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High care and intensive care.
Resuscitation
Resuscitation – when to do it
If in doubt, start resuscitating while you are thinking further.
The ethical concept of ‘medical futility’ is the key to the decision making process. Medical futility[1] is a state where, even with good quality care, a patient is not likely to live a meaningful independent existence.
Don’t automatically be nihilistic if people are old – they sometimes do very well.
The key feature is reversibility. If somebody has an underlying good prognosis or even though quite frail has had a sudden acute, reversible event (diagnosable as such), then try. If the acute event is unclear, it is more likely to be something like a CVA or massive myocardial infarct, and the outcome is unlikely to be good.
Resuscitation – how to do it
- Start cardiac resuscitation – a limited amount of ventilation will occur during the process by its very nature. (Try a ‘thump version’ first). Initial oxygenation may not be as urgent as originally thought, although this probably depends on the cause of the arrest[2] (and the two articles alluded to in this editorial applied to out of hospital resuscitation by lay-person bystanders.)
- Note the time.
- Start hand bagging using an airway and mask.
- Inject adrenalin 1 ml of 1:1000 (i.e. 1 mg) into a drip and flush it through. If there isn’t a drip, put it into a big vein that you are comfortable about accessing – preferably the subclavian or internal jugular, but if you aren’t happy with these and can feel a groin pulsation with the CPR, use the femoral vein.
- Continue with the CPR, keeping an eye on the time – there are no hard and fast rules, and drowning victims and hypothermic patients may have marvellous outcomes even after a considerable time; in most other situations however, if you aren’t getting anywhere after 20 to 30 minutes, you are unlikely to succeed.
- If you aren’t having any luck, give another 1-3 ml of adrenalin 1:1000 in increments intravenously.
These are the key components. All the rest looks impressive, but is just embellishment of the above – endotracheal intubation, a central line, and DC cardioversion are all worth a try, but if you can do the first bit, then somebody else can come along and help with the rest.
DON’T spend ages trying to intubate if you aren’t very familiar with the technique.
DON’T spend ages trying to get central venous access if you aren’t very familiar with the technique .
DON’T do cardiac compression the way they do it on TV soapies. The correct way is the way you were taught. The thorax has to get a bit squashed with each push, otherwise it doesn’t work…
Perspective – rapid response teams and clinical outcomes
A narrative review[3] identified a number of observational studies giving mixed results but only one large (125 132 patients) cluster randomised study[4], and this showed no effect on mortality (OR 1.03, 95% CI 0.84-1.28) or cardiac arrest rate (OR 1.31, 95% CI 0.79-1.13.) This serves as a reminder that in medical patients with multiple organ dysfunction, resuscitation is not often successful, and attention should be given to identifying patients at risk and fixing their problems timeously.
Ventilation
When to ventilate – be alert:
An asthmatic who seemed to be coping and is now getting restless, or an asthmatic who was unhappy and has now gone quiet without an improvement in peak flow.
Any unconscious patient who doesn’t cough on suctioning.
A paralysed patient (Guillain-Barre or myasthenia gravis) with an FVC of less than 1.5 litres, or 20 ml/kg. (Remember that measuring peak flow is misleading under these circumstances.)
Any gasping patient, whether with cardiac failure or chest disease.
Any shocked patient where you don’t see the cardiovascular situation improving in the very near future, and who seems to be losing consciousness.
Progressive hypoxaemia on pulse oximetry.
When not to ventilate:
When it would be medically futile – end-stage COPD, malignancy with poor prognosis.
If you aren’t happy to intubate – wait until you can get someone to help.
When you expect to be able to reverse the situation with just a little more time. However, be very careful of this one. The little bit more time often turns into quite a lot of wasted time, and then an unseemly rush to keep things going.
Non-invasive ventilation
As a step prior to intubation and full ventilation in alert patients, it is worth considering CPAP/BiPAP which is achieved using a tightly sealing face mask in a non-intubated patient. CPAP just requires a mask with an expiratory valve, usually set at 5 to 10 cm H2O. BiPAP needs a leak tolerant machine, and controls pressure in both inspiration and expiration. It is suitable in COPD, where controlling the inspired pressure (IPAP) may help lower the CO2, and in pulmonary oedema, where expiratory pressure (EPAP) is helpful. Typical initial settings might be:
- IPAP 10 cm H2O
- EPAP 4 cm H2O
- rate 14 bpm
The machines can usually be set to spontaneous (like pressure support), timed (like controlled mandatory ventilation) or a mixture of the two (spontaneous breathing, but mandatory breaths if the gap between two inhalations is too long.) In patients with COPD it may be possible to set a short inspiratory time and a short rise time (time taken to reach IPAP.) In cardiogenic pulmonary oedema, CPAP but not BiPAP has been shown to reduce mortality, although both reduce the need for intubation[5]. Simplistically CPAP=EPAP=PEEP and helps oxygenation; IPAP increases tidal volume and helps reduce CO2 retention. A patient desaturating on CPAP is not likely to improve with BiPAP
When starting patients on BiPAP wean the patient onto the modality using verbal support and a continuous initial presence, with 2-3 cm H2O increments in pressure as tolerated.
Mechanical ventilation
The principles are relatively easy, but things can go dismayingly wrong, even if the best hands, in a very short time. There are a few principles:
- Make sure the ventilator is working and that all the necessary pipes are present.
- Check that the laryngoscope has a functioning light and the blade is big enough – you can intubate nearly any adult with a large blade, but can fail miserably on a big person with a small blade.
- Check the Ambu bag yourself.
- Suction working? Suction catheter?
- Endotracheal tube the right size? 7.5 or 8 if you don’t know better. Check the cuff yourself. Remember to take the air out again after putting it in…
- Magill’s forceps present?
- Drip up and functioning?
- Oxygen working?
- Assistant available to apply cricoid pressure?
- Is the patient correctly positioned? (Supine, head extended.)
- Have you explained what you are going to do?
- Sedation drawn up? Diazepam or midazolam.
If you sedate the patient, remember that you are making a critical situation potentially much worse. The usual reason for this is not the failure to put the tube in per se, but the need, if you fail, to mask ventilate an unconscious hypoxaemic individual now often bleeding from the nasopharynx, and with laryngeal stridor due to trauma or blood. If you do get into this unhappy situation, stay calm, mask ventilate by hand (ensuring that the Ambu bag is connected to the oxygen!) and either seek help or else re-position the head, suction carefully, and try again.
Basic ventilator settings
There are many variables that can be adjusted on modern ventilators, but the principle should be to sort out the important bits first:
Many of the settings have to do with the alarms – leave these for later.
Decide on the mode of ventilation. If you are not too sure, go for SIMV.
Choose a tidal volume – about 5 ml/kg. For a 70 kg man this is about 350-400 ml.
Depending on the machine, you can then use either the inspiratory flow rate or respiratory rate (12 – 16) to set the peak airway pressure, which should be less than 35.
The only variable left is the amount of time available to exhale – the more airways obstruction there is, the longer the desired expiratory time. (i.e. you might aim for and I:E ratio of 1:4, whereas without obstruction 1:2 or less may be adequate).
Set the PEEP to 5 cm water unless the patient has asthma or COPD, in which case do not use any PEEP.
Ventilator modes and other settings
It is possible to get quite confused with all the variations that are available. If you are stuck, go back to basic ventilator settings, and make sure most of the other things you have fiddled with are ‘off’.
SIMV – in this mode the ventilator delivers a fixed number of breaths within a finite time. The patient may trigger a breath, but once started, a fixed volume is delivered, regardless of the pressure needed to do this. Between these mandatory ventilations, the patient can breathe at will.
SIMV with pressure support. This is like SIMV in terms of the mandatory volume-limited breaths and the opportunity for spontaneous breaths between, but when the patient tries to breathe, the machine helps by pushing – it maintains the inspiratory pressure at a constant level.
Assist sensitivity. This sets the amount of pressure the patient must generate (how hard he or she must suck) before the machine recognises the change in pressure as an attempt at taking a breath. Once this value is exceeded, a breath will occur – either a volume limited one if one of these is due, or if it is within the assist window and pressure support is on, then a pressure supported breath.
Problems with ventilated patients
Restlessness
- Correct hypoxia and hypotension (see below)
- Alleviate pain (non-steroidals or opiates as appropriate)
- Check that the urinary catheter isn’t blocked
- Consider delirium tremens
- See that the ventilator setting are reasonably comfortable
- If you are fairly sure that there are no other reversible factors, sedate with a morphine-diazepam infusion after an initial bolus. Omit the morphine if asthmatic and be careful if there’s a possibility of unresolved intracranial hypertension.
Can’t keep the oxygen saturation up.
- Is the patient peripherally shut down? Saturation readings will be inaccurate.
- Is the ET tube really in the trachea, and patent?
- Are you ventilating both lungs? Reduced air entry on the left usually means the tube is in too far – pull it back a couple of centimetres and listen again.
- If the BP is okay, incrementally increase the PEEP up to 15.
- Increase the inspired oxygen concentration.
- Try changing the I:E ratio.
Persistent hypercarbia.
Usually ignore this despite the understandable urge to hyperventilate the patient. Check first that the tube is correctly positioned. Obviously, if all else is okay and you aren’t pushing other variables in order to maintain oxygenation and blood pressure, then it is reasonable to increase either rate or volume or both in order to blow off the carbon dioxide. Permissive hypercapnoea refers to deliberate Underventilation with some increase in CO2 – usually okay so long as pH >7.2.
Inspiratory pressures too high
- Tube kinked or blocked with secretions – suction the patient yourself.
- Tube down right main bronchus?
- Inspiratory flow rate too high.
- Tidal volume unnecessarily high.
- Patient fighting the ventilator.
Sudden ‘collapse’
- Pneumothorax – beware of missing it on a supine X-Ray. (A clue may be that the costophrenic angle is sharper and deeper on the affected side.)
- Tube blocked or ventilator disconnected.
- Inotrope infusion has run out.
- New arrhythmia faster than previous sinus rate.
- Pulmonary embolus or myocardial infarction.
- In surgical patients, bleeding.
- Septicaemia (temp and white cell count may not be elevated.
- A new neurological event – e.g. cerebral haemorrhage or infarct.
- A drug you’ve given?
Troubleshooting the ventilator itself
Check the basic settings – tidal volume of 400-700 ml, rate of 10-16/min, I:E ratio (inspiration:expiration time) about 1:2. PEEP of 5-10. If there are major deviations from these ranges, consider whether this could be the cause of the problem – if you need different settings to ventilate the patient adequately, then adjust the alarm settings accordingly.
Problem – low expired volume. This causes the alarm to go off because of insufficient volume returned from the patient to the machine. The causes are a leaking ET tube cuff, a loose connection (often where the flow sensor pipe connects to the expiratory limb of the circuit). After checking that the alarm is correctly set, check all the connections yourself. If the patient is well don’t get too perturbed. In particular, do not replace an ET tube with a leaking cuff in the middle of the night, unless it is essential in order to ensure adequate oxygenation. Things have a habit of going wrong in this situation, so try to avoid it.
High peak airways pressure. Is the tube down the right main bronchus? Is it blocked? (Listen and suction.) Decrease the inspiratory flow rate a bit and see if this will help, if the plumbing isn’t blocked.
The machine triggers, but won’t deliver a breath. Check you aren’t in neonatal ventilation mode – this is a frustrating facility offered on some machines, which can cause considerable puzzlement. The remedy is usually just to flip the appropriate switch.
Any other alarm going off – the usual reason is it has been set incorrectly. Think about it carefully, and adjust accordingly.
Weaning from ventilation
Although often life-saving in the short term, pumping air down a plastic pipe into someone’s lungs is not ideal, and every attempt should be made to avoid needlessly prolonging this exercise. Consider initiating weaning once the original pathology is under control, rather than necessarily fully reversed. Ideally, the patient should be fully awake, apyrexial, and saturating adequately on an inspired oxygen concentration of 40% or less and only minimal PEEP.
There are many different ways of weaning, but in general once the patient is comfortable breathing on his or her own on bland ventilator settings, it is worth trying on a T-piece. If this doesn’t work (desaturation, respiratory distress), then put back onto ventilation and try again the next day. Extubation can happen as soon as the patient is seen to be managing fine on a T-piece, assuming the tube is not there for airway protection in a patient with reduced consciousness.
Perspective –post-extubation laryngeal oedema
Despite modern low pressure high volume cuffs, laryngeal oedema after extubation can still happen in up to a fifth of patients, particularly if intubated for more than two days. In a double-blind randomised trial[6] of methylprednisolone 20 mg every four hours starting 12 hours before planned extubation the incidence of post-extubation oedema was 3% versus 22% in controls (NNT 6, CI 4 – 7), with 4% of the active group requiring reintubation versus 8% of controls (NNT 26, CI 14 – 96). It would be reassuring to see corroboration of this result from further studies.
Suspected ARDS
ARDS is characterised by the presence of inflammatory cytokines and increased interstitial fluid in the lungs. It should be suspected in any patient who is sick enough to warrant ICU attention, across the spectrum from motor vehicle accidents, polytrauma, surgical sepsis, pneumonias, to severe myocardial infarction. It manifests as progressive hypoxaemia with a diffuse infiltrate on CXR, and increasingly ‘stiff’ lungs requiring progressively higher pressures for adequate ventilation.
Management:
Heparin prophylaxis – 5000 units SC 8 hourly.
Hydrocortisone in low dose (100 mg 12 hourly).
Consider recruitment strategies. (Increase PEEP to 30 with patient lying on stomach with a pillow under the abdomen and torso, and stop the ventilator cycling. Leave for 30-60 seconds, then restart the ventilator with a PEEP of about 15 for an hour or so.)
Treat intercurrent infections.
Ensure that all other reversible factors have been reversed as far as possible (e.g. elimination of surgical sepsis)
Sedation in ICU
Most ICUs have a favourite cocktail, which is rarely the same as that in other ICUs, but is often considered the ‘only’ thing that works. Sedation is often considered as the panacea for all ventilatory problems, but should be used with great care.
General principles of ICU sedation
Patients in pain need regular adequate analgesia rather than sedatives. Homeopathic doses of analgesia given as part of a favourite twilight cocktail rarely address the problem. If in any doubt, calculate it out – would you like to get 1 mg of morphine per hour if you had a broken femur?
Address all other causes of restlessness before simply increasing sedation. Simple things like a blocked urinary catheter can render sedation apparently ineffective.
Combinations of a benzodiazepine and an opiate are very popular and have some theoretical advantages, but some benzodiazepines are considerably more expensive than others – in particular, high doses of midazolam are quite costly, although its water solubility means that it is less sclerosant to veins. It starts to accumulate after a few days of use and loses the advantage of short action.
There is no law against baseline sedation with nasogastric medication in a stable patient who has been on a ventilator for some time and where there is no urgency to wean. Interactions with feeds need to be considered, but are not insurmountable.
Morphine may exacerbate wheezing in patients with asthma or COPD.
Antibiotics in ICU
Antibiotic policies in ICUs develop as a legacy of previous prescribing practices within the community, the hospital, and the ICU itself. There is a logical tendency amongst intensivists to use ‘strong’ antibiotics for sick patients. This means that the starting point becomes shifted up a level, with initial antibiotics being broad-spectrum moderately expensive cephalosporins and quinolones, and movement then being somewhat limited in a resource constrained environment. Special considerations:
The antibiotic naïve patient sent in from a rural area who has not been languishing in a general ward for some time may well respond to straightforward choices.
More unpleasant organisms require combination therapy – Proteus and Pseudomonas species should rarely be treated with a single agent. Possible options would be a quinolone and an aminoglycoside, or ceftazidime and a quinolone.
Klebsiella species resistant to cephalosporins, particularly ceftriaxone and cefotaxime, develop rapidly in situations where these antibiotics are ‘preferred empiric therapy’ so take care if you see that you and your colleagues are prescribing nothing else.
Peculiar organisms commonly considered non-pathogens in relatively well patients loom with disconcerting apparent importance when isolated from tracheal aspirates of very ill patients. Remember that many of these organisms (e.g. Acinetobacter) are found in most ICUs, and their pattern of resistance usually identifies them as old acquaintances. If they are all over the furniture, they will be all over the patients you put on the furniture. Sometimes they are important pathogens, but they then usually show a pattern of persistent isolation from the same type of site in the same patient.
Don’t under-dose ICU patients – antibiotic doses should be at the top end of the suggested ranges, bearing in mind the need to take account of renal or liver failure.
When ICU patients are sent on surgical adventures (e.g. for an exploratory laparotomy) get cultures of all fluids and tissues available!
Inotropic support.
Dopamine and other inotropes are valuable in the management of volume replete patients who are underperfusing critical organs. Inotropes are NOT a substitute for adequate volume replacement, and should not be used to boost a lowish blood pressure that is not causing harm. They are of value in sepsis and multi-organ failure, and may have a limited role to play in selected patients with pump failure.
Low dose dopamine (less 5 mcg/kg/min) is still considered controversial although evidence in favour of its use is not accruing to any convincing extent. A meta-analysis[7] dealing specifically with its use in severely ill patients found no evidence of survival benefit or of a reduction in the need for haemodialysis.
Much has been written about the purported advantages of the three commonly used agents for pressor effects. (Isoprenaline is no longer available.) The drugs are dopamine, dobutamine, and adrenaline. A very simplistic approach is to reserve dobutamine for those where a tachycardia is particularly undesirable (e.g. in the setting of ischaemic heart disease) and to use adrenaline if dopamine on its own is not yielding an adequate effect. In spite of all the confusing physiology, there isn’t really any convincing evidence that any particular agent or combination of agents yields any clear survival benefits, but again this may be because of weak trial design. The dose is always titrated against response – there is no ‘correct’ dose.
Mysterious medications
Amiodarone infusion
This toxic drug is going through a fashion revival. It is probably over-used at the moment, and its long term side effects should be considered before initiating therapy (thyroid problems, peripheral neuropathy, pulmonary fibrosis and interstitial pneumonitis, hepatotoxicity). It has a half-life of nearly two months.
It is usually given for prophylaxis and treatment of tachyarrhythmias (e.g. recurrent VT) in patients with cardiomyopathy. Oral load is with 200 mg 3x/d for a week and then slow reduction to a maintenance dose of 200 mg/day. In a more acute situation give 400 mg 4x/d for the first day, or even start with an IV dose of 5 mg/kg as an infusion over 1-2 hours, e.g. for a 70 kg man this would be 300 mg or 2 amps of 150 mg in saline. It is fashionable to then give a further 900 mg or so IV over the next 24 hours as a continuous infusion; whether this leads to more rapid arrhythmia control than the oral/NGT load is unclear.
Adenosine
Benefit in paroxysmal SVT is sometimes dramatic, but it is not always successful. It is now reasonably priced. It probably won’t work if the patient was given theophylline. Avoid it if the patient is asthmatic, as it can cause bronchospasm. Many patients feel uncomfortable after being given it (flushing, shortness of breath, chest discomfort) but the effect is short lived: the drug has a half-life of <10 seconds.
Dose: 3 mg rapidly (over 1-2 seconds) IV into a fast flowing drip. If it hasn’t worked in a minute or so, give 6 mg. If still no effect, try 9 or 12 mg.
Perspective – adenosine, verapamil and carotid sinus massage.
A number of studies show similar success rates for restoring sinus rhythm when comparing verapamil and adenosine in patients with symptomatic paroxysmal supraventricular tachycardias. One small study suggested that benefit might be rate-related, with adenosine working better for very fast rates (75% success if rate >160 bpm, and only 25% if rate < 140 bpm.) Carotid sinus massage only worked in 32%[8]:
Anti-thymocyte (anti-lymphocyte) globulin
Anti-lymphocyte globulin is used to achieve transition from very severe aplastic anaemia to less transfusion dependent states. A single course only works in about 40% of patients, although this may improve to 60% with a second course. The medication is not as good as bone marrow transplantation, and this option should be considered if there is a possibility of a compatible family donor. If it is to be given, a suitable infusion regimen is:
Give 500 mg methylprednisolone as an IV infusion over 2 hours before each ATG dose. Then give ATG 40 mg/kg/d IVI over 4 hours daily for 4 days. The addition of cyclosporin thereafter may increase the response rate still further.
Calcium infusions
Finding a validated calcium infusion regimen is problematic. There are many variations, and the amount infused needs to be adjusted to the severity of the hypocalcaemia. For an equivalent volume of the 10% solutions, calcium chloride contains about three times as much elemental calcium (27 mg per ml versus 9 mg per ml) as the gluconate, however the chloride is a more sclerosant to peripheral veins. In an emergency inject 10 ml of 10% calcium gluconate over two minutes intravenously. Repeat once only, if necessary. If an infusion is required, put 10 ml of 10% calcium gluconate solution into 1000 ml of 5% DW and infuse over 12 hours.
Cyclosporin
It has a narrow therapeutic range – in other words it is quite easy to veer from subtherapeutic to toxic and vice-versa.
Dose response is unpredictable, so therapy needs to be monitored with levels.
Many drugs, and some foods, interact with it, e.g. ketoconazole and grapefruit.
An added complication in patients given the drug after renal transplantation is that a rising creatinine may be due to either rejection, sometimes related to inadequate dosing, or to toxicity. In general, check the level and ask for advice.
Perspective – therapeutic range of cyclosporin concentration.
Various laboratories may have considerably different ranges, so check the range on the laboratory reply form. Use an EDTA tube and take trough samples about 10-12 hours after the last dose. During the first six months after a transplant, the risk of rejection is higher in patients with whole blood levels less than 80-200 nmol/l (100-250 ng/ml) and the risk of cyclosporin toxicity is increased in those with concentrations higher than 170-330 nmol/l (200-400 ng/ml.[9]) Doses are often in the range 2-6 mg/kg/day although higher doses (10-15 mg/kg/d) may be used initially. Very many drugs interact with cyclosporin, so check before prescribing anything new, and if levels suddenly change, consider whether the patient may have been getting other medication elsewhere.
Hyperimmune globulin
An established indication is for the treatment of acute Guillain-Barre syndrome. (See under Guillain-Barre for a discussion of the magnitude of benefit.) It has also been reported to be of benefit in ITP refractory to corticosteroids and splenectomy, autoimmune haemolytic anaemia not controlled by splenectomy, and refractory myasthenia gravis. A standard regimen is 0.4g/kg/day for 5 days, giving a total dose of 2g/kg[10]. Cost – about the same as 1000 FBCs.
Labetalol infusion
Use for hypertensive emergencies as an infusion at a rate of 2 mg/min to a maximum of 100 mg IV, or as 20 mg boluses every 10 minutes.
Magnesium infusion
Tetanus is sometimes associated with autonomic instability and magnesium is touted as an antidote; occasional patients with torsade de pontes may also benefit from magnesium. Patients with symptomatic magnesium deficiency require quite vigorous magnesium replacement. There are a number of regimens available, one of the more straightforward of which is 3g in 200m1 of 5% DW over 2-3 hours. (The 50% solution contains 1g in 2 ml, and 1 g of MgSO4 is equivalent to 4 mmol.) An alternative for less acutely ill patients is 1g IMI 6 hourly.
Nitrate infusion
Indicated for patients with unstable angina not responding to heparin, aspirin, sublingual isosorbide, and who for logistic reasons are unable to undergo urgent catheterisation. It is also used for accelerated hypertension. The intravenous infusion solution contains 25 mg in 5 ml (50 mg in 10 ml) and should be infused at a rate of 10 mcg/minute, increasing by 10 mcg/min increments every 3 minutes until pain relief or mean arterial pressure below 70 mmHg (or has dropped by more than 20 mmHg). Tachyphylaxis develops relatively rapidly.
Nitroprusside infusion
Put 100 mg in 200 ml of 5% dextrose and infuse at 10 mcg/min, increasing by 10 mcg/min to 40-70 mcg/min. Protect from light and beware of cyanide toxicity (tachypnoea, tachycardia, coma, fits). Don’t use it for long – you should be able to get the patient onto more conventional antihypertensives within a day.
Vancomycin
Mistakenly rapid intravenous administration can lead to histamine release resulting in hypotension, chills, nausea, palpitations and an itchy red rash mainly in the upper half of the body – the so-called ‘red man’ syndrome. Dilute 1g in 200 ml of saline or 5% dextrose and infuse over at least one hour. Dose: usually 1g 12 hourly.
Dose in renal impairment: Validated recommendations on the dose in renal failure are scanty – a common recommendation is to give 1g every 10 days if you really do need to use it and the patient has a GFR of <10, and for GFRs between 10 and 50, give 1 g every 3 to 10 days. For GFRs above 50, the recommendations are equally tenuous, but perhaps 1g every 48 hours is reasonable.
Diagnosing brain death
This applies when one of the normal criteria for death is not met, usually because the patient is being ventilated. A few tests, if all negative, predict the impossibility of independent survival. First check that:
- The core temperature is >35 C,
- The fingerprick glucose is normal.
- The patient is not profoundly hypotensive (e.g.. systolic above 90 mmHg)
- Any sedation has worn off (deduce this from the drug half lives).
- There is no ongoing intoxication. (This is often easier said than done, and if in doubt consider getting drug levels, and observing for another 24 hours.)
Note that the presence or absence of spinal reflexes is not relevant, and that if you leave the ventilator off for long enough (significant hypoxaemia) the diagnosis will be self-fulfilling. If in doubt, oxygenate the patient carefully and try again later.
Perspective – prognosticating after a cardiac arrest
Patients who remain unconscious after an arrest pose some dilemmas for clinicians attempting to guess the chance of recovery. In intubated patients, the performance of a full Glasgow Coma Scale evaluation is not possible, and medication given during the resuscitation may interfere with pupillary size and reaction to light.
The definition of what constitutes a poor outcome also varies – usually death, coma, and persistent vegetative state, but some definitions include inability to live independently. One systematic review[11] provided some pooled measures – at 24 hours, absent motor response had a LR+ of 4.9, absent papillary response 10.2, and absent corneal 12.9. At 72 hours an absent motor response was associated with a LR+ of 9.2. For all 1914 comatose survivors of cardiac arrest included in this review, there was a 77% probability of a poor outcome (= the pre-test probability.) Note that these are not statistically independent, so you can’t multiply LRs together in this instance.
|
Pre-test probability |
0.01 |
0.05 |
0.1 |
0.25 |
0.5 |
0.75 |
0.9 |
0.95 |
0.99 |
|
Revised probability | |||||||||
|
Corneal absent |
0.12 |
0.40 |
0.59 |
0.81 |
0.93 |
0.97 |
0.99 |
1.00 |
1.00 |
|
Corneal present |
0.01 |
0.03 |
0.06 |
0.17 |
0.38 |
0.64 |
0.84 |
0.92 |
0.98 |
Triage for ICU
Triage is about determining which patients it is most worthwhile to treat in ICU when there are bed pressures. If a patient has a terminal illness which is likely to cause his or her death in the next couple of months, then no matter how sick that patient is, another patient with perhaps slightly better out of ICU prognosis in the short term might be considered worth admitting if the long-term prognosis for cure was high. For instance, a healthy 24 year old with pneumococcal pneumonia and a PaO2 of 7.5 would be favoured over another 24 year old, also with pneumonia and a PaO2, but with active cerebral toxoplasmosis and a CD4 count of 25.
This process of patient selection is deeply uncomfortable for most doctors, and is a form of explicit rationing brought about by the resource constraint of inadequate nursing and other healthcare personnel, as well as a limit on the number of ICU beds.
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Schneiderman LJ, Jecker NS, Jonsen AR. Medical futility: its meaning and ethical implications. Ann Intern Med. 1990;112:949-54. ↑
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Weisfeldt ML. In CPR, less may be better. New Engl J Med 2010;363:481-3. ↑
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Winters BD, Pham J, Pronovost PJ. Rapid response teams – walk, don’t run. JAMA. 296:1645-7. ↑
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Hillman K, Chen J, Cretikos M, et al. MERIT Study Investigators. Introduction of the medical emergency team (MET): a cluster-randomised trial. Lancet. 2005;365:2091-2097. ↑
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Weng C, Zhao Y, Liu Q, et al. Meta-analysis: non-invasive ventilation in acute cardiogenic pulmonary edema. Ann Intern Med 2010:152;590-600. ↑
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Francois B, Bellissant E, Gissot V, et al. 12-hr pretreatment with methylprednisolone versus placebo for prevention of postextubation laryngeal oedema: a randomized double-blind trial. Lancet. 2007;369:1083-9. ↑
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Kellum JA, Decker JM. Use of dopamine in acute renal failure: a meta-analysis. Crit Care Med. 2001;29:1526-31. ↑
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Ballo P, Bernabo D, Faraguti SA. Heart rate is a predictor of success in the treatment of adults with symptomatic paroxysmal supraventricular tachycardia. Eur Heart J. 2004;25:1310-7. ↑
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Reynolds DJ, Aronson JK. Cyclosporin. BMJ.1993;306:396. ↑
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Dalaks MC. Intravenous immunoglobulin in autoimmune neuromuscular diseases. JAMA. 2004;291:2367-75. ↑
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Booth CM, Boone RH, Tomlinson G, et al. Is this patient dead, vegetative, or severely neurological impaired? JAMA. 2004;291:870-9. ↑