus HDU

Which patients should be admitted to an HDU (High Dependency Unit)?

What factors need to be considered when assessing suitability for admission to

How would you decide if a patient should be admitted to ICU or HDU?

Differences between care in HDU and ITU:

What are the problems in admitting emergrncy patients to ICU?

What is 'multiple-organ failure' (MOF)?

Definitions of system failure:

What is the purpose of scoring systems?

What is level 1, 2 and 3 care?

Can you give some examples of each type ?

What are the characteristics of an ideal scoring system?

What scoring system are you aware of?

Briefly describe the GCS?

How is this system used?

What is the predicted risk of death with an APACHE score of >40 ?

Brifly describe the APACHE sore ?

When should APACHE scoring be done in the ITU setting ?

What is the effect of a reduced APACHE score following treatment on outcome ?

Give examples of some of the commonly used scoring systems

POSSUM or the Portmouth corrected version, P-POSSUM:

What are the drawbacks in using scoring systems?

What are the limitations of IUT scoring systems?

Airwy & Intubation

How would you define airway obstruction?

In what situations does it occur?

What are the clinical features of airway obstruction?

How would you clinically assess an airway?

What are the immediate management possibilities?

What methods are there of managing a compromised airway?

Are there any contraindications to the airway adjuncts?

A patient in A&E has a completely obstructed airway that an experienced

In elective practice, when would you perform a tracheostomy?

Describe the steps of an elective tracheostomy?

What are the complications of tracheostomy?

Acute lung injury

What is 'acute lung injury' (ALI)?

Acute respiratory distress syndrome

How would you define acute repiratory distress syndrome (ARDS)?

What are the criteria for diagnosing ARDS?

What are the criteria for the diagnosis of ARDS?

What are the causes of ARDS?

What clinical condition are commonly associated with the development of

What pathophysiological processes underline ARDS?

What is pathology seen in ALI \ ARDS?

What is the pathophysiology of ARDS?

endothelial and alveolar cell damage results in increased permeability, pulmonary

What are the principles of treating ALI/ARDS ?

What are the aims of mechanical ventilation for ARDS?

What is the mortality from ARDS?

Principles of cardiovascular monitoring

What non-invasive means of cardiovascular monitoring do you know?

What invasive means of cardiovascular monitoring do you know?

What information can be gained from pulse oximetry?

What factors might make pulse oximetry unreliable ?

How does pulse oximetry work?

What are the problems and complications of arterial pressure monitoring?

What are the complications of central venous access?

Key learning point

What is A-a gradient?

Arterial blood gases