Sonographic lung changes in canine hypoadrenocorticism (HOAC), C-reactive protein in canine HOAC and discussion of critical-care related corticosteroid insufficiency (CIRCI)
Gosh we (mostly) love a challenging case at VPS…and this is a challenging one.
A previously-healthy three-year-old male Labradoodle presented with malaise of several days duration progressing to marked hyperpnoea, abdominal discomfort, vomiting with fresh blood and sparse, sanguinous nasal discharge.
Routine haematology and biochemistry, including electrolytes, were largely unremarkable although C-reactive protein was markedly elevated.
On thoraco-abdominal ultrasound examination, before intravenous fluids, the most striking finding was diffuse, marked increase in B lines (interstitial syndrome). Echocardiographic findings were broadly unremarkable.
Although his left adrenal measured maximum 6.0mm diameter (within normal limits), the right gland was thin. There was diffuse hyperechoic change of the gastric mucosa and some degree of gastric hypomotility.
On first consideration, the rather dramatic pneumopathy in the absence of cardiac changes tended to suggest something along the lines of acute respiratory distress syndrome (ARDS)…maybe sepsis or Leptospirosis:
J Vet Intern Med 2010 Nov-Dec;24(6):1277-82
Pulmonary abnormalities in dogs with leptospirosis
B Kohn, K Steinicke, G Arndt, A D Gruber, B Guerra, A Jansen, B Kaser-Hotz, R Klopfleisch, F Lotz, E Luge, K Nöckler
https://pubmed.ncbi.nlm.nih.gov/20738768/
…and something along those lines initially seemed compatible with an elevated CRP.
However, his R adrenal at least was suspiciously thin (no history of exogenous steroid treatment) and basal cortisol was <10 nmol/l.
It turns out that CRP often is elevated in canine hypoadrenocorticism (HOAC):
https://www.vin.com/apputil/content/defaultadv1.aspx?id=8172839&pid=19132&
‘The mean CRP was 62.2 mg/L, with an inter quartile range: 20.45–89.66 mg/L (reference 0–25 mg/L). Seven out of nine dogs had an elevated CRP‘
….and indeed, in our case, an ACTH stimulation test revealed absolutely no increase in cortisol after ACTH (still <10 nmol/l). The patient responded completely, over the course of a few days, to dexamethasone treatment and presumably does have (‘atypical’) HOAC.
We did give some consideration to the possibility that this dog’s adrenal insufficiency could be a critical care-related corticosteroid insufficiency (CIRCI) with some other primary cause:
The Veterinary Journal Volume 273, July 2021, 105677
Critical illness-related corticosteroid insufficiency in dogs with systemic inflammatory response syndrome: A pilot study in 21 dogs
M.Marchetti, A.Pierini, G.Favilla, V.Marchetti
https://www.sciencedirect.com/science/article/abs/pii/S1090023321000721
That’s a really interesting article. But the take home message is that none of those dogs with putative CIRCI had basal cortisol <38nmol/l. In fact many had relatively high cortisol levels. Rather it is lack of appropriate change in cortisol in response to (0.5umol/Kg) ACTH which the authors used as the inclusion criterion (change <75nmol/l).
It turns out that our patient is not the first report of pneumopathy in association with canine HOAC:
Front. Vet. Sci., 10 November 2022
Sec. Veterinary Emergency and Critical Care Medicine
Volume 9 – 2022 | https://doi.org/10.3389/fvets.2022.1015739
Case report: Hypoadrenocorticism crisis complicated by non-cardiogenic pulmonary edema in a dog
Mathieu V. Paulin* and Elisabeth C. Snead
https://www.frontiersin.org/articles/10.3389/fvets.2022.1015739/full
The details of this single case are strikingly similar to our Labradoodle. Right down to the sanguinous nasal discharge. The authors speculate that the mechanism might have involved neurogenic pulmonary oedema (NPE)…one subclass of non-cardiogenic pulmonary oedema. NPE, in human medicine, can be triggered by a variety of metabolic derangements including hypoglycaemia or electrolytes changes.
Another differential diagnosis to add to the list for interstitial syndrome on lung ultrasound.
