DrG -

NIV in Asthma... No point right?

2011-06-18T16:33:00.000-07:00

Yet more NIV excitement,

To find it, take a look at the brand new shiny blog here http://drgdh.wordpress.com/.

The DrG blog is moving there permanently, all new stuff will go up on the new site.

See you there!

DrGDH

Haemolyitc uraemic syndrome - its not just for kids anymore!

2011-06-07T14:35:00.000-07:00

Going completely off track again (blame my goldfish like attention span) I wanted to think about Haemolytic Uraemic Syndrome. This is a bit of a topical subject at present, with most of Europe panicking about a virulent strain of verocytotoxin-producing E. coli that has been found on German vegetables. So far 24 people have died and hundreds have been diagnosed with HUS.

What has people worried is that this bug has been causing a comparatively high number of cases of HUS, and has been causing it in adults. HUS is most often seen in children.

So, as its in the news, and something that I had only a vague idea about I thought it was worth a few lines, so lets see where we end up....

The majority of HUS is a consequence of enteral infection with certain strains of enterohaemorrhagic E-coli (usually picked up from unwashed vegetables, or undercooked meat) The natural history of the disease begins with enteritis, which is frequently notable for bloody diarrhoea. In most people this is self limiting, however in 2-7% of cases HUS develops.

HUS occurs due to the toxins produced by the bacteria. The toxin enters the systemic circulation via the compromised intestinal mucosa. Once in the blood stream it plays havoc with the kidneys. The toxin causes endothelial damage, which in turn causes activation of the clotting cascade and thrombosis of capillaries. As well as causing kidney injury (hence ‘ureamic’) via ischaemia and direct cellular toxicity, a consumptive thrombocytopenia occurs as platelets are used up. The haemolysis occurs due to RBC’s getting damaged as they pass through the damaged capillaries
.

It is important to note that while the kidneys are the most commonly affected, almost any organ can be damaged, e.g HUS can cause cardiac failure, pancreatitis or even vitreous hemorrhages if the eyes are affected.

So how do these patients present? The diagnosis requires both a prodromal illness (commonly diarrhoeal) and evidence of organ damage. The typical patient will have a recent history of bloody diarrhoea, anaemia (usually Hb of <8g/dl) and now have evidence of kidney injury such as oligura, hypertension or deranged renal function. The classic finding on investigation are schistocytes (basically damaged and fragmented RBC’s) on peripheral blood smear.

So what to do about it? Good supportive care is the key here - manage the dehydration and electrolyte derangements. Blood transfusions may be needed if anaemia severe. If the renal function does not respond then renal replacement therapy may be needed (i.e dialysis/haemofiltration). A small number of patients end up with permanent renal dysfunction.

Most do pretty well with the care above, about 85% recover with supportive care. If this doesn’t happen, the the next line of treatment is plasmaphoresis and exchange. The patients plasma is removed and replaced with FFP. The idea here is that the toxin responsible for the HUS is removed along with the plasma. This is done daily until improvement occurs.

There are several other treatments still in the experimental stage - and this outbreak is sure to stimulate interest. This NEJM article discusses the use of complement blockade in HUS refractory to plasma exchange

The use of antibiotics is also worth a mention. The underlying problem in these patients is a bacterial infection, so it seems reasonable to give antibiotics a try. Of course, nothing is that simple. In HUS it seems that antibiotics can possibly make things worse by damaging the E-Coli organism and increasing the amount of toxin released. (in fact HUS is one of the reasons we are advised to avoid antibiotics in diarrhoeal illness - they can increase the risk of HUS developing in the first place).

That said - antibiotics continue to be tried in severe cases. (Worryingly this outbreak in Europe seems to be a particularly awkward resistant ESBL producing strain; Augmentin? Tazocin? Cephalosporins? No good here!) It will be interesting to see what case reports etc are published about this outbreak.

(Interesting debate here about affect of antibiotic use in agriculture fueling emergence of antibiotic resistant bugs, but I’ve waffled far too much already)

So where does this leave us in the ED? HUS should be considered in any patient (particularly children) who are unwell following an diarrhoeal illness (especially if bloody). Look for signs of kidney injury - (oliguria, deranged renal function) and anaemia. If suspected a blood smear should confirm haemolysis is occurring. Most will get better with supportive measures, a few will need renal support, and a few will need plasma exchange to get rid of the toxin.

Phew... I really didn’t mean to write so much, but with the newspapers discussing HUS on the front page, how could I not join in? Hopefully we’ve learnt something useful....

FEAST video

2011-06-03T06:24:00.000-07:00

Many thanks to @AndyNeill for pointing out this video about the FEAST trial I discussed in my last post, amazing stuff.

Fluid therapy in shocked children - NEJM article

2011-05-27T05:23:00.000-07:00

I have mentioned this article on twitter already, but I think it is such an important piece I wanted to write about it in a little more detail. I would also like to express my admiration for the authors here; a study challenging established practice is always difficult, especially in paediatrics, and even more so in a resource poor environment.

The article in question is the FEAST trial, published in the NEJM. It is a RCT conducted in 3 West African countries. They included 3141 kids with 'severe febrile illness' and evidence of shock (low GCS and/or respiratory distress, AND evidence of poor perfusion). Excluded were children with gastroentetritis, or those shocked because of trauma or burns. The 29 children with severe hypotension were grouped separately (difficult to justify withholding fluid bolus from them!) and effectively excluded.

The 3141 children were randomised between:

20mls/kg bolus of saline over 1 hour (repeated if signs of shock persisted)
20mls/kg 5% HAS over 1 hour (repeated if signs of shock persisted)
Maintenance fluid only.

All children received standard care otherwise (maintenance fluid, abx, antimalarials etc). The protocol was amended during the study and the fluid bolus volume increased to 40mls/kg.

The primary end point was mortality at 48hrs, a solid an end point as you can get.

As you may have guessed from the interest surrounding this study, the results go against our established practice. Mortality in children receiving a fluid bolus was 3.3% GREATER than those who did not; a relative risk of 1.45 (95% CI, 1.13 to 1.86; P=0.003). There was no difference between the NaCl and HAS groups.

Now this is a dramatic finding, and is sure to generate a lot of discussion. Fluid bolus therapy is a mainstay of paediatric critical care and any challenge to this needs to be carefully scrutinised. To my eye, the results seem valid. The sample size is large enough (although the trial was stopped early as the clinical effect became apparent), well randomised and the multi-centre nature of the trial does not seem to have produced significant hetrogenicity. There was very little crossover between groups.

There are points that need thinking about though:

We already know that excessive fluid therapy can be bad for children (cerebral and pulmonary oedema can be a real problem). However very few children developed these problems in this group.

How applicable to are these results to practice in the developed world? These children were very sick (presentation of illness tends to occur later in the developing world), will have had different pathology (quite a few had malaria) and the clinical environment would have been very different (no CVP monitoring here!).

Also, remember that children who were severely hypotensive were not included, no one is suggesting that we do not give fluid boluses in them.

So, should we all now go away and stop giving fluid boluses to sick children (and rewrite a large chunk of the APLS manual)? Not yet, but this result certainly raises questions that need to be urgently answered. It will be interesting to see the responses and debate about this over the next few months.

For me this touches on a larger issue, the need we have in emergency/critical care to chase 'normal' physiology. Many of the symptoms of shock we look for are evolved responses to a severe illness. Are we doing harm by trying to correct them, rather than letting the body sort itself out?

Last but not least, this article illustrates the importance of challenging custom and practice. just because 'we've always done it this way' doesn't mean it's right!

Lots to think about here. Would be very interested to hear everyone's opinion on this. Thoughts? Comments? Disagree with my intepretation? Please leave a comment, or get into a twitter debate @DrGDH. Thanks for reading!

DKA guidelines

2011-05-25T10:32:00.000-07:00

Quick one this time, these guidelines for DKA was released by the NHS last year. While I am not going to take on a whole ‘management of DKA’ post, I thought that the guideline had enough interesting points to warrant a few lines. It is also a nice concise piece of guidance, and explains the basic pathophysiology well.

The main thing that struck me was the emphasis on managing the ketonaemia rather than focusing on the hyperglycaemia. I admit I have been guilty on fixating on the blood sugar level as a way to gauge my management; this guideline focuses much more on the blood ketones (or bicarbonate/pH as a surrogate for this).

The big change in management for me is the use of a weight based dose for the insulin infusion. This is a change from the traditional ‘sliding scale’. Specifically this guideline recommends:

Infusion of 0.1 units/kg/hr of insulin

Aiming for:

Reduction of blood ketones by 0.5mmol/L/hr

Reduction in venous bicarbonate by 3mmol/L/hr.

Reduction of blood sugar by 3mmol/L/hr

If these are not achieved then infusion rate can be increased by 1 unit/hour until these targets are met. Blood glucose is not a reliable indicator of resolution of acidosis so bicarbonate and/or ketones should also be measured.

I like this a lot, a much more structured and measurable way to manage these (potentially sick) patients than my previous practice. Kind of a EGDT for DKA!

NIV in pneumonia

2011-05-17T16:23:00.000-07:00

I wanted to include a bit specifically on pneumonia because, at least in my experience, it is a common use for NIV. Outside of critical care, NIV tends to be tried in people with pneumonia and respiratory failure (who are not suitable for IPPV) as a ‘ceiling of treatment’.
The evidence is nowhere near as conclusive as it is for COPD. The original trials that revealed a positive benefit in COPD (see previous entry) tended to exclude those patients with pneumonia.
In addition, the majority of the trials tend to be conducted in a critical care setting, with patients rapidly switched to invasive ventilation if they are not improving. This makes it difficult to generalise the results to our patients on a general ward for whom NIV is the ‘ceiling of treatment’.

In 2004 Keenan et al published a systematic review in Critical Care Medicine. They found a reduced rate of intubation in patients with hypoxaemic respiratory failure (they excluded those with CPO). They also noted a possible mortality benefit but commented on the heterogeneity of the studies they looked at.
This is a recurring problem, there are studies with very different results out there; because the patient group with respiratory failure will include a wide range of pathology. Some of them, e.g. those patients with CPO or COPD, we know may benefit from NIV. This is well illustrated in this piece by Phua et al. They looked at 111 patients in hypercapnic respiratory failure from a variety of causes. Unsurprisingly the patients with COPD came out the best, with a rate of failure of NIV of 19%. In those with other diagnosis the risk of failure of NIV was 47%. Those with pneumonia were at the greatest risk of failure; 65%. These patients were all managed in an ICU setting on an all singing/dancing ICU ventilator, not the portable things that I use on the wards and in the ED. So we can imagine that outside of that setting the failure rate would be even greater.

The theme from evidence seems to be that a significant proportion of patients with pneumonia will fail a trial of NIV (i.e end up intubated or palliated). However there are benefits to be found. Jolliet et al found a similarly high failure rate - 66% of patients with pneumonia ended up intubated. However in those who did not had shorter stays and improved mortality. Now this could of course all be due to treatment bias (the patients who were less poorly and stayed on NIV may have done better anyway), but it is easy to see why avoiding IPPV would be a good thing.
Now what to conclude from all this? Patients with pneumonia and respiratory failure do not do well on NIV, and many end up intubated. However, it may avoid intubation in some patients, especially those with underlying COPD. This makes it reasonable to try NIV on these patients in a critical care setting where close monitoring and rapid access to IPPV is available. Bear in mind however that these patients may have other reasons to intubate and ventilate them, e.g. septic shock - most studies exclude patients who are haemodynamically unstable.
The situation is much less clear in those patients outside of ICU who are deemed not suitable for IPPV. In view of the possible benefit we have identified it is probably worth trialling NIV in these patients. However this must be accompanied by a clear plan of action in the case of failure - e.g. planning to institute palliative measures if no improvement over first 12 hours. This is vitally important if we are to ensure that a futile, uncomfortable therapy is not continued longer than necessary.

Super. This NIV thing is getting well out of hand. The next post will be to explain how I go about using it in practice; then that will be it for NIV.

Blog, presentations etc...

2011-05-10T14:00:00.000-07:00

Neglected the poor blog for a bit, will do some proper work soon.....

In the meantime, the Brain Failure presentation from the med student acute care talk is here for those who asked for a copy:

NIV in cardiogenic pulmonary oedema

2011-04-28T03:02:00.000-07:00

(apologies in advance for the terminology used here, some of it is not strictly kosher.... CPAP is not technically NIV, and BiPAP is actually a trade name. For my purposes, BiPAP is a bilevel pressure support, and NIV covers any use of non invasive support)

We have discussed the use of NIV in patients with exacerbations of COPD. This is well established and the reason why NIV has become a common sight on our wards.

There are other groups of patients who may benefit from NIV. Patients with cardiogenic pulmonary oedema (CPO)have been managed using non invasive ventilation for many years. In 1985 it was noted that CPAP clinically improves patients with CPO. Since there has been extensive work confirming improvements in symptoms, physiology and reductions in intubation rates and mortality (like this). The evidence has been better for CPAP than BiPAP, and one metanalysis suggested BiPAP may increase the rate of MI.

Now in 2008 there was a big trial published in NEJM called the 3CPO trial. This was good stuff; multi-center, randomised, and well powered (1156 patients). They divided patients with a respiratory acidosis and CPO into 3 groups: normal 02 therapy, CPAP and BiPAP. All patients got medical therapy. And what did they find? There was little difference between the two NIV groups. Compared with standard therapy, NIV improved acidosis and dyspnoea. But it didn't improve mortality or reduce intubation rates! D'oh!
Now this was at odds with established practice, and people were quick to object..., saying the sickest patients were not included. However the authors point out that the mortality rate was similar for patients were were included and those not included in the study, which suggests patient selection bias was minimal.

A careful look through the methods reveals a possible explanation; the power calculation was designed to have an 80% chance of detecting a 6% mortality benefit. Now as mortality benefits go this is pretty generous. Add the fact that the study did not quite achieve the number patients it required for this calculation (1200), and it is conceivable that a mortality benefit was missed.

We could spend a long time arguing the pros and cons of this study. Bottom line: Should we use NIV for our CPO patients? Yes we should. There has been no suggestion of harm (the risk of MI with BiPAP has not been supported by 3CPO), and the fact it improves symptoms is reason enough. There is enough suggestion of benefit to mean we should consider it for patients not improving with medical therapy. CPAP or BiPAP? Still a difficult question, CPAP tends to be better tolerated in my opinion, but the increased minute volume BiPAP provides may be useful in severe respiratory acidosis.

Love a trawl through pubmed on a sunny morning! Pneumonia and NIV next....

It's not a drug....... It's a gas!

2011-04-11T13:55:00.000-07:00

While not strictly a NIV topic, the issue of oxygen therapy in COPD patients comes up time and time again. A case report in the current BMJ (http://www.bmj.com/content/342/bmj.d1557.full) has got me thinking about it once more.

The point the case report is making is that COPD patients can suffer rebound hypoxia if their supplementary oxygen is removed. I was more interested in the clinical scenario and what learning points we can bring out from it.

The story is as follows: an elderly lady with confirmed COPD was admitted with SOB. On admission her oxygenation was fine on 24%. She was managed with the traditional COPD/pulmonary oedema/pneumonia cocktail and sent to the ward. The admitting doctor prescribed her oxygen, noting that: "oxygen therapy should be given at 24-28% via a Venturi mask, aiming for a target SpO2 range of 88-92%.” Top banana so far...

Later on the ward our lady took a turn for the worse. Her Sp02 was noted to be 85% so her oxygen was increased to 4l/min via nasal cannula. Here is where we start beating our heads against the wall:

Why were nasal cannula used, when Venturi masks were prescribed? All too often masks are changed to nasal cannula on wards because they are easier for staff and patients. But oxygen is a drug, with right and wrong doses. Too much or too little can cause problems. BTS guidelines explicitly state that oxygen should be prescribed, and dose, method of delivery and target spo2 should be noted. Here, the dose and method of delivery are changed despite what was on the prescription (can you imagine this happening with GTN or potassium chloride?)

So why do we not like nasal cannula? Simple, you don't know how much oxygen you are giving your patient! With a Venturi mask, you know the patient is getting 24% or 28% oxygen etc. With nasal specs, you are giving a volume of oxygen each minute. Think about it: if your patient is given 4l of oxygen via nasal cannula, and is breathing a minute volume of 6l a minute, then 2/3 (66%) of it is oxygen. However, if they get sick and start breathing faster, say 12l a
minute then 1/3 of it (33%)is oxygen. So you really don't know what the hell is going on when you strap nasal specs to your patient.

Back to our patient. After the oxygen was increased, she was found drowsy and hypercapnic. This probably occurred because she was receiving a high concentration of oxygen via the nasal specs (the mechanism for this is disputed.... that's for another day). Now the doctor who arrived to review her found her Spo2 was 100% decided to remove the oxygen to 'treat' the respiratory failure.

This is idiocy. Plain and simple. This lady had been found to be hypoxic and unwell very
recently, and we decide to take the oxygen away. Unsuprisingly she got very unwell (with a Sp02 of 59.6%).

So what should we have done here? If we treat oxygen as a drug then the answer is obvious: give the right dose! The key here is to get the Sp02 right. Change the oxygen, check the Sp02 and adjust as needed. This needs time and careful observation. The moral is that if you change something, check what effect it has had. If our friend above had checked the Sp02 soon after taking the oxygen away it would have been clear it wad a bad idea.

Right, I've waffled quite a lot here, but this kind of thing really gets on my nerves. To summarise:

1. Prescribe oxygen - dose, delivery method and target Sp02.
2. Nasal specs are bad news in sick patients.
3. Get the Sp02 right! All of the concerns about too much oxygen and hypoxic drive become moot if we target the correct Sp02 (94-98% in most people, 88-92% in COPD). If a patient has appropriate saturations and is still hypercapnic, then they need ventilatory support.

More Non-Invasive Ventilation

2011-03-31T08:40:00.000-07:00

In the last entry we discussed selecting COPD patients for NIV. Today we are going to think things that might make a patient unsuitable for NIV.

As with most medical interventions, there are absolute contraindications (things that make NIV impossible or extremely dangerous) and there are relative contraindications (things that make NIV less suitable, but it may still be appropriate).

The absolute contraindications for NIV are mostly common sense. Many of them are factors that mean the patients has an unsafe airway. A patient with an unsafe airway needs airway management, and probably invasive ventilation if respiratory support is required. NIV can make airway management more difficult and problematic (think about a vomiting patient with a NIV mask on...... not pretty).
Upper airway obstruction, vomiting, facial or airway burns and recent ENT surgery are all things that make NIV too dangerous to contemplate. Recent upper GI surgery is also a contraindication. The other important contraindication is an undrained pneumothorax. Any kind of positive pressure ventilation can force air into a pneumothorax, making it larger, and potentially causing it to tension. If the patient has a chest drain, then no problem.

As with everything else, an important contraindication for NIV is refusal of consent in a competent patient.

There are another group of patients for whom NIV is relativily contraindicated. We say this because they are usually excluded from the research populations, so we cannot say for sure that NIV will help them. These are patients who are probably better off going to ITU for intubation and invasive ventilation. However, this may not be appropriate. The discussion about who is and isn’t suitable for ITU is long and contraversial, but there will be a group of patients with COPD who are not admitted to ITU, because it is consideried futile. In these patients NIV may be used as a second line therapy.

Severe acidosis: Patients with a pH of <7.26 have a higher mortality and are more likely to fail on NIV (see the latest numbers from the national audit here). Therefore most guidelines suggests that they be referred to ITU for invasive ventilation or NIV in a critical care environment.

Low GCS: a GCS of <8 implies an unsafe airway. As we discussed above, NIV in a patient with an unsafe airway is not a good idea. However, if patients are not suitable for invasive ventilation, then it makes sense to try it. There will be a group of patients who are obtunded by their high C02, and may recover reasonable quickly with NIV.

Hypoxia: If a patient is hypoxic despite high flow oxygen, then ITU need to know. With some NIV ventilators it is possible to deliver high concentrations of oxygen that will help these patients, but even so, critical care is the best place for these patients so they can be watched.

(IMPORTANT: many of the portable NIV machines you see on wards are air driven. This means they cannot deliver high concentrations of oxygen, so putting a hypoxic patient on them will make matters worse. Get to know the machines you use and what they can and can’t do).

To sum up all that...

Some patients are absolutely not appropriate for NIV; and these are mostly those with potential airway problems. There are also a group of patients for whom optimum management would be invasive ventilation, but may be suitable for NIV if this this is deemed inappropriate. These patients include the comatose and the hypoxic.
Patients who are severely acidotic (pH <7.26) do better when managed in a critical care environment whether they end up intubated or not, so should be discussed with ITU.

Next up is NIV in other groups such as patients with pulmonary oedema or pneumonia.

Compartment Syndrome

2011-03-20T14:59:00.000-07:00

Completely off topic again, but a patient today has got me thinking about compartment syndrome.

Compartment syndrome, simply put, is the damage done to tissues by an increased pressure in a body 'compartment' - usually a muscular compartment in the arms or legs. Most common in the limbs, it can occur in any space in the body; abdominal compartment syndrome is well documented. I will be focusing on compartment syndrome in the extremity.

CS has a myriad of causes. The most common and widely quoted is traumatic injury especially fractures (tibial fractures are a frequent cause). The other frequently mention cause is drug overdose - lying on a hard surface in an awkward position for a lengthy period of time can causes CS. A great study from 1979 by Owen et al looked at pressures in muscular compartments in collapsed patients. Resting your head on your forearm can cause a pressure of 48mmHg, one leg atop another 78mmHg, and lying with your arm under you can subject your tissues to 178mmHg!. It is easy to understand that these pressures even over a short time can cause damage.

Other causes of CS include excessive muscle activity (v. strenuous exercise, seizures), infections causing muscular inflammation, bleeding into a muscle, compression from a tourniquet or cast.

Whatever the cause - the underlying pathology is the same. The pressure in the compartment is increases to the point where blood flow is compromised. If this persists over time, then the tissues become ischaemic and inflamed. This causes oedema, acidosis and further rises in pressure. This vicious circle continues until tissue necrosis sets in.

I find the concept of tissue perfusion pressure useful here. The tissue perfusion pressure can be thought of as:

Capillary perfusion pressure - interstitial fluid pressure

It is simple enough to see from this that if the pressure in the interstitial fluid is raised, then the tissue perfusion will fall. If this continues then the perfusion falls to the point where oxygen delivery to the tissues is compromised and eventually capillaries collapse. The tissues become hypoxic and the damage begins. Exactly what pressure is needed to cause this is not clear, but most seem to think that a pressure of 30mmHg in a compartment needs sorting out.

CS is one of those conditions that can be so devastating that you need a high index of suspicion for it if any risk factors are present. When assessing a patient, the most worrying sign is pain, often severe and out of proportion. Pain that increases with passive movement and stretching of the muscle is often the earliest sign.

As pressure increases the next thing to be affected are nerves. A careful neuro exam is vital to assess motor and sensory dysfunction. As pressure increases further the tissues may feel hard to the touch ('woody' is often the word used). Signs of arterial compromise (loss of pulses) are a very late sign.

If CS is suspected, the compartmental pressures can actually be measured. It is simple enough to do with the right kit and a knowledge of the anatomy involved.

The cornerstone of management is fasciotomy. This is simply means a surgeon makes incisions in the fascia surrounding the compartment to release the pressure. Often more troublesome are the systemic effects. If CS has progressed far enough and necrosis has set in then the dead muscle can release unpleasant things into the circulation; this can lead to renal failure. Keeping the patient well hydrated improves tissue and renal perfusion and can help prevent complications.

To sum up........

CS is caused by increased pressure in a body 'compartment', most commonly in the lower leg. This increased pressure compromises the capillary blood supply to tissues. A high index of suspicion must be maintained, especially in patients with fractures of the long bones or those who have been collapsed for a period of time. Severe pain, exacerbated on passive movement is the key early sign. Compartment pressures can be measured at the bedside. Fasciotomy is the definitive management.

Blimey...... Right, next time I will be back on NIV.

2011-03-08T00:51:00.000-08:00

Bit of a delay in getting on with this entry, but here we are. In the first entry I discussed the definitions of NIV and a little background, Today we will discuss the kinds of patients NIV is used on,

We have already said that NIV is a common sight on the wards. The main reason for this is its usefulness in patients having an exacerbation of their COPD. An acute exacerbation of COPD is one of the most common diagnosis needing admission to hospital (second only to pneumonia) and represents a huge cost to the NHS. NIV has been shown to improve outcomes in COPD exacerbation, as well as reducing hospital stay and costs (which in this day and age is more important than ever).

This is an intervention with a good evidence base, and has been going on a long time. In 1995 Brochard et al found reduced mortality (9% vs 29% p=0.02), reduced need for invasive ventilation (26% vs 74% p<0.001) in patients managed with NIV rather than ‘standard’ therapy. A subsequent trial by Plant et al in 2000 found similar improvements in outcomes and a cost benefit analysis of the same trial found that an average UK hospital could prevent 6 deaths and 9 ICU admissions a year and save £12000-53000 by using NIV. No wonder it is so popular! NIV is included in all the big guidelines for COPD management, including those published by NICE and the British Thoracic Society.

An acute exacerbation has many definitions, but simply it is an worsening of the symptoms of COPD. This means increased breathlessness and increases sputum production. From a physiological stand point the problems encountered are all to do with respiratory compromise. Patients may present in respiratory failure, and the presentation classically associated with COPD is ‘type II’, i.e hypercapnic or acidotic failure (I really don’t like the terms type 1 and type 2 - why over complicate things and give yourself something else to remember? ‘Hypercapnic failure’ and ‘hypoxic failure’ make much more sense).

So why does it help? The problem in patients with a respiratory acidosis is a failure of ventilation. This is a product of decreased respiratory effort (due to fatigue) working against an increased airway resistance (due to mucous and bronchospasm). This means the amount of air they can physically move in and out of their lungs (their tidal volumes) is reduced. As the patient tires they are unable to get rid of the C02 being produced and the level in the blood increases. This has many detrimental effects, the most important being reduced level of consciousness and eventually coma.

Putting the patient on NIV increases their minute ventilation. It delivers a tidal volume to the patient, and the pressure support decreases the work of breathing. This should increase the amount of C02 excreted and therefore treat the hypercapnia.

From what we have said above, we can work out that the patients who are going to benefit from NIV are:

Those with a diagnosis of acute exacerbation of COPD
With a respiratory acidosis (ph < 7.35)
Who have not improved rapidly with standard management (i.e nebulisers, controlled 02, steroids)

Of course it is not as simple as that. There are certainly great benefits to using NIV in exacerbations of COPD, and there are good quality trials to support this. However, some patients may not be suitable for NIV, and some patients may benefit from alternative management. Also, some patients without COPD may benefit from NIV. In the next section (this one has got a bit mammoth already) we’ll talk about inclusion and exclusion criteria, and also touch on NIV in other patients, such as those with pneumonia or pulmonary oedema.

Non Invasive Ventilation

2011-02-22T14:28:00.000-08:00

This is another of my favorite subjects, and something that anyone working on a medical ward will deal with NIV at some stage. We're going to split this up into 3 or 4 entries, and I want to start with going through exactly what NIV is and what it is for.

Defining NIV can be a challenge, simply because there is a lot of terminology and acronyms out there. Simply put NIV is the delivery of ventilatory support without a endotracheal tube. This is accomplished using a tightly fitting face or nasal mask. The most commonly encountered type of NIV is bilevel positive airway pressure (BiPAP). In BiPAP the ventilator delivers a high inspiratory pressure (IPAP) and a lower expiratory pressure (EPAP). The change in pressure delivers a tidal volume to the patient.

There are several benefits to supporting a patient in this way:

1. The work of breathing is reduced, which is vital in a tiring patient. As a patient gets tired the respiratory effort decreases. This reduces the amount of air they can move in and out of their lungs (minute volume). Eventually this reaches the point where patient cannot shift their CO2 and they become hypercapnic and acidotic. By decreasing the work of breathing and improve minute volumes CO2 is shifted and the acidosis improves.

2. Recruitment. The application of the EPAP means alveoli are splinted open and prevented from collapsing. This means there is more lung getting ventilated, and blood that would be flowing through collapsed lung sections is now flowing past nicely perfused alveoli and getting oxygenated.

3. Delivery of high concentrations of oxygen. By delivering oxygen under pressure higher concentrations can be given to patients than the 50-60% that can be given with normal oxygen masks (note - some of the smaller, portable ventilators that you may find on the wards are air driven. This means that the pressure is generated using air and the oxygen only enters the system at the mask. These ventilators are not capable of giving a high concentration of 02 - make sure you know what your machine is capable of).

I haven't mentioned CPAP yet. Constant positive airway pressure delivers the same pressure throughout as the patient breaths. This has many of the benefits listed above, but no actual ventilation takes place and minute volume is not directly improved, and therefore it is not a suitable treatment for hypercapnic acidosis.

That a lot of typing so I'll stop here. Next time I want to talk about the indications for NIV and which patients are and aren't suitable for it.

Nutrition in Pancreatitis

2011-02-15T11:36:00.000-08:00

Ok, last but not least. Should we feed patients with pancreatitis?

The answer is a resounding 'it depends' (isn't it always!?). Traditionally patients with pancreatitis were not fed. The (seemingly sensible) idea is that gut rest reduces stimulation of the pancreas and reduces the production of all those enzymes that are causing havoc in the first place. This make sense, and indeed is absoluitly fine in patients with mild pancreatitis. These patients will, after a couple of days of IV fluids, sort themselves out and they can start eating again once their symptoms are improving.

However, can we use the same approach with severely ill patients? These patients may be unwell for a long time, and starving anybody for days and days on end is not a good idea, especially those catabolic, critically ill patients who need all the calories they can get to help recover. For a long time these patients were fed intravenously; but this has its own problems, most notably parental nutrition increases the risk of infection. If you remember from the post on antibiotics in pancreatitis, pancreatic infections are bad news.

It was in the 1970's that people first began considering the risk/benefit of feeding patients with severe pancreatitis. It was suggested that feeding directly into the jejenum might reduce the pancreatic stimulation while avoiding the intravenous route. There was subsequently a great deal of research into this possibility.

So what was the outcome of all this work? It seems safe to conclude that patients who are fed early via the nasojejenal route do better than patients fed intravenously, there are several metaanalyses that support this.
Although results vary, there has not been any suggestion that outcomes are worse when NJ feeding is used, so it would seem a good idea to use this route and avoid intravenous feeding.

The main downside to all this is that placing a nasojejunal feeding tube is not a straightforward task. It is often done endoscopically but there are methods that allow placement at the bedside. It is certainlyt more difficult than placing a NG tube.

Interestingly, there is a growing amount of evidence that NG feeding can be used in these patients. The evidence base is small however and more work is needed. If this was confirmed it would be a important finding.

That seems about enough for now. So to sum up......

In severe pancreatitis: NJ feeding good! TPN bad! NG feeding......maybe!

Neurological Examination

2011-02-11T00:54:00.000-08:00

This is the link to the neuro exam presentation from 9/2/11, enjoy!

http://prezi.com/ra62x-7b-dyl/neuro-teaching/

Swine flu and hyperimmune plasma

2011-02-07T05:45:00.000-08:00

Another diversion from pancreatitis today, but thought this was cool enough to warrant a few lines. We have been discussing hyperimmune plasma on the unit today, specifically for H1N1 flu.

Now this isn't something that we are going to come across very often. It is pretty experimental and available on a compassionate basis, only for patients who are critically ill with H1N1 and who have not responded to conventional meds.

So what is hyperimmumne plasma? This is the cool part. They find patients who are recovering from flu (convalescent), and use their plasma (which is loaded with flu antibodies) to treat the sick ones. This is pretty awesome, like something Dustin Hoffman would think of while trying to catch that monkey. They have also used this technique to treat things like rabies and measles.

Again, not relevant to most people's day to day practice, but you've gotta love stuff like this. If you want to know more there is a meta-analysis here. As I said above, for H1N1 this is experimental; this meta-analysis looks at H5N1 (bird flu). This review from Chest gives a good overview of the management of H1N1 in general.

Fantastic, I'm definitely going to finish pancreatitis soon. The last bit will be about nutrition in pancreatitis.

EMJ Feb 2011

2011-02-02T13:09:00.000-08:00

Another month, and another bright red journal lands on my doormat, must be EMJ day!

Quite a bit of interesting stuff this month, starting with the cover telling us that '50-70% of emergency medical personnel can be described as resilient and stable". Which makes me somewhat concerned about the 30-50% of unstable people I work with...

Acute respiratory failure is the subject of the next article, in what seems to be the start of a series of educational features. This one focuses mainly on NIV and it's role in the ED. It's a good overview of NIV in general. NIV is becoming increasingly common in many areas of the hospital and patients on NIV are increasingly managed by junior doctors, so overviews such as this are very useful.

Note the reference to the 3CPO trial - this is a piece of work all acute/emergency docs should be aware of - a large multi centre RCT found that NIV improves symptoms and ABG results in cardiogenic pulmonary oedema, but not mortality (this is controversial) Interestingly CPAP and BIPAP were not found to be much different.

My other highlight this month is a piece on echo in life support. This is written by the some of the same guys who run the emegergency ultrasound courses on Ipswich and Cambridge. I'm a big fan of bedside ultrasound; it going to become much more common place in the future. This piece demonstrates that even in the ten seconds available to scan during ALS, useful information can be gleaned.

Antibiotics for pancreatitis??

2011-01-31T13:42:00.000-08:00

After a brief distraction by an interesting case of discitis, I'm reading up on pancreatitis again - this time its antibiotics.

As I mentioned i n the first pancreatitis post, pancreatitis has two main stages. The first is the SIRS response resulting from the inital insult. Following this, patients can either get better, or go on to develop pancreatic necrosis. This can be sterile or infected necrosis. As you would imagine, infected necrosis is bad news.

So when thinking about antibiotics we have several questions (or 'learning objectives' if you want to get all PBL about it):

1. Do antibiotics benefit patients in the early stages? Can they reduce the risk of necrosis?
2. Do antibiotics reduce the risk of necrosis becoming infected?
3. In infected necrosis what antibiotics should we be using?

Lets look at each of these in turn:

1. Early panceatitis - antibiotics are not of any benefit in patients not displaying signs of severe pancreatitis. Non-necrosis pancreatitis is not at risk from infection and antibiotics will do little to alter the course of the SIRS response. They do not reduce the risk of progression to necrosis. However, the case is less clear in severe acute pancreatitis or where necrosis is present.

2. Where necrosis is present on CT, antibiotics may be beneficial. The evidence is somewhat ambigious here. A recent meta-analysis by a Petrov et al found no significant benefit for antibiotics, but a non significant trend towards lower mortality was noted. The updated Cochrane review came up with a similar result. It is interesting to note however that even the Petrov meta-analysis (the most comprehensive one out there at present) only included 467 patients - could this be underpowered to detect a benefit?

3. What antibiotics? To pick an antibiotic we need to know two things - what bugs are we after (type and sensitivities), and will our antibiotic get to them (penetrance into tissue). The paper by Buchler et al I mentioned in the last post found that the majority of infected necroses were caused by gram negatives; mostly GI bugs such as e-coli. This is consistent with the current theory that infected necrosis occurs via translocation of bacteria from the gut. The most commonly cited drugs in trials seem to be carbopenems, which have been shown to penetrate necrotic pancreas well.

So far so good. However its not all plain sailing. There has been the suggestion that throwing broad spectrum antibiotics at these patients is not without problems. It has been postulated that an increased number of gram positive and fungal infections occur when antibiotics are used prophylacticaly. Now, you don't have to be an expert to realise that having fungus growing in your necrotic pancreas is really, really bad news. Of course, then someone suggest that we should be giving everyone antifungals too.... (the evidence is still out on this one, but it goes to show that for each question you answer, more will pop up!)

So, in take-away form (i.e wrapped in greasy newspaper): antibiotics in pancreatitis only if severe acute (i.e the really sick ones) or if necrosis seen on CT. Even then, the evidence is on the fence, and we may be causing harm.

So, years of hard work and rigorous research and....... we're not sure.

Discitis - one of those rare things you need to know about.....

2011-01-28T14:39:00.000-08:00

Slight distraction from pancreatitis, I've been reading about discitis.

Discitis is an inflammation of the vertebral disc space, usually associated with infection. Its pretty rare but its something that you have to be aware of - it can be difficult to diagnose and
can have serious complications. Anyone presenting with back pain and signs of infection needs working up for spinal infections as a matter of urgency. There are two peaks of incidence - 7and
50yrs of age.

Discitis rarely appears spontaneously. It is seeded from another infection, commonly UTI, pneumonia or soft tissue infections. Infection can also be caused by dirty needles in injecting
drug users. Discitis can rarely occur after spinal surgery. In kids, there is usually no other source of infection found.

Back or neck pain is the most common presentation, often with an insidious onset over weeks or months (in kids the presentation is much more acute, associated with refusal to walk). Invariabaly there is local tenderness. The back pain is worse on moving, better if still, and it doesn’t get any better with the usual back pain measures such as rest, NSAIDs.

As with most orthopaedic and soft tissue infections - gram positives are usually the cause, specifically staph aureus. If a UTI is the primary cause then gram-ve bugs such as e-coli could
be the cause. Pseudomonal discitis can occur in IVDUs

If suspected discitis is best imaged using MRI. CT can be a more easily available option, and CT is useful for guiding biopsy so samples can be obtained for culture. Plain x-rays can detect
discitis and associated vertebral osteomyelitis but only at a late stage. Other investigations include the usual sepsis stuff; blood cultures and the like. ESR can be useful for monitoring
response to treatment.

Treatment is with antibiotics, broad spectrum to start then guided by culture results. A long course is needed: 6-8 weeks. Surgery is sometimes indicated if antibiotics aren't doing the job, or as an emergency if there is neurological deficit.

So.... discitis to go: suspect if back pain and signs infection, usually seeded from another infection. MRI is best, CT OK, CT guided biopsy for culture. Most common bug is staph aureus.
Needs 6-8 weeks antibiotics, surgery if no improvement or neurological involvement.

Pancreatitis in ICU

2011-01-26T15:44:00.000-08:00

Have been reading a lot of pancreatitis lately. Today I'm on about surgery for pancreatitis.

In the 1970's and 80's patients with severe acute pancreatitis underwent early laporotomy and they didn't do well. This makes sense when considering the natural history. The early stage of pancreatitis is characterised by a SIRS response and surgery would only excarbate this. If these patients don't get better they end up with a necrotic pancreas. This can sometimes get infected, which is bad (imagine your pancreas dissolving into a mass of infected black goop). Surgery is essential to remove this source of sepsis.

A guy named Hartwig did a great bit of work in 2002. They looked at pancreatitis patients admitted over 17 years. Over this time the recommended management changed from early laprotomy to late surgery on those with pancreatic infection only. Mortality in patients treated with surgery fell from 39% to 12% - a great improvement in anyone's book. Outcomes for patients managed with no op did not really change, suggesting it was not improvements in supportive management that accounted for this improvement.

So, if we think that late surgery is better, who do we operate on? How do we decide who needs surgery? Buchler et al trialled a treatment regime using CT guided fine needle aspiration to find the infected pancreases that needed removing. If someone got sicker or seemed septic then a FNA was performed. If this was positive then they were whisked off for surgery, if not , they stayed put. This approach seems to work, and is rapidly becoming accepted.

So....... surgery for everyone is bad. Surgery for infected necrosis...... good. FNA to look for infection if patients not improving.

Next bit will be feeding in pancreatitis, or antibiotics in pancreatitis, or something to do with pancreatitis, provided I don't get bored of it.