Todd Fraser on 14-05-2013
Another interesting case was sent to me this week, and on the basis of the response to last weeks, I thought this might be an interesting theme to explore. I'll add some more interesting cases in the next few weeks
This patient is a 70 year old, 80kg man with a history of smoking related chronic obstructive pulmonary disease. He has had a week of flu like symptoms, and presented with severe respiratory distress and fevers. He rapidly failed NIV and then was intubated.
Following intubation, his ventilation is extremely difficult. On Volume SIMV with a rate of 15 and Vt of 500 mls, PEEP 10cmH2O, he has Peak inspiratory pressures of 35, a CO2 of 90mmHg, and arterial saturations of 88%. His pH is 7.05 with a base excess of -12mmol/L, and he is now anuric with acute renal failure (by RIFLE). His vasopressor requirement is increasing. One side of his chest is moving, one side is not. The chest xray, and a subsequent CT, demonstrate a densely consolidated right lung - almost no aerated lung is visible.
- How would you improve his saturations? What would you aim for?
- Will ventilating the pneumonic lung damage the normal lung?
- How do you manage his acidosis, particularly given the increasing vasopressor requirements?
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I would exclude rapidly correctable causes of his hypoxia, in particular blocked kinked ETT, excessive secretions, one-lung intubation, or a pneumothorax. Assuming the hypoxia is solely related to the severity of his pneumonia, I would treat as ARDS and employ a high PEEP low tidal-volume strategy and permissive hypercapnia and consider adding prostacyclin or nitric oxide. Broad spectrum antibiotics of course, and urgent microbiology. I would also use nebulised ipratropium and salbutamol.A target SpO2 would ideally be guided by a a base-line ABG, otherwise >92%, and aim to reduce the Fi02 from 1.0 as soon as is practicable. The normal lung is at risk of damage, especially with high PEEP and high, rapid tidal volumes, but the balance here is to maintainarterial oxygen content but not at the cost of damaging the good lung. A narrow path.
You raise a very interesting point there Anthony, the risk of damaging the good lung.
Using a DLT in this scenario could potentially address the issue of markedly different lung compliances. I have never seen this approach, but would love to try. Some potential challenges include the skill requirement to place and manage DLTs, along with their propensity to migrate and change positions, and occlusion of the RUL. Presumably one reason why this isn't seen/tried more often is that these infective processes are I think more likely to be multi lobar and bilateral rather than unique to one lung. If the problem were so clearly one-sided it may be tempting to perform a bronchoscopy and lavage (bearing in mind the current severity of the hypoxaemia) along with physiotherapy
The interesting thing about the ARDS type ventilation is that there isn't that much evidence for permissive hypercapnoea. Everyone quotes the ARDS-Net trial, but in that study they used a high pressure strategy in the control arm versus a low pressure strategy in the intervention arm as well as the different volumes, and when they intervention arm inevitably became acidotic, the respiratory rate was turned up so that the minute ventilation was essentially the same. This meant that the CO2s were also very similar, and weren't that high. When the pH dropped below 7.20, they gave bicarbonate infusions.
A DLT will be totally unhelpful - if the lung is that consolidated, no air is going in there anyway. You're better off treating it like a single lung vent and reducing the volumes you can reasonably achieve.
As for bicarbonate, little evidence of either of these issues - in theory, if you add bicarb you push pH up even if CO2 increases, not decreases, so should improve arterial pH. If its a closed system (and this case sounds like it, i.e. can't increase ventilation at all) then CO2 can potentially move across membrane and result in cellular acidosis, but my understanding is this has largely been debunked.
The oxygen target question is quite interesting I think. Given his history of COPD, it would potentially mean his target is lower than the non-smoking population.
I would agree with the de facto-single-lung strategy, although I would add some aggressive pulmonary toilet as well, doing whatever we could to clear out some recruitable space in that consolidated lung. I would use a pressure mode, and probably something like APRV/BiLevel to maximize recruitment and gas exchange in the remaining good lung. In a 70 year-old COPDer, a saturation of 88-90% should be adequate, and might take some of the pressure off (no pun intended) from worrying about the FiO2.
I'd also do lying him on his good lung - this may improve bloodflow to better vented lung, and may improve drainage of pus from bad lung
That's the beauty of the pressure mode, in my opinion (especially an APRV-type mode)...the affected lung will gradually be recruited as it's able. Sigh breaths (if you stay in SIMV) and periodic pressure-based recruitment maneuvers will also help gently "rebuild" the available lung units in a much more lung-friendly manner than a volume mode. In addition, you'll snag more of the units that are closed from atelectasis rather than infection (there are bound to be some), and you need all you can to improve gas exchange and bring that CO2 down.
As Gemma has commented...the consolidated lung is useless for ventilation purpose at least for now, so ventilation strategy could be like that of OLV, we can go for optimum peep by serial ABG and keep the best peep. DLT would be not very useful and will be more of issue than solution, CT scan of chest to the actual extent of affected lung's involvement and recruit ability..bronchoscope to fix any mucosal plugging, we can reduce the TV and increase the RR to manage the CO2. If lower lungs are involved predominantly then prone positioning may help. This is not a de facto ARDS scenario but a case of unilateral pneumonia, positioning may also help....
Who intubated him in the first place? I would advocate a carefully considered approach. His mortality is quite high.
Consider list of P's (Permissive hypoxaemia,Permissive Hypercapnoea,Prostacyclin inhalation,Paralyazing with Cistracurium infusion,Pressure control ventilation+/-IRV, Plateau pressure<30,Positioning to facilitate secretions drainage and physilogic recruitment) and Pray..
Once bronch'ed would anyone consider HFOV if persistently hypoxic despite paralysis and IPPV
Controversial statement Angaj - why would you say that? Yes, its quite high, but I think you'd need a bit more information before suggesting that he not be intubated...
In light of the PROSEVA trial, would anyone prone ventilate this man?
Yes why not.Proning is free though some technical risks but very effective physiologic recruitment technique if combine with optimal PEEP in
Proning is fine and good, but I wouldn't look for it to be much benefit in this specific case until the bad lung is improved because you'll still likely have significant V/Q mismatch. I'd still keep the patient good-side-down as much as possible until we started to see some resolution in that right lung.
I meant "semi-prone" as we called it if apply in this particular patient.
When the case was sent to me, it was noted that the patient was treated with GTN nebulisers as the patient was retrieved and they didn't have prostacyclin (or Nitric Oxide obviously). Has anyone ever tried this? Did it work? I've done a quick literature search and haven't found much on it.
@Djhdoc, why would you HFOV this man? he sounds to have one good lung and one that doesn't work. there is no evidence for HFOV in this group, or any other if you believe OSICLLATE and OSCAR. how is it going to help?
@Angaj - I'm not sure there is enough there to decide not to intubate this man, though I'm sure that's something that needs to be discussed with the patient and the family, taking into account further information about his background history