hello everybody,
hello everybody,
Gizmo is a 12 years old pommeranian that presented with signs of congestive failure.Responded to Furosemide Focused heart US showed normal LA/AO and subjectivelly normal function. We moved south and found hypoechoic spleen with multiple difuse hyperechoic nodules. LN’s adjacent to spleen, pancreas base and portal are all enlarged round with hyperechoic reactive fat around. Also pancreas body and left limb are heterogeneous. Suspect this is consitent with neoplasia and might be the reason for this Pumonary edema, lung infiltration? Was wondering what are my differentials?
I think an FNA of the spleen will be my next step.
Thank you,
CC
Comments
That spleen is infiltrated
That spleen is infiltrated and hepatic LN are enlarged (arrow on my still of your video). Round cell neoplasia til proven otherwise. FNA th espleen and liver and you will find the underlying cause likely. MCT possible here too so give benadryl first but more like an LSA pattern. Occasionally fungal does this too.
The non cardiogenic pulmonary edema diffs include mets, SARDS (paraneioplastic and PTE or pneumonitis. If you check the la/ao ratio immediately you can tell cardiogenic from non (NCPE). Small breeds get SARDS a lot especially chronic respiratory. I’ve seen SARDS in Shiht-zus and Pekinese more than other breeds personally.
here are my noted on NCPE:
NCPE: no elevation of LA pressure (La/ao normal)
Pulmonary hemorrhage can mimic NCPE
NCPE Causes:
Increase capillary permeability or hydrostatic pressure
Caudal lung interstitial pattern
PCWP< 18 mmHg
Causes:
Post obstructive: POPE: negative pressure edema: laryngeal dysfunction, aspiration pneumonia, brachycephalic: stenotic nares, elongated sp, reverted laryngeal saccules, Everted tonsils, hypo plastic trachea> acute stress heat exercise intubation POPE aspiration pneumonia>> negative pressure hypoxia sympathetic overstimulation> increase pulmonary vascular volume and pressure > NCPE > surfactant depletion + hypoxia & sympathetic stim > blood pooling > Hypoxia
–hypoxia during a POPE event may damage the alveolar epithelium and cause pulmonary vasoconstriction through endothelin
POPE Parameters
paO2<80mmHg
Sao2 <95%/93%
Compensatory hyperventilation can increased PaO2 to normal levels
PCWP: Swan Ganz catheter via jugular vein to deep pulm artery= LV end diastolic pressure and la pressure > 18 mm Hg = Cardiogenic volume overload
Sedation removes compensatory hyperactivity of upper airway dilating muscles in brachycephalic breeds
Neurogenic NCPE: seizures, electrocution (NCPE manifests after 1 hour) head trauma CNS hemorrhage creates hydrostatic and permeability changes with a catecholamine storm initiated by the medulla. Volume shift from systemic circulation to pulmonary circulation occurs. Neuro peptide y and endothelin one cause Edema through permeability and vasoconstriction respectively
-An acute increase in hydrostatic pulmonary capillary pressure and secondary damage to tight junctions of the alveoli
ALI/ARDS induced NCPE: sirs, pancreatitis, neoplasia, pneumonia, sepsis, uremia, parvo
Diffuse inflammatory reaction causes pulmonary endothelial and epithelial disruption, edema progresses to fibrosis
Criteria: arterial hypoxia, acute onset, pulmonary Edema, pulmonary inflammation, known risk factor.
Cough with pink foamy sputum in severe cases
All lung fields affected not just caudal dorsal lung***
Drowning NCPE: transfusion related acute lung injury 2-6 hours post-transfusion
Smoke inhalation NCPE: tissue hypoxia, thermal damage, irritation> secondary pneumonia
OTHER NCPE:
Drug reaction
Anaphylaxis
O2 toxicity
PTE
That spleen is infiltrated
That spleen is infiltrated and hepatic LN are enlarged (arrow on my still of your video). Round cell neoplasia til proven otherwise. FNA th espleen and liver and you will find the underlying cause likely. MCT possible here too so give benadryl first but more like an LSA pattern. Occasionally fungal does this too.
The non cardiogenic pulmonary edema diffs include mets, SARDS (paraneioplastic and PTE or pneumonitis. If you check the la/ao ratio immediately you can tell cardiogenic from non (NCPE). Small breeds get SARDS a lot especially chronic respiratory. I’ve seen SARDS in Shiht-zus and Pekinese more than other breeds personally.
here are my noted on NCPE:
NCPE: no elevation of LA pressure (La/ao normal)
Pulmonary hemorrhage can mimic NCPE
NCPE Causes:
Increase capillary permeability or hydrostatic pressure
Caudal lung interstitial pattern
PCWP< 18 mmHg
Causes:
Post obstructive: POPE: negative pressure edema: laryngeal dysfunction, aspiration pneumonia, brachycephalic: stenotic nares, elongated sp, reverted laryngeal saccules, Everted tonsils, hypo plastic trachea> acute stress heat exercise intubation POPE aspiration pneumonia>> negative pressure hypoxia sympathetic overstimulation> increase pulmonary vascular volume and pressure > NCPE > surfactant depletion + hypoxia & sympathetic stim > blood pooling > Hypoxia
–hypoxia during a POPE event may damage the alveolar epithelium and cause pulmonary vasoconstriction through endothelin
POPE Parameters
paO2<80mmHg
Sao2 <95%/93%
Compensatory hyperventilation can increased PaO2 to normal levels
PCWP: Swan Ganz catheter via jugular vein to deep pulm artery= LV end diastolic pressure and la pressure > 18 mm Hg = Cardiogenic volume overload
Sedation removes compensatory hyperactivity of upper airway dilating muscles in brachycephalic breeds
Neurogenic NCPE: seizures, electrocution (NCPE manifests after 1 hour) head trauma CNS hemorrhage creates hydrostatic and permeability changes with a catecholamine storm initiated by the medulla. Volume shift from systemic circulation to pulmonary circulation occurs. Neuro peptide y and endothelin one cause Edema through permeability and vasoconstriction respectively
-An acute increase in hydrostatic pulmonary capillary pressure and secondary damage to tight junctions of the alveoli
ALI/ARDS induced NCPE: sirs, pancreatitis, neoplasia, pneumonia, sepsis, uremia, parvo
Diffuse inflammatory reaction causes pulmonary endothelial and epithelial disruption, edema progresses to fibrosis
Criteria: arterial hypoxia, acute onset, pulmonary Edema, pulmonary inflammation, known risk factor.
Cough with pink foamy sputum in severe cases
All lung fields affected not just caudal dorsal lung***
Drowning NCPE: transfusion related acute lung injury 2-6 hours post-transfusion
Smoke inhalation NCPE: tissue hypoxia, thermal damage, irritation> secondary pneumonia
OTHER NCPE:
Drug reaction
Anaphylaxis
O2 toxicity
PTE
WOW that’s great info!
I
WOW that’s great info!
I suspect paraneoplastic syndrome. Will
recommend FNA of spleen liver and if accessible LNs.
Thank you so much.
CC
WOW that’s great info!
I
WOW that’s great info!
I suspect paraneoplastic syndrome. Will
recommend FNA of spleen liver and if accessible LNs.
Thank you so much.
CC