00:00 Okay, so let's begin with the clinical presentation. 00:04 The very first exposure actually is relatively asymptomatic, largely because the individual hasn't yet developed an immune response to the relevant antigen. 00:14 However, once the immune reactivity has been established, the stage is set. 00:19 First up, an acute attack of hypersensitivity pneumonitis typically follows a pretty dramatic exposure to the culprit antigen. 00:26 Think about someone walking into a barn full of moldy hay or spending the day in a very dusty bird feather processing plant. 00:33 About four to eight hours after that exposure, patients often develop what feels like a severe flu or pneumonia, sudden cough, chest tightness, and shortness of breath, but notably without the classic wheeze you'd expect if it were asthma. 00:48 They can also run a fever, get chills, feel generally unwell, malaise, and even experience nausea or headache. 00:55 On exam, you'll see that rapid breathing and hear diffuse fine crackles when you listen with a stethoscope, almost like the lungs are crackling away, but without the classic signs of infection. 01:06 Now here's a key teaching point. 01:08 Although it can clinically mimic a viral or bacterial infection, the big clue is the timing, those abrupt symptoms about half a day after a heavy exposure. 01:17 And then miraculously, if you remove the person from that environment, they feel almost back to normal within one to two days. 01:24 So if you see that pattern, rapid onset, flu-like picture, and quick resolution after avoiding the antigen, you should think acute HP rather than classic pneumonia. 01:34 All right, now let's transition to subacute and chronic HP, which is more insidious. 01:40 In these cases, patients often can't point to a single bad day when everything went downhill. 01:46 Instead, over weeks to months, they develop a progressive dry cough and increasing shortness of breath. 01:53 They may start feeling fatigued more easily, lose their appetite, and even drop a few pounds. 01:59 On exam, you still see that rapid breathing and diffuse crackles. 02:04 But if the disease has been simmering for a long time, signs of fibrosis begin to creep in, cyanosis and digital clubbing, for instance, and a chest that doesn't expand as easily. 02:15 The tricky part here is that patients may not recall an acute episode, and they often don't know exactly what triggered it. 02:23 Next, let's talk briefly about laboratory and pathology findings, just the essentials. 02:29 In terms of blood work, you might see elevated serum IgG antibodies against the suspected antigen, but here's the catch. 02:36 Positive IgG means you've been exposed, not necessarily that HP is causing your symptoms. 02:42 There are a lot of false positives and false negatives, so don't rely solely on IgG. 02:48 You may also see nonspecific markers of inflammation, like an elevated erythrocyte sedimentation rate, ESR, or C-reactive protein, CRP. 02:57 And in the acute phase, lactate dehydrogenase, LDH, can be up. 03:03 But again, these are general inflammation markers, so they can't confirm HP. 03:08 Now, moving on to bronchoalveolar lavage, which is actually the most sensitive test for HP. 03:14 If you perform a bronchoalveolar lavage in a suspected case, you'll find a marked increase in lymphocytes. 03:20 You'll also see a low CD4 to CD8 ratio, and in acute disease, a bump in neutrophils. 03:27 Remember, this is a lymphocyte-driven injury. 03:30 Lastly, if you end up needing a lung biopsy, usually transbronchial or surgical, you'll see lymphocytic infiltrates along the parabronchial tissues and alveolar walls, poorly formed granulomas hanging out near the respiratory bronchioles, and, if the disease has gone on long enough, a bit of fibrosis. 03:51 But for you med students, it's enough to know that you're looking for lymphocytes and granulomas in small clusters, plus fibrosis in advanced cases. 04:00 Alright, let's cruise into pulmonary function and imaging. 04:04 On spirometry, HP most commonly shows a restrictive pattern. 04:09 The lungs just can't expand as well because of inflammation and eventually fibrosis. 04:15 Occasionally, in more advanced or mixed cases, you might see an obstructive component too, but don't sweat the exact numbers. 04:22 Just know that in chronic HP, diffusion across the alveolar membrane is impaired, so the diffusing capacity for carbon monoxide is down. 04:30 In the acute or subacute forms, these numbers can actually return to normal if you remove the antigen and give some supportive care. 04:38 Now on to imaging. 04:40 High resolution CT of the chest is the go-to here. 04:43 It's way more sensitive than a plain chest x-ray. 04:47 In early or subacute HP, you'll see central lobular ground glass or nodular opacities that favor the mid and upper lung zones. 04:55 If you compare inspiratory and expiratory images, you might pick up air trapping, a sign that small airways are affected. 05:02 As the disease progresses into chronic stages with fibrosis, reticulation increases and you can see traction bronchiectasis or even honeycombing in severe end-stage cases. 05:13 You might also notice some emphysema, but again, the classic distribution is upper lobe predominant which helps distinguish it from other forms of pulmonary fibrosis. 05:22 Contrast that with the chest x-ray, which is often unremarkable in early HP or may simply show vague, patchy infiltrates. 05:29 In chronic HP, you could see more of those micronodular or reticular opacities, especially in the upper lobes. 05:37 The takeaway is, if you suspect HP, order an HRCT, not just a chest x-ray. 05:42 Okay, now let's transition to management. 05:45 First and foremost, avoid the antigen. 05:49 That means either physically moving the patient out of the problematic environment, for example, moving out of a moldy house or away from a bird's cage, or removing the antigen from the environment itself. 06:00 Sometimes patients can use protective equipment like high-efficiency masks or filtered air helmets, but truly, the most effective strategy is elimination. 06:10 However, if you're dealing with subacute or chronic HP, especially if there are clear inflammatory features on HRCT, think ground glass opacities, or lymphocytosis on BAL, you might give a short course of glucocorticoids. 06:26 Immunosuppressive agents such as azothioprine or mycophenolate mothetal are options in chronic cases that haven't responded to steroids, but these are less well-studied in HP. 06:37 They may be considered when fibrosis is already established or if steroids aren't enough. 06:43 Finally, for patients with end-stage fibrotic HP who continue to decline despite all other measures, lung transplantation may be the only way to restore quality of life, which is why it's critical to catch HP early and remove the offending antigen. 06:59 And with that, we have covered the most relevant aspects of hypersensitivity pneumonitis. 07:04 Thanks for watching.
The lecture Hypersensitivity Pneumonitis: Diagnosis and Management by Richard Mitchell, MD, PhD is from the course Disorders of the Pulmonary Circulation and the Respiratory Regulation (release in progress).
A patient develops sudden onset cough, chest tightness, and fever approximately 6 hours after cleaning a barn with moldy hay. The symptoms resolve within 48 hours after leaving the environment. This presentation is most characteristic of which condition?
The most sensitive laboratory test for diagnosing hypersensitivity pneumonitis reveals which characteristic finding?
High-resolution CT imaging in early hypersensitivity pneumonitis typically demonstrates ...?
The most critical initial management approach for a patient diagnosed with hypersensitivity pneumonitis involves which intervention?
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