Talk:Pulmonary contusion
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Pulmonary contusion is currently a good article nominee. An editor has indicated a willingness to review the article in accordance with the good article criteria. Further reviews are welcome from any editor who has not contributed significantly to this article, and can be added to the review page, but the decision whether or not to to list the article as a good article should be left to the first reviewer.
Date: 06:41, 14 May 2008 (UTC) |
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[edit] GA Review
This review is transcluded from Talk:Pulmonary contusion/GA1. The edit link for this section can be used to add comments to the review.
I am currently reviewing this "Pulmonary contusion" as a "Good Article" candidate. Axl (talk) 12:24, 10 June 2008 (UTC)
This sentence is from 1.1 "Associated injuries", paragraph 2: "Pulmonary lacerations, in which lung tissue is torn or cut, may also result from blunt and penetrating forces in the same injury that causes a pulmonary contusion and may be associated with the latter injury." It is too long and should be simplified, perhaps split into two sentences. Axl (talk) 17:09, 10 June 2008 (UTC)
In "Causes", paragraph 2: "However, except with shotgun wounds, pulmonary contusions that accompany gun and knife wounds are not usually severe enough to have a major effect on outcome, and penetrating trauma causes less widespread lung damage than does blunt trauma." So do shotgun wounds produce more serious pulmonary contusion? If so, this deserves a separate sentence. Axl (talk) 17:20, 10 June 2008 (UTC)
From the "Mechanism" section: "After the shock wave passes, the gas in the lung may expand beyond its original volume and may tear alveoli; this is the implosion effect." Gas in the lung expanding beyond its original volume? This really doesn't sound like "implosion". Can someone clarify and expand on this mechanism please? Axl (talk) 17:31, 10 June 2008 (UTC)
- I'm having trouble finding anything about the origin of the name. The implosion effect is mentioned in dozens of sources, but always with the same sentence about the gas expanding after the pressure wave has passed. My instinct is that the term comes from the initial compression of the gas that leads to the overexpansion, but I haven't seen this confirmed anywhere (though I did find the word "rebound" in a source and added that to the article). Ideally I'd just look at the original studies the reports are citing for who coined the term--hopefully they'd have an explanation--but I don't have access for before the mid '90's for most journals. I can keep working on this, but I'm not sure how much luck I'm going to have. Any suggestions? delldot talk 12:04, 11 June 2008 (UTC)
- Okay, I'll search around in the library. Axl (talk) 12:25, 11 June 2008 (UTC)
- Thanks much, good luck. This is cited in Cohn, it might be the origin of the term: Huller T, Bazini Y. Blast injuries of the chest and abdomen. Arch Surg. 1970 PMID 5409672 delldot talk 12:40, 11 June 2008 (UTC)
- Okay, I'll search around in the library. Axl (talk) 12:25, 11 June 2008 (UTC)
From "Pathophysiology": "Lung water increases over the first 72 hours after injury." What is "lung water"? Perhaps this means "pulmonary edema"? Axl (talk) 17:41, 10 June 2008 (UTC)
- An excess accumulation of lung water leads to pulmonary edema. As I understand it, they are not synonymous, because there's a normal lung water content in a healthy person;[1][2] however you only ever hear about it in the context of edema and it looks like they're informally treated as synonymous. How is this tweak? delldot talk 07:18, 11 June 2008 (UTC)
From "Pathophysiology", subsection "Consolidation": "When alveoli consolidate as a result of bleeding into them, it causes the pressure within the capillaries of the lungs to rise; this increased pressure can get so high that blood and serum leak from the capillaries and lead to intrapulmonary shunting." Is this really true? I would have expected the initial injury to cause a transient rise in pressure leading to capillary damage and haemorrhage into the alveoli. This impedes gas transfer locally, at the site of capillary damage. Reduced oxygenation of blood then leads to (arterial) vasoconstriction at the site of lung/capillary damage. Thus I expect that the "consolidated" lung leads to shunt which then leads to vasoconstriction and raised pulmonary arterial pressure. Unfortunately I don't have direct access to the quoted reference. Axl (talk) 17:57, 10 June 2008 (UTC)
- Your mechanism sounds reasonable, but I haven't found a source that says all of that exactly yet; I'll keep looking though. Here's what the source I used (PMID 8895709) says: "...the extravasation of blood into the alveolar space and subsequent consolidation lead to an increased intravascular pressure. When the pulmonary capillary pressure exceeds the pressure at which the vessels can retain blood and serum (7 mm Hg), an intrapulmonary shunt develops." Do you think I accurately represented the source with the sentence you quoted? I can keep looking for more detail on pathophysiology. delldot talk 09:06, 11 June 2008 (UTC)
- In that case I can't fault your interpretation of the reference. However I am not convinced that the second sentence is correct: "When the pulmonary capillary pressure exceeds the pressure at which the vessels can retain blood and serum (7 mm Hg), an intrapulmonary shunt develops." I would expect shunt to develop before the capillary pressure rises that high. Again, I'll search the textbooks. Axl (talk) 12:48, 11 June 2008 (UTC)
From "Consolidation": "Findings from animal studies indicate that even when only one side of the chest is injured, inflammation may spread to the other lung and lead to respiratory failure in both lungs." Is this ARDS? Axl (talk) 18:03, 10 June 2008 (UTC)
- The source just calls it a "significant inflammatory response". It doesn't cite sources for that sentence, but does for the one before it. PMID 10963530 makes no mention of inflammation, PMID 11493780 is about inflammation spreading to the uninjured lung but makes no mention of ARDS. I'm not sure this inflammation has all the features of ARDS, and from the second study it looks like the time courses may be different (beginning within a couple hours in that study, whereas ARDS develops over a day or two). So I'd hesitate to call that ARDS, but on the other hand, we do know that ARDS develops after pulmonary contusion, it's discussed in complications. Should I take out the inflammation mention and limit the discussion to the complications section? delldot talk 14:07, 11 June 2008 (UTC)
From "Pathophysiology", subsection "Ventilation/perfusion mismatch": "Since contused lungs become stiff and lose compliance, more pressure may be needed when ventilating the patient to fill the lungs with the same volume of air." This is true, but is irrelevant to ventilation/perfusion mismatch. Axl (talk) 18:06, 10 June 2008 (UTC)
- Good catch. This is actually covered already under treatment, so I just removed this unnecessary sentence. delldot talk 07:22, 11 June 2008 (UTC)
From "Prognosis and Complications": "It is less common for ARDS to develop as a result of pulmonary contusion in children than in adults." And from "Epidemiology": "Pulmonary contusion is equally serious in children and adults." I presume that the development of ARDS is more likely to lead to death? Does the lower incidence of ARDS in children reflect the young compliant chest wall that allows contusion with a weaker (i.e. lower energy) trauma? If this is the case, why is contusion equally serious in children and adults? Both of those sentences have the same reference, but again I don't access to it. Axl (talk) 18:57, 10 June 2008 (UTC)
- I found a contradiction of the ARDS fact in another source. I've made some changes, what do you think? To try to answer the question, it might be that the second sentence is comparing pulmonary contusion alone without taking into account its complications, but i"m not sure. delldot talk 08:37, 11 June 2008 (UTC)
