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.

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.

09/02/2026

The syringes on my desk today weren’t just medicine. They were an ending, held gently.

Some days euthanasia is quick. A quiet room, a peaceful goodbye, everyone ready.

Other days it’s hours long. Today was one of those days. Multiple patients, multiple families, multiple sessions that stretched on for hours.

Because here’s the thing people don’t always say out loud about this job: euthanasia is a gift we get to give. We get to end suffering instead of prolonging it. We get to make sure the last thing an animal feels is calm, not fear, in the arms of their favorite people in the world.

That is sacred work. I mean that.

But it’s also work that asks something of us every single time. Working emergency, we get to see families that are ready to say goodbye, but more often than not we have to help families through traumatic events and conversations, guiding them to make informed decisions on one of the hardest decisions they will make… saying goodbye.

In those long rooms today, I learned about a dog adopted the week someone’s daughter was born, now grown and leaving for college. A cat who was the last living connection to a husband who passed three years ago. A senior dog who was, in someone’s own words, “my only friend.”

People don’t just let you into the room. They let you into the whole story. You become a confidant, a grief counselor, a shoulder, sometimes literally, all in the span of one vet visit.

I love this part of my job. Genuinely.

And it costs something. Every time.

A few things I remind myself:

❤️‍🩹 Feeling wrecked after a hard euthanasia isn’t a sign you’re bad at your job. It’s the tax on being good at it.

❤️‍🩹 You are allowed to step outside for five minutes. Your team should know this is normal, not a red flag.

❤️‍🩹 Debrief with someone. Your team, a colleague, your person at home. Compassion fatigue grows in silence.

❤️‍🩹 Multiple heavy losses in one shift compound. That’s not weakness, that’s just how grief math works.

❤️‍🩹 It is okay to cry. In the bathroom, in the car, quietly, alongside them.

How do you take care of yourself after days like this?

Genuinely asking, because some days I’m still figuring it out…

08/20/2026

🇨🇴💙 Aprender, compartir y ayudar.

Después del reciente terremoto que afectó a Colombia, un grupo de colegas se unió para crear estas Jornadas Académicas Solidarias, con el propósito de poner nuestro conocimiento al servicio de una causa que hoy necesita de todos.

Me hace mucha ilusión poder participar en esta iniciativa y estaré acompañando y representando a GIVE: Global Instruction for Veterinary Empowerment, una organización que trabaja para promover la educación veterinaria y generar un impacto positivo a través de nuestra profesión. 🐾❤️

📚 ¿Quieres participar en las charlas?
Las jornadas serán completamente virtuales y las grabaciones estarán disponibles durante 30 días, para que puedas acceder al contenido y aprender a tu propio ritmo.

Puedes inscribirte a través de Instagram en Educación veterinaria | Hibrida.

❤️ Se espera un aporte solidario mínimo de $25.000 COP, pero si está dentro de tus posibilidades, te invitamos de corazón a aportar lo que más puedas. Cada aporte cuenta y nos ayudará a adquirir insumos médicos, medicamentos, alimentos e implementos de aseo para animales y personas afectadas.

💙 También puedes hacer una donación directa:

📱 Nequi: 313 481 1349
🔑 Llave:

Más que una jornada académica, esta es una oportunidad para que como comunidad veterinaria podamos aprender, compartir y contribuir.

📅 16 al 21 de agosto
💻 Virtual por Zoom
🎥 Grabaciones disponibles por 30 días
❤️ Aporte mínimo: $25.000 COP

🌎 Conoce más sobre GIVE: www.give.vet

Si no puedes participar, también puedes ayudar simplemente compartiendo esta publicación para que llegue a más personas.

Inscríbete, aprende y ayuda.
Porque juntos podemos convertir el conocimiento en solidaridad y nuestros aportes en ayuda real para Colombia. 🇨🇴🫶

07/24/2026

Scroll this panel and almost everything is unremarkable. Renal values normal, liver enzymes normal, even the pancreatic markers are boring.

Then you hit sodium at 175 and potassium at 2.6…

That combination in the face of other normal values is primary hyperaldosteronism until proven otherwise. Not the rare zebra it used to get labeled, it’s underdiagnosed because most hypokalemic or hypertensive cats get treated symptomatically and never worked up further.

What’s happening:
An adrenal tumor or bilateral zona glomerulosa hyperplasia is secreting aldosterone independent of the renin-angiotensin system. That drives sodium and water retention (hypertension) and potassium wasting (myopathy). Textbook teaching says sodium usually stays normal thanks to aldosterone escape. This cat didn’t get that memo, and honestly the Na this high alongside a K this low makes the picture easier to point to.

The work up:
Textbook next step is aldosterone level, renin, adrenal ultrasound.
This owner couldn’t do any of it.
So we started spironolactone (1 to 2 mg/kg PO q12h) with potassium gluconate.

That’s not a shortcut, it’s the same medical management a confirmed diagnosis lands on anyway when surgery isn’t happening. Not every patient will be able to do a full work up.

What you have to be honest about: a K that climbs and a cat that stops ventroflexing supports the diagnosis, it doesn’t confirm it. You haven’t ruled out unilateral versus bilateral disease, and a nonresponse should send you back to the differential list, not to a higher dose.

Recheck electrolytes and blood pressure 1-2 weeks after any dose change. Get a BP on every hypokalemic cat regardless of budget, that number is what prevents a blind cat.

If finances have ever dictated your workup… sometimes response to treatment is your best diagnostic.

07/22/2026

This 4 year old yorkie had a seizure at home. Came in lateral, hypothermic 97.7F, bradycardic 76bpm, hypotensive 70 mmHg. Her blood glucose was 26 mg/dl.

The owner said it came out of nowhere. Just found her seizing on the kitchen floor.

We asked about toxins, trauma, previous medical concerns… went through our differentials (shunt, liver, kidneys, SIRS/sepsis, endocrine, cancer), point of care bloodwork was normal except for the hypoglycemia, pocus was unremarkable.

Asked about toxins again and ran down a list of possible causes: ma*****na, plants, OTC meds, sugar-free foods…

- “No, just some freeze-dried pineapple treats yesterday.”

An internet search later… read the label.
Birch bark extract.

Birch bark extract is a source of XYLITOL.

It’s showing up in “natural” and “healthy” pet treats, human snacks, and even some dental products, often without xylitol itself ever appearing on the ingredient list. If you only trained your eye to scan for the word “xylitol,” this one slips right past you.

Dogs release insulin in response to xylitol at a much higher rate than they do to actual glucose. That insulin surge can happen fast, sometimes within 30-60 minutes, and it doesn’t care that the “sugar” was disguised in a birch extract. The result: profound hypoglycemia, and in more severe cases, hepatic necrosis and coagulopathy.

What to actually do:
• Treat the seizure and the hypoglycemia simultaneously, don’t wait for one to fix the other
• Anticonvulsant of choice if actively seizing, my go to is midazolam
• IV dextrose bolus, then a CRI, glucose checks are your endpoint, not a one-time fix
• Monitor liver values and coagulation status even if she looks okay initially, hepatotoxicity can be delayed
• Ask about ALL foods, not just “did she get into anything toxic.” Owners don’t think of pineapple treats as a toxin

If a seizuring patient comes in and glucose reads low, ask about treats, chews, gum, even toothpaste. Xylitol is hiding in places none of us were trained to look.

She’s home now. Owner tossed every “healthy” treat in her cabinet just to be safe.

Check your own dog’s treats tonight. You might be surprised what “natural” is hiding!

07/16/2026

We don’t think about pneumothorax when we hear “asthmatic cat,” but it happens, and it’s one of those complications that catches people off guard because the chest tap findings feel backwards. Air where you expect fluid, in a cat you were treating for a totally different problem.

The mechanism: chronic bronchoconstriction and mucus plugging create air trapping distal to the obstruction. Over time that raises intrathoracic pressure enough to rupture a bulla or bleb, usually subpleural. Air escapes into the pleural space, and now you’ve got a cat that was already working hard to breathe, breathing even harder for a completely different reason.

Radiographically this is a trap. Severe bronchial disease already gives you a busy, speckled lung pattern that can hide retracted lung margins, especially on VD/DV views where a mild-to-moderate pneumothorax is easy to miss. Lateral views are your friend here: look for that gap between the cardiac silhouette and the sternum, and for lung margins pulling away from the thoracic wall dorsally.

Clinically, the tell is usually a cat who was stable-ish on bronchodilators and steroids and then acutely decompensates. Increased respiratory effort out of proportion to auscultation, muffled heart/lung sounds, or a sudden shift from expiratory push to a more restrictive, shallow pattern.

Management is twofold and neither part is optional: thoracocentesis for the acute crisis, and treating the underlying asthma aggressively so you’re not just resetting the clock on the next rupture. Watch for recurrence, some of these cats need a chest tube if it’s a persistent leak rather than a one-time event.

Teaching point I’d want everyone to walk away with: in a chronic feline respiratory patient who suddenly gets worse, don’t just assume asthma flare. Reassess the whole chest.

07/08/2026

Normal lake day. Dog fetches, drinks, has a blast. A couple hours later he’s vomiting, still drinking water, then dull, then can’t stand. Dad rushes him in terrified, he’s seizing on the way.

On exam: stuporous, no menace response, intermittent seizures, extensor rigidity, horizontal nystagmus. Breathing 80-90 times a minute and working for it, muddy gums. Heart rate around 80… uh oh.

First blood gas explained it all:
• Na 123 (should be ~145)
• Lactate >10
• pH looked ok on paper, but the metabolic acidosis underneath was brutal (HCO3 6, base excess -19)

Acute freshwater intoxication with severe hyponatremia and cerebral edema. Textbook.

Mechanism, quick version:
He drank more free water than his kidneys could clear in that window. Sodium dilutes fast. Because this happened over hours, not days, his brain hasn’t had time to dump idiogenic osmoles, the protective adaptation seen in chronic hyponatremia. So the edema hits harder and faster here. But it also means we can correct faster than in a chronic case, without the same osmotic demyelination risk. Still capped at the 24hr ceiling though (12-24 mEq/day), this isn’t a free pass.

Treatment:
• Bolus hypertonic saline (3-7.2% NaCl), 3-5 mL/kg over 15-20 min, for hyponatremic encephalopathy

Goal: bring down acute brain swelling fast (monitoring MGCS, ONSD, watching for Cushing’s reflex).

From there, no isotonic fluids yet. We ran a continuous low-rate hypertonic cri with blood gases q2h, controlled correction instead of one-and-done. Once sodium was almost normal, we transitioned to isotonic maintenance fluids.

Electrolytes normalized within hours. Neuro signs didn’t. Nystagmus and ataxia stuck around even with normal bloodwork, the edema resolves on its own timeline, separate from the numbers. ONSD on POCUS let us watch intracranial pressure actually come down, reassuring in real time.

Took two full days before he walked again. First sitting up, eating hand-fed chicken, then standing, then real steps. Dad there for almost all of it.

Went home walking on all four legs, still a little ataxic with intermittent nystagmus. But grateful, he was going home with Dad ❤️

07/01/2026

This dog is presented after being run over by a car. Mildly tachypneic on presentation, few superficial abrasions, lame on one hind limb, but otherwise stable-ish. POCUS shows B-lines, thinking contusions… need chest rads and limb rads… you know… standard trauma workup.

Then we go to get chest rads.
Acutely becomes dyspneic.
My nurses stop the rads, place the dog sternally, give flow by oxygen and called me over urgently… (great work reading their patient!)

I look at the rads they were able to get and now it makes sense. The stomach was herniating through a rent in the diaphragm, and positioning for radiographs was enough to shift it further into the chest.

Why it’s easy to miss early:
* Tachypnea gets written off as pain or anxiety
* B-lines can coexist with a hernia, both mess with lung inflation
* Some dogs compensate for hours before they don’t

Red flags:

* Muffled or asymmetric heart/lung sounds
* Borborygmi in the thorax (absence doesn’t rule it out)
* Tachypnea that isn’t improving with analgesia
* Abdomen that feels empty or an organ that looks off on POCUS

Whoever is holding that patient for films is in the best position to catch the moment it decompensates. If it happens the second you extend a trauma patient for a view: stop, support positioning, get oxygen on, speak up. That timing is diagnostic, not just a bad moment.

Once you know, stabilize before chasing a perfect picture. Surgery is definitive but timing depends on the patient, not the schedule, and acute respiratory compromise can move you to the OR faster than planned.

Suspect this early in blunt trauma. Think twice before you flatten a dog on a table just to get the film.

06/26/2026

Cat was hospitalized for AKI.

Initial blood gas: pH 7.1, uremic metabolic acidosis
We started treatment. Fluids, antibiotics for suspected pyelonephritis, supportive care. Expected the acidosis to improve.

It didn’t. It got worse.

pH 6.95!!!
HCO₃ 7.78, BE -24.4, BUN 268, Creatinine too high to read on blood gas, 12 on chemistry panel.

A patient with acidosis should be making acidic urine.

That’s the whole point of the distal tubule. When urine pH is 8 and blood pH is 6.95, the kidneys aren’t compensating. They’re part of the problem.

Distal Renal Tubular Acidosis (RTA):
The collecting duct can’t excrete H⁺. Bicarbonate never gets regenerated. Acidosis doesn’t respond to treatment because the organ responsible for fixing it is broken.

In cats, common underlying causes:
- pyelonephritis
- oxalate nephrolithiasis
- hepatic lipidosis
- hyperthyroidism.

This is usually secondary. Find and treat the cause.
BUT the pH still has to be addressed acutely…

So this is one of the only times I will actually reach for Na Bicarbonate. At least until the kidney recovers.

• Dose: 0.5-1 mEq/kg slow IV diluted 1:3, or: 0.3 × BW(kg) × base excess, give half the dose over 1-2 hours, recheck blood gas after
• Target pH >7.2, not 7.4
• In RTA, supplementation often continues beyond the acute phase.

Watch for overcorrection: paradoxical CNS acidosis, ionized hypocalcemia (already borderline here at iCa 1.00), volume overload.

Alkalinization shifts calcium to the bound fraction. This cat has almost no buffer room. He started twitching and became bradycardia at 160bpm and on recheck iCa was 0.89, we gave Ca gluconate 10%, 1 ml/kg over 20 min, and signs resolved.

This cat’s pH slowly improved to 7.28, he finally lifted his head and heart rate improved…

Remember:
Non-responsive metabolic acidosis. Don’t just push more fluids. Check the dipstick. Rule out renal tubular acidosis.

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 ☺️

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