Basic surgical skills course

Apologies for delay in postings. Completed the basic surgical skills course at Queen Elizabeth hospital last week. It was the first time the course has been trialled to run over 2 days outside the Royal College of Surgeons (normally 2.5 days). This of course meant earlier start (8am), late finish (1800), and shorter lunch break (30mins). Of course any surgical doctors will agree the above timetable almost feels like a holiday.

The course content was not altered in anyway,and there were plenty of time allowed to complete all the tasks. At the end of the course, 100% of participants preferred the 2 day course over the 2.5 days as it meant less annual leave/study leave were required to complete the course.

Having completed a similar course as an undergraduate (instructed by Mr Paraskeva at Imperial college), i found it relatively straightforward course, and it greatly helps if the candidates are familiar with the 'Reef knot'.

I particularly enjoyed the 'debridement of necrotic tissue' part of the course, as well as stacking the sugar cubes using laparascopic instruments in a box trainer. I was slightly dissapointed with my 'tower of 8', as the 9th cube slipped from the grasper and then  ricochet off the sidewall and flattened my hard work.

Although the basic surgical skills course deals a low blow to the bank balance (currently ranging from £650-£700), If the 2 day course is implemented it might mean a reduction in cost. However, the course it self uses up a lot of resources including many consultant's time who have to give up their clinic/theatre list in order to tutor the trainees.

In summary, a very useful and a thoroughly enjoyable course that is not just for surgeons, but for any medical professionals who perform minor surgery (GP, Dermatologist, A&E etc).

The courses are usually very popular, and sell out months in advance, so i recommend contacting centres at the earliest oppurtunity to reserve your place.

Please visit the royal college of surgeons website for more information regarding the course http://www.rcseng.ac.uk/education/courses/basic_surgical_skills.html?searchterm=bss

Romesh

Physiology of The Respiratory System III: Blood flow, Gas exchange and the regulation of Ventilation

Thank you for still sticking with us, I know respiratory physiology isn't everyone's cup of tea but it is essential to know the basics as they frequently come up in exams. So in this final blog on the matter, I'll give an overview of the important concepts goerning blood flow, gas exchange and reglation.

Blood Flow
A good understanding of pulmonary anatomy will be useful to tackle this bit. Pulmonary blood flow is regulated by levels of pCO2 and pO2. Hypoxia or hypercapnia result in vasoconstriction which allows blood to be diverted to better oxygenated areas (this is called hypoxic vasoconstriction). Flow is determined by perfusion pressure and resistance. The three pressures that determine blood flow in the lung are:

1. Hydrostatic pressure in the pulmonary arterioles
2. Pressure in the pulmonary veins
3. Pressure of air in the alveoli

The blood flow in the lung can be divided into zones:

1. Zone 1: this is the apex of the lung. Blood flow is low in this region as alveolar pressure is similar to pressure  in the pulmonary arterioles so smaller vessles become compressed. 
2. Zone 2: here the pressure in the arterioles is higher than alveolar pressure so blood flow is better.
3. Zone 3: The pressure in the arterioles is at its greatest in comparison with the pressure in the alveoli thus blood flow is highest here. This area corresponds with the bases and explain why vasculitic disease affects the bases.

Ventilation and Perfusion
The ventilation to perfusion ratio varies through out the lung and depends on the pressure in the arterioles:

• V/Q = infinity in alveoli that are ventilated but not perfused.
• V/Q = zero in alveoli that are perfused but not entilated.
• At the apex, V/Q = 3 which means that the alveoli are ventilated better than they are perfused. Whilst at the bases V/Q = 0.6 which indicates that the alveoli are perfused better than ventilated. 
• The ideal V/Q is found 2/3 of the way up the lungs.

 Gas Exchange
The diffusion of gases is affected by:

1. Pressure gradient: this is the partial pressure and involves the flow of air from an area of high pressure to lower pressure
2. Diffusion coefficient: this is the ease with which a gas can diffuse and is determined by its solubility in water as well as molecular weight.
3. Tissue factors: the tissue at site of diffusion should have a large surface area and short diffusion distance.

Sysemic venous blood is pumped into the pulmonary arteries from the right ventricle. This blood has a pO2 of 5.3 kPa and pCO2 of 6 kPa whereas alveolar pO2 is 13.7 and pCO2 is 5.3.  Thus oxygen will diffuse into the bood as it has a lower partial pressure whilst carbon dioxide will diffuse into the alveoli. This results in oxygenated blood transported back to the heart via the pulmonary veins. Physiological shunting (passage of blood through the lungs without going through the alveoli) occurs as bronchial blood mixes with the oxygenated blood therefore the partial pressure of oxygen in systemic blood is lowered to 13kPA. Pathological causes of shunting include pneumonia, ASD, VSD and Patent ductus arteriosus.

Oxygen is predominantly transported by haemoglobin and only a miniscule amount is dissolved. The oxygen dissociation curve shows the relationship between the partial pressure of oxygen and the concentration of oxygen in the blood. The position of the curve is altered by several factors:

1. Right shift decreases oxygen affinity thus oxygen is released at higher partial pressure. This is caused by raised temperature, increase in levels of 2,3-diphosphoglycerate (2,3-DPG) and increased H+. Right shift of the dissociation curve is called the Bohr effect.
2. Left shift increases oxygen affinity and thus oxygen is released at lower partial pressure. 

Foetal Haemoglobin and Myoglobin
Adult Hb has two alpha and two beta chains whilst foetal Hb has two gamma chains as well as two alpha. The change in globin chain results in greater affinity for oxygen thus allowing the foetus to extractblood from the maternal circulation. The curve for HbF is to the left of adult Hb as there is greater affinity for oxygen. Myoglobin has an even greater affinity for oxygen and so its curve is even further to the left as it is an oxygen storage molecule which only releases O2 when the partial pressure has dropped significantly. The function of myoglobin is to provide additional oxygen during anaerobic respiration.


Carbon Dioxide
CO2 is transported in three ways:

1. Carbamino groups which are formed between CO2 and proteins/peptides. 
2. Dissoved
3. HCO3- makes up arund 70% of transported carbon dioxide. It forms when carbon dioxide diffuses into red blood cells and reacts with water to give carbonic acid which dissocites to H+ and HCO3-. The H+ binds haemoglobin and the bicarbonate diffuses into the plasma. The reverse of this process occurs in the alveoli (bicarb diffuses into the cell to produce CO2 which can be expired).

The CO2 dissociation curve differs from that of oxygen as it has no plateau phase as blood can not become saturated with CO2, carbon dioxide is far more soluble than oxygen and the normal rnge for CO2 is narower (5.3-6kPa). The curve is influenced by partial pressure of oxygen thus the amount of CO2 carried increases as oxygen levels fall (this is called the Haldane effect).

Regulation

• Neurological: this occurs via the medulla oblongata, Pons, cerebral cortex and Limbic system. In the medulla inspiratory neurons rhythmically fire action potentials which stimulate the diaphragm and external intercostals to contract this is followed by intervening periods of inactivity when expiration occurs. Expiratory neurons in the medulla are inacive during quietrespiration but during increased respiration fire action potentials to stimulate the internal intercostals and abdo muscles to contract thus producing forced expiration. In the pons, the apneustic centre prolongs inspiration and reslts in short expiratory efforts whilst the pneumotaxic centre inhibits inspiritory neurons to shorten inspiration. Neither of these centres are essential for respiration. The cerebral cortex can override neurons in the medulla to increase ventilation or reduce it/hold breath. Finally, in extreme emotional states, the limbic system may influence respiration.
• Chemical: central and peripheral chemoreceptors monitor changes in arterial PCO2, pH and PO2. Central chemoreceptors are found in the CNS close to the resp centre in the medulla and are especially sensitive to changes in pCO2. As CO2 diffuses into the blood in the brain, it reacts with water to give H+ which causes a fall in pH. This fall stimulates the central chemoreceptors which increases the resp rate in an attempt to blow off CO2. The opposite occurs with low CO2. Peripheral chemoreceptors are located in the carotid bodies and are less important than central chemoreceptors. They respond to changes in arterial pH and low levels of pO2. Thus a fall in arterial pH due to metabolic acidosis will stimulate respiration and thus lower the level of CO2 to bring pH back to normal. The response to low oxygen is only seen when pO2 is less than 8kPa. The importance of this mechanism is witnessed in chronic lung disease whereby persistently elevated carbon dioxide levels cause the patient to become accustomed to it and thus lose the effect low pCO2 has on chemoreceptors. Thus they rely on low levels of pO2 to stimulate respiration and is called the hypoxic drive. 

Hypoxia, hypoxaemia and respiratory failure
Hypoxia is a reduction of oxygen in the tissues and is classified as:

1. Hypoxic hypoxia: due to low arterial pO2 and caused by high altitude, PE, hypoventilation, lung fibrosis and pulmonary oedema.
2. Anaemic hypoxia: decrease in amount of haemoglobin which leads to a decrease in oxygen and is due to haemorrhage, reduced red cell production, haemolysis and carbon monoxide poisoning.
3. Stagnant hypoxia: due to low blood flow which maybe due to vasoconstriction or reduced cardiac output.
4. Histotoxic hypoxia:  this occurs when the enzymes involved in cellular respiration become poisoned and thus are unable to use oxygen. The main cause of this is cyanide poisoning.

Hypoxaemia is a reduction in the concentration of oxygen in arterial blood. It is caused by:

1. Hypoventilation: this may result from CNS depression, trauma, neuromuscular disorders and chest wall deformity. It may be treated using oxygen therapy.
2. Impaired diffusion: this can be caused by asbestosis, sarcoidosis and ARDS. It maybe treated by oxygen therapy.
3. Shunt: this is not improved by oxygen therapy.
4. V/Q mismatch: this usually occurs in chronic lung disease and results in mismath between ventilation and perfusion.
5. Reduction in inspired Oxygen tension

Respiratory failure is present if PaO2<8kPa and is subdivided into:

• Type I: PaCO2 < 6kPa and is due to ventilation-perfusion mismatching. The PaCO2 is normal or low as the increase in ventilatory rate results in compensation by remaining alveoli for any increase in CO2. Causes of Type I resp failure include pneumothorax, pneumonia, contusion, PE and ARDS.
• Type II: PaCO2 > 6kPa. This is largelydue to hypoventilation and caused by COAD, neuromuscular disorders, airway obstruction, central respiratory depression and chest wall deformity.

Well that's it for respiratory physilogy, hope it was useful.

Amel

Physiology of The Respiratory System II: Lung Function Tests

The assessment of lung volumes is important in dignosing respiratory disease and monitoring progression. Spirometry is used to measure lung volumes. It is important to know the definition of each lung volume in order to be able to intepret spirometry findings and their relevance:

• Tidal Volume (TV): air breathed in and exhaled during quite respiration
• Inspiratory reserve volume (IRV): maximum volume of air that can be inspired on top of normal inspiration
• Expiratory reserve volume (ERV): maximum amount of air that can be forcefully expired after normal expiration
• Functional residual capacity (FRC): volume of gas left in the lungs after expiration during normal breathing. This can be determined using the helium dilution method. This involves the patient breathing normally from a spirometerfilled with a known volume of helium and air thus as they breath in and out, the helium is diluted into the air that is left in the lungs 

FRC = (initial helium concentration of spirometer) x Volume/(final helium concentration) 

• Residual volume (RV): volume remaining after maximal expiration. It can't be measured directly but is calculated as RV= FRC - ERV
• Total lung capacity (TLC): the sum of all volumes plus the residual volume
• Vital capacity (VC):volume of air expelled from maximal inspiration to maximal expiration

Dead space
The concept of dead space is important to grasp as this is the volume of air which does not take part in gas exchange. The are two types:

1. Anatomical: the volume of gas which does not mix with air in the alveoli. It can be determined using Fowler's method. This involves the patient breathing through a tube connected to a nitrogen analyser. The patient initial takes a single breath of pure oygen, holds their breath for several seconds and breathes out. This will determine deadspace as only the alveoli will have maximal concentrations of nitrogen whilst the higher up airways will have purer concentrations of oxygen as they did not participate in gas exchange. Thus if a curve is drawn, air initially expired will not have nitrogen as it is part of the anatomical deadspace whilst nitrogen concentrations will increase as alveolar air is expired.
2. Physiological: this is the volume of gas that reaches the alveoli but due to a lack of perfusion does not take part in gs echange. It can be determined using the Bohr equation

Volume of deadspace= Volume expired CO2(1-(Fraction of expired CO2/Fraction of alveolar CO2))

Alveolar Ventilation rate
This is the rate at which gas exchange occurs in the alveoli.
Alveolar ventilation rate= (TV-dead space) x Respiratory rate

Peak Expiratory Flow rate
This is a cheap and simple test that can be performed at the bedside. A patient is asked to take a maximal inspiration and then blow out as fast as possible into the peak flow meter. It is useful in assessing the severity of asthma attacks and monitoring treatment.

Closing Capacity
This is the volume of the lungs at which airways at the base of the lung start to close. It is normally 10% of vital capacity and can be assessed by getting the patient to breath a maximal inspiration of 100% O2 then expiring fully through a nitrogen analyser. A graph can be plotted which will show 4 phases:

1. Pure dead space is exhaled so its 100% oxygen
2. a mixture of deadspace and alveolar gas (increasing concentration of nitrogen)
3. pure alveolar gas (reaches a plateu)
4. abrupt increase in nitrogen as airways at the base of the lung close and therefore not participating in gas exchange so the expired air is coming from the apex which has received less oxygen thus the nitrogen is more concentrated.

 Factors that affect the closing capacity include increasing age, supine position and anaesthesia which increase it.

Diffusion Capacity
This tests the diffusion capacity of the alveolar membrane and pulmonary vasculature. It is measured by inhaling small amounts of carbon monoxide and measuring its levels in the blood.Diffusion capacity is most commonly reduced in pulmonary oedema (as diffusion distance is increased) and emphysema (causes loss of alveolar surface area).

Flow-Volume and Volume-Time Curves
These can be plotted using spirometry results and are important because certain pathological processes such as obstructive lung disease cause typical curves.

Well that's it for now from me. Watch out for the third and final respiratory physiology tutorial. By the way if there are any specific topics you'd like us to cover/discuss just leave a comment/send an email and we'll get on to it.

Amel

Physiology of The Respiratory System I: Mechanics of Ventilation

Although I generally find physiology a tad on the dry side, a good foundation in this is vital for success in Surgical exams and patient care. I thought we could start with the respiratory system as I'm currently doing a Resp job.

Components of the Respiratory system

1. Nasal passages
2. Olfactory system
3. Conducting airways
• Nasopharynx
• larynx
• trachea
• bronchi
• bronchioles
• Alveoli

Functions of the respiratory system

1. Cleaning, humidification and warming/cooling of air: this is achieved by the nose hairs, mucociliary escalator and air flow through the conchae.
2. Respiratory gas exchange: flow of gases depends on pressure gradient between atmosphere and alveoli which can be represented as V (rate of air flow)  = Palveoli - Patmosphere/R (resistance). Thus bronchoonstriction leads to reduced air flow due to increased resistance.
3. Facilitation  of olfaction and sound production

Mechanics of Ventilation

Inspiration is an active process. At the start of inspiration the intrapleural pressure is about -4cmH2O. This decreases to around -9cmH2O when respiratory muscles contract to increase increase chest volume. This change in intrapleural pressure causes lung expansion and generation of of a negative intralaveolar pressure. The result of this is that atmospheric pressure is higher leading to air inhalation.  (NB at rest around 500mL of air is inhaled, during excercise pressure can decrease down to -30cmH2O and thus 2-3L of air can be inhaled).

Expiration is passive due to elastic recoil of the lung. However, during excercise, contraction of the accessory muscles of respiration (internal intercostals and abdominal muscles) can generate intrapleural pressures of up to +20cmH2O to expel air more quickly.


Pressures and forces acting on the Lung
Three forces act on the lung:

1. Elasticicity of the lungs: under normal conditions this keeps the lungs stretched whic results in a force that pulls inwards on the visceral pleura.
2. Surfactant: lines alveolar surfaces and produces surface tension thus producing an inward pressure which accounts for 2/3 of elastic recoil. Surfactant also increases lung compliance thus reducing work of breathing, prevents fluid accumulation in alveoli and reduces alveolar instability [ΔP (alveolar distending pressure) T (tension)/r (radius)] by stopping them from collapsing.
3. Negative intrapleural pressure: opposes the above two forces and is created by the chest wall and diaphragm pulling the parietal pleaura outwards. This results in the two layers of the pleura being pulled in opposite directions leading to a negative pressure.

 The pressure in the alveoli is equal to atmospheric pressure which is 0cmH2O. As intrapleural pressure is between -4 and -9cmH2O this results in a transmural pressure which keeps the lungs distended.

Compliance
This is the ease with which lungs can be inflated and can be expressed as:

Compliance = ΔV (change in volume)/ΔP(change in pressure)

It is governed by elsticity of the lung parenchyma and surface tension. Thus compliance is reduced in scarring or fibrosis of parenchyma, pulmonary oedema, deficiency of surfactant, reduced lung expansion (e.g. motor neurone disease/muscular paralysis), supine position, mechanical ventilation (due to reduced pulmonary blood flow), age and breathing 100% O2. Conversely, emphysema increases lung compliance to destruction of elastic fibres in the lung parenchyma. 

Regional differences in Ventilation

In the upright position the apices are less ventilated than the bases. This is due to gravity and the fact that the pressure-volume curve is sigmoid shaped and thus the two parts lie on diferent areas of the curve. This is because the bases lie on the diaphragm and are compressed whereas the apices re already stretched by their own weight this inflation begins further along the pressure-volume curve.

Well that's it for now, I shall be writing another two posts on Respiratory phyiology. The next shall be on Lung Function tests and the final on Blood flow, Gas exchange and the regulation of Ventilation. For more info, I found the following webites useful: www.acbrown.com/lung/www.acbrown.com/lung/Lectures/RsVntl and www.medicine.mcgill.ca/physio/resp-web. Hope this has been useful.

Amel

Reperfusion injuries and compartment syndrome

Having spent 6 hours in theatre yesterday assisting with re-perfusing an acutely ischaemic leg in a patient with multiple previous vascular surgical history, today was a pretty busy day managing the post-operative complications that can arise due to reperfusion of the muscles. Serious complications of re-perfusion includes hyperkalaemia (release of potassium from dead/necrotic muscles), renal failure secondary to release of creatinine kinase into the circulation (again from ischaemic muscles) which is nephrotoxic, and compartment syndrome.

Having had no blood supply to the leg for few hours, the reperfusion of the muscles of the lower limb can lead to tissue/muscle oedema secondary to release of inflammatory mediators from damaged tissues. This initially leads to compromised venous return and therefore leads to venous congestion. This leads to further increase in the intra-compartmental pressures, and a vicious circle is set up. If the intra-compartmental pressure exceeds the perfusion pressure; this can lead to irreversible ischaemic damage to the muscles. If compartment syndrome develops, urgent release of the compartment pressure by a fasciotomy is required to prevent irreversible ischaemic damage to the muscle groups.

For further details on re-perfusion injuries and compartment syndrome; visit our website www.iwanttobeasurgeon.com (Website currently under construction)

Remember; If a patient has pain out of proportion to the injury sustained; suspect compartment syndrome, and early recognition and action can help save the limb.

Romesh

First update

Seems like Amel has been pretty busy over the last few days blogging. Congratulations to Amel and Tarik for their poster presentation, no doubt it wil tick all the right boxes when it comes to Core surgical training application.

In my end, i have been relatively busy with my vascular job, which i am thoroughly enjoying. I had very little exposure tovascular surgery as a student, however this job has opened  my eyes to the joys of vascular surgery, in particular the wide range of extraordinary surgeries that are being performed everyday such as visceral hybrid repairs, arch hybrid repair, type 1-4 thoracoabdominal aneurysm repairs, carotid endarterectomies, carotid-carotid bypass etc. I shall blog about these interesting procedures in the near future.

In addition to the free MRCS advice given by Amel, i just would like to add a few more tips.

 Consider tutoring groups of medical students, this will help refresh examination skillls, as well as help you to examine a wide variety of patients who you may not see otherwise. For example: being a vascular house officer, i am only exposed to vascular patients, this means that for the next few months i will not see/examine many general surgical patients. By tutoring a group of final year students, in addition to learning vascular surgery, i will be exposed to general surgical, and orthopaedic patients. This will no doubt be invaluable when i prepare for the MRCS Part B. In addition, the students can also fill out feedback form for the teaching you provide, which wil of couse tick the 'teaching experience' part of your job application form/interview.

So keep tuned for blogs on further MRCS advice, tips, hints, as well as posts on current vascular surgical procedures.

Romesh

MRCS Part B - Part deux

Going to meet Essie for coffee next week. She MRCS Part B in October and passed as an F1 (never having done a single surgical job). She'll give me an update on what came up, which books she used, how she revised etc... will keep you posted!

MRCS Part B

So the next Part B exam is coming up in May. As the exam is relatively new, it can be a bit of a cahllenge preparing as there isn't the wealth of information out there for other exams. The format for the exam is OSCEs with 18 stations (4 of them rest stations). On application (DEADLINE is 19th March!!) you are asked to decide he following:

1. Choose a region in which you will be assessed on Anatomy, History taking and physical exam.
2. Choose a region in which you will be examined on History taking and physical exam.
3. Choose a region on which you will be assessed on physical exam alone.
4. The rest of the exam will be basic surgical skills, communication etc...
5. The regions available are Thorax and Trunk, Head and neck, Limbs and Spine as well as Neuro. You can only pick one region per assessment and can't pick the same region more than once.

Advise from other people who have sat the exam and passed has been:

1. Revise your anatomy very well as there are anatomy stations. However, on applying you get to pick which region you would like to be examined on.
2. Read up on physiology and pathology.
3. There is no substitute for clinical experience so increase your exposure by going to clinic, theatre etc...remember people are supposed to sit the exam in their surgical training years although more and more junior people are sitting it early.
4. Get a good clinical tutor who can take you through examining patients correctly and test your knowledge as preparation for the exam.
5. If you work in groups and know people who are sitting the exam; revise together as you can get constructive feedback.
6. The area of going to revision courses is still contentious but most people go to courses in order to get a structure for their revision and polish their performance. I will try and research some of the courses and give feedback on this blog.

So here you are. A little breakdown of the exam. I must admit I'm finding it difficult to get meaningful advise about how to prepare for the exam but like any exam, I guess knowing your stuff well and seeing as many patients as possible is key to being successful.  Things that do not help in focusing on revision is knowing that you can only take this exam 4 times and the cost of the exam as well as revision courses/books. Its important to remember though that even failure in the exam itself should not be seen as a collossal negative as it can just act as a mock for the next time you sit it. Good luck and watch this space for more info on revision tools for Part A and B.

Amel

MRCS approaches

The spectre of MRCS looms ever closer and we will be blogging regular posts to help with preparation. Ideally, you should have started thinking about revisng for Part A by now as the exam's in April. Revision tips and advice will be published by Mr T very soon. From experience, I found that there are a few things that were vital in my passing the exam:

1) Anatomy revision: REVISE REVISE REVISE anatomy as the first paper has anatomy & Physiology only. I really liked "Instant Anatomy" (little orange book) as it was concise, split into logical chapters and had diagrams that were easy to memorise.

2) "Basic Sciences for the MRCS" by Rafftery is invaluable for learning physiology and if you want to brush on some pathology. The anatomy section is a little weak (as I unwittingly told the author whilst I was awaiting to sit the second paper and really didn't stop to think why someone who looked quite senior would ask what I thought of the book!!!) but you can't have everything. If you're good at learning anatomy from text rather than need viusal aids (as I do) then the anatomy sections will do very nicely for you. One thing to make note of is that although dry, make note of the little details like paths of major nerves and embryonic development as they do come up in the exam.

3) PASTEST question bank all the way! Honestly, I'm not being paid/sponsored by them before the accusations start flying but those questions were life savers. I did not revise any pathology as that was my strong point and I wanted to focus on anatomy and physiology which I was dire in. I did every single question on the database and the pathology was spot on! Its the exact same level and many of the exam questions were very similar.  Also make sure you dont just do EMQ/SBAs as although the exam is in that format, T/F questions will test your knowledge to a higher detail and all practise is useful to building knowledge. The anatomy and physiology questons were also very useful but you definitely need to revise these to a bit more detail for the exam.

4) Try to get a few days off as zeros/annual leave around the exam if at all possible so that you can touch up on areas of weakness.

Anyway, that's it for now. Watch this space for more MRCS Part A and B information from all of us.

Amel

The story so far...

In spite of lack of activity since our last post we have been busy in the non virtual world. Just presented a poster at the Associations of Surgeons In Training (ASIT) annual conference with Mr T. Amer. (above).  Surprising number of familiar faces (you know who you are). Rom and I have also been trying to finish off a couple of audits and research projects. We will actually be uploading some articles on how to write papers as well as design projects very soon. The plan for the net two weeks is as follows:

1) wrap up audit on surgical prophylaxis 

2) Get website up and running

3) submit posts at least 3 times per week to this blog.

Anyway off to work on website. Do watch this space it'll be worth it, I promise).

Amel