Critical Care Veterinarian

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Critical Care Veterinarian

Board Certified Emergency and Critical Care Veterinary Specialist Her dedication to teaching is not just a profession; it's a calling.
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Dr. Mariana Pardo is a trailblazing force in the world of veterinary medicine, exemplifying the transformative power of dedication and education. In 2009, she embarked on her journey at Universidad Mayor, Chile, where she laid the foundation for her remarkable career. Her pursuit of excellence led her to the University of Georgia and the University of Florida, where she honed her skills through no

t one, but two emergency and critical care internships. Driven by an insatiable hunger for knowledge, she then pursued her emergency and critical care residency at Cornell University. Dr. Pardo is more than just a skilled practitioner; she is a bilingual ambassador for knowledge and change. As an international speaker, she bridges the gap between cultures, sharing her expertise far and wide. Her prolific contributions extend beyond the lecture hall; she has authored multiple articles and book chapters, leaving an indelible mark on the field. In a digital age, Dr. Pardo has leveraged the power of social media through her platform , bringing accessible continuing education to a global audience. She is on a mission to give back to the Latin American community, generously participating in numerous continuing education programs. However, Dr. Pardo's influence extends beyond her professional achievements. She is a passionate advocate for diversity and inclusion in veterinary medicine, and her commitment is evident in her role as a member of the American College of Veterinary Emergency and Critical Care’s Diversity, Equity, and Inclusion Committee. In 2024, Dr. Pardo's life journey led to the inspiration to create Global Instruction for Veterinary Empowerment or GIVE, a registered 501(c)(3) nonprofit organization that has the mission of creating global veterinary advancement by empowering sustainable specialty-level care in areas where these services are not available or cost-prohibitive. Dr. Pardo's journey is an inspiring testament to the heights one can reach through unwavering dedication, education, and a deep commitment to making veterinary medicine more inclusive and accessible for all.

05/27/2026

This dog presented for progressive abdominal distension and swelling of the limbs. On exam, the edema was soft, ventral, and pitting, and the abdomen was markedly fluid-filled.

This is a classic presentation of systemic venous congestion from right-sided congestive heart failure.

When the right side of the heart cannot move blood forward effectively, venous pressures begin to rise. That increased hydrostatic pressure forces fluid out of the vasculature and into tissues and body cavities.

The result:
💧Peripheral pitting edema
💧Ascites
💧Sometimes pleural effusion as well

At the same time, decreased effective forward perfusion activates the RAAS system, causing:
🧂 Sodium retention
💦 Water retention
📈 Worsening congestion

So even though these patients are fluid overloaded, the body continues trying to retain more fluid.

Abdominocentesis can significantly improve comfort and ventilation in patients with severe ascites, but draining the abdomen does not treat the underlying disease process. The primary problem remains elevated venous pressures and congestion.

Common causes of right-sided CHF in dogs include:
▫️ Tricuspid valve disease
▫️ Pulmonary hypertension
▫️ Pericardial disease
▫️ Dilated cardiomyopathy
▫️ Heartworm disease

And remember: not all ascites + edema are cardiac.

Other important differentials include:
• Severe hypoalbuminemia (PLE/PLN/liver failure)
• Portal hypertension
• Renal disease
• Neoplasia
• Lymphatic obstruction
• Vasculitis/sepsis
• Iatrogenic fluid overload

Don’t just remove the fluid.

Always ask yourself WHY the fluid formed in the first place.

05/25/2026

35kg English pointer. Rawhide chew, 24 hours with lodged esophageal foreign body, anxious and pacing.

Endoscopy showed it lodged near the cardia, we spent 2 hours with ratgators, a Foley catheter behind it, forceps. Nothing moved. The mucosa was already angry from manipulation. We recommended specialty surgery but that wasn’t an option financially… Euthanasia was on the table.

So we offered an esophagostomy approach… I mean it’s just a bigger e-tube incision… right? 😖

So we put on our big girl panties, and went for it… we got it out!!!

Checked after with scope: one small pressure ulcer, diffuse swelling. NG tube, sucralfate, pantoprazole, dexamethasone, Clavamox, short course of steroids.

Esophageal foreign bodies aren’t just about getting it out. The longer it sits, the deeper the pressure necrosis. Short-term complications can include perforation (which gets you cervical abscess, subcutaneous emphysema, or thoracic catastrophe: pneumothorax, pyothorax, mediastinitis). Aspiration pneumonia from manipulation or partial entry to the airway. Overall complication rates run 15–22%, and our 2-hour endoscopic maneuvering was right at that edge.

Strictures may develop 1–3 weeks post-injury, but can emerge as late as 4–6 weeks. With dental chew-induced esophagitis, stricture rates hit 24% in one series. That swollen mucosa we saw? That’s the warning sign. If the injury extends past mucosa into muscle, it heals with scar tissue and narrows the lumen. Then you’re managing dysphagia long-term, chasing aspiration risk, possibly doing repeat endoscopic dilations.

That’s why we gave dexamethasone sp and a steroids taper, not standard across the board, but for moderate-to-severe esophagitis, they can blunt the fibrotic cascade.

We were happy to be able to send her home… and these owners will never go near rawhide again…

Sometimes it pays off to be brave ☺️

05/17/2026

We tried everything.

Maropitant. Ondansetron. Mirtazapine. Capromorelin. We warmed the food. We switched proteins. We hand-offered. We used baby-voice while asking “who’s a good boy”… We stared at this dog like maybe sheer willpower could make him eat.

He wasn’t having any of it.

Then dad walked in.

Sat on the floor. Pulled out a spoon. And this dog, who had refused food from every single one of us for days, started eating.

Not a lot. But enough.

And honestly? That moment did more for his recovery than the last anti-emetic I reached for.

Here’s the thing we don’t talk about enough in ECC: the human-animal bond is not a soft, sentimental add-on. It’s physiology. It’s parasympathetic tone, stress reduction, cortisol reduction. It’s the difference between a patient who shuts down in a kennel and one who decides today’s the day to try.

We have a whole pharmacy of appetite stimulants and prokinetics. They matter. But sometimes the missing ingredient isn’t a drug, it’s the person whose voice that animal has heard every day of its life.

This is one of the biggest reasons I love working in an on open concept. Owners can sit with their pets. Talk to them. Cuddle them and comfort them and give them a reason to fight. We don’t lose anything by letting them in. We gain a co-therapist who knows things about that patient we’ll never learn from a chart.

To the techs and nurses reading this: you already know. You’re the ones who notice when a patient perks up the second their person walks through the door. Advocate for that. Make space for it. It’s medicine.

Sometimes the best intervention is a dad with a spoon.

05/12/2026

The blood in that photo? All from one cat. One sitting.

This 6yo MN DSH, came in for lethargy, Pu/Pd and not wanting to move. Physical exam showed ataxia, squinting at the lights and very bright red gums. PCV: 82%. TS 6.8 g/dL, Polycythemia!

Differentials:
• Relative → dehydration, splenic contraction. Nope. (euhydrated, TS normal).
• Secondary appropriate → chronic hypoxia, R-to-L shunt, severe pulmonary disease. Nope. (Clean echo, clean rads).
• Secondary inappropriate → EPO-secreting tumor, renal classically. Nope (Abdominal US clean).
• Primary or Polycythemia vera → diagnosis of exclusion, to fully confirm need low/normal serum erythropoietin (EPO) levels and a bone marrow biopsy.

Acutely we need to perform a phlebotomy:
• 10-20 mL/kg whole blood, isotonic crystalloid replacement at roughly the same volume.
• Jugular access, butterfly + 3-way stopcock. Slow pull.
• Target PCV ~55-60% acutely. NOT NORMAL PCV. You’re breaking viscosity, not bleeding the cat dry.
• Watch mentation, MM, BP, lactate, PCV immediately after.

We removed 10 ml/kg initially, PCV dropped to 62%, mentation improved. He blinked at me like a normal cat for the first time. We repeated another 10 ml/kg phlebotomy 6 hours later and it dropped to 56%, he was eating, and moving normally.

Long-term: hydroxyurea + maintenance phlebotomies guided by symptoms and PCV trend, not the calendar.

A bright red cat with weird neuro signs isn’t always a toxin or a stroke. Sometimes the blood is just too thick to flow.

05/10/2026

Society has a way of making women feel like they have to pick a lane.

Career or family. Ambition or presence. The version of yourself that achieves or the version that nurtures.
I delayed becoming a mom for a long time. And I built something in that space that I’m genuinely proud of, beyond what I ever thought I’d be capable of. I don’t regret a single year of it.

And then I had three kids who completely wrecked me in the best possible way, and I realized: I would have never forgiven myself if I’d missed this.

But here’s what I want to say carefully, because this is not a post about motherhood being the thing that completes you.

It’s about whatever that thing is for you, the version of your life you’re quietly deferring because the systems around you weren’t built to hold all of it at once.

Maybe it’s kids. Maybe it’s a relationship. Maybe it’s a completely different kind of life than the one your career has been building toward.

And here’s the other thing nobody says enough: we were never supposed to do any of this alone. The village wasn’t a metaphor, it was the actual plan. Somewhere along the way we convinced ourselves that needing help was a weakness, that asking for it was an imposition.
It isn’t. Reach out. Show up for someone. And please, let people show up for you.

We keep asking women to sacrifice. We don’t ask nearly enough of the structures that force the choice.
You shouldn’t have to choose. And we should be a lot louder about that.

Today I’m holding my 3 extra tight, grateful that I get to be a mom ❤️👦🏼👧🏼👦🏼❤️

Happy Mother’s Day to everyone finding their version of enough, whatever shape it takes.

05/08/2026

This is your worst nightmare… you go to scruff a cat.. and their skin TEARS!!!

Not because you were rough or did anything wrong. The skin was diseased, and has been changing, over months, before anyone touched it.

Feline hyperadrenocorticism is rare and it ican cause some pretty significant skin changes. Chronic, excessive cortisol shuts down collagen synthesis at the fibroblast level, causing paper thin skin. No elasticity.

More than 50% of cats with HAC develop skin fragility like this (Hardy et al., JFMS Open Reports 2023; Boland & Barrs, JFMS 2017), and unlike dogs, who almost never get this complication, cats are uniquely vulnerable.

Nobody fully knows why.

The diabetes piece matters too. Around 80-90% of cats with HAC have concurrent DM (Cook & Evans, JFMS 2021), and it’s almost always insulin resistant.

So if you have a diabetic cat that just won’t regulate, HAC deserves a spot on your list. Not the first spot, most hard-to-regulate diabetics don’t have Cushing’s, but it belongs there.

What I want you to actually take from this image though: look at the skin before you restrain.

Feel it. If it moves like tissue paper, if it looks translucent, if this cat is also a difficult diabetic with muscle wasting and a pot belly, change how you handle them.

The scruff is a reflex. It needs to become a decision.

05/01/2026

This dog came in with AHDS. Severe. The kind where puddles of blood pool by his rear.

After 20 ml/kg IV crystalloid: no measurable BP, weak pulses, obtunded, the monitor suddenly shows VTach at 240 bpm.

Here’s where it gets easy to freeze.

The arrhythmia feels like the emergency. But look at the POCUS on the above: volume underloaded, contractility not where it should be for this level of hypovolemia. The heart isn’t failing on its own terms. It’s ischemic, it’s underfilled, and it’s been on a grain-free diet for two years. There’s a lot going on in that ventricle.

We gave a lidocaine bolus and started a CRI. But we didn’t stop resuscitating. Because the VTach here isn’t the problem, it’s a symptom of the problem. A heart that’s starving for volume and oxygen will do weird things. Treating the rhythm without treating the cause is just pointless.

What the POCUS gave us in real time:
• Confirmation of severe hypovolemia (not fluid overload masquerading as poor contractility)
• Reduced systolic function, likely ischemic in origin, possibly compounded by diet-associated cardiomyopathy
• A reason to keep going with resuscitation despite an ugly ECG

The skipped beats you can see are the arrhythmia breaking through. The CRI hadn’t fully kicked in yet. This is what that transition looks like.

The takeaway:
VTach in a crashing, hypovolemic patient is not an automatic reason to pause resuscitation. Treat the rhythm, yes. But keep filling the tank.

POCUS lets you see both problems at once, which is exactly when you need it most.

04/30/2026

POCUS PEARL: the medullary rim sign 🐱

Scanning kidneys on a cat for something unrelated and you catch it: a bright hyperechoic band hugging the corticomedullary junction. Sharp. Clean. Doesn’t shadow.

That’s the medullary rim sign. And it’s not normal.

What it is:
Calcium salt deposition in the tubular epithelium of the outer medulla. The outer medulla runs hypoxic at baseline, so it’s the first thing to go when there’s ischemia, toxin exposure, or chronic metabolic stress. Mineralization follows damage.

Your differentials:
• Hypercalcemia (lymphoma, idiopathic, primary hyperparathyroidism, hypervitaminosis D)
• CKD
• Nephrotoxins (lilies, ethylene glycol, aminoglycosides)
• FIP
• Renal lymphoma

Hypercalcemia and CKD are your most common culprits. MRS alone won’t tell you which, it just tells you the kidney has been through something.

What to do next:
Ionized calcium, full chemistry, UA. Survey the rest of the abdomen while you’re in there.

Techs: if you see a bright band at the corticomedullary junction, flag it. That’s a reportable finding.

The kidney’s trying to tell you something.

04/28/2026

Blocked cat. You know the presentation: straining, painful non-expressive bladder, the look on their face that says please help me.

But this one had a little extra. POCUS showed a stone sitting in the urethra.

We don’t always catch urethral calculi on point-of-care ultrasound. The urethra is small, the stone can be distal, and the angle doesn’t always cooperate. So when you see that hyperechoic focus with posterior acoustic shadowing in the right spot?

Screenshot it. That’s a good day.

Why it matters clinically:
Most obstructed cats have functional obstruction (mucus plug, urethral spasm) rather than a true stone.

But when there IS a calculus, your management changes:
• Hydropulsion may not cut it
• You’re thinking about whether this cat needs more than just unblocking
• Recurrence risk is different, and so is the conversation with the owner
• Stone type matters: struvite vs. calcium oxalate = very different dietary/medical plans

For my techs: If you’re doing the initial POCUS assessment on an obstructed cat, don’t just check bladder size. Run the probe caudally and see what you find. It won’t always be there, but when it is, you’ve just changed the whole game plan before the doctor even walks in.

Urethral calculi account for a minority of feline obstructions, but they’re disproportionately important to identify early. Don’t skip the scan just because you’re “pretty sure” it’s a plug.

Have you caught one of these on POCUS? Drop it below.

04/27/2026

A cat walks into the ear with a history of itchy ears for the past month…

Not an emergency. Not critical care. Just a very itchy cat and a humbling reminder that derm exists… and this is not my forte.

BUT… as I examine his ears I feel hopeful that this may be one of the few derm things I DO know!

Dark, crumbly, coffee-ground discharge in the ear canal + intense pruritus + some pinna excoriation.

I take a sample of both ears and look under the microscope, there it is Ear Mites!

We clean the ears and give Revolution.
Another life saved!

That’s it. That’s the post. Sometimes the answer is just: it’s mites, go see your vet, here’s what works.

Now if someone could explain why they came to the ER for this, I’m all ears. So is the cat. 🤣

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