ICU Edge: How a Simple Bite Nearly Led to a Chest Tube

It was just after 12 PM when I got the call from the respiratory therapist.

“The vent alarm keeps going off, and her tidal volumes are low.”

I sprang into action. I rushed over to the room and saw the patient – a middle-aged woman, intubated and heavily sedated after decompensating the night before due to encephalopathy in the setting of worsening sepsis and acute kidney injury. Her oxygen saturations were sagging, and the ventilator’s low tidal volume alarm screaming for attention.

“The cuff is definitely blown,” I said. I grabbed a syringe, attached it to the pilot balloon, and tried to inflate it. "Nothing. No resistance. Just the empty give I felt in the dead space."

 A blown cuff is a classic ICU problem. When the cuff deflates or won’t hold pressure, air escapes around the tube, leading to poor ventilation, low tidal volumes, and the dreaded ventilator alarms. I should have taken a moment to physically inspect the pilot balloon when initially exchanging the endotracheal tube (ETT)  — a key teaching point I’ll come back to later.

The usual culprits ran through my mind:

  1. Ruptured/Blown cuff – They can rupture from overinflation, manufacturing defects, or trauma during intubation.

  2. Pilot balloon leak – A small tear or leak in the pilot balloon or its tubing can cause slow deflation.

  3. Faulty inflation valve – If the valve isn’t sealing properly, the cuff won’t stay inflated.

  4. Tracheal damage – Rare but serious, tracheal injury can prevent the cuff from seating properly.

We needed to act fast. The leak was so profound that it was no longer a closed system to deliver adequate tidal volumes to ensure ventilation and oxygenation. If left untreated, this would lead to respiratory acidosis, hypoxia, and eventual cardiopulmonary collapse.

 I decided to do a tube exchange – quick, clean, straightforward. We prepared the room for an intubation in the instance that the airway was lost during the exchange, gathered our supplies, and exchanged the tube without incident. The new ETT and cuff  held pressure beautifully. I left feeling confident that we’d solved the problem.

The next day, I was back in the ICU when the respiratory therapist approached me with that look. “It’s happening again,” she said.

Sure enough, the vent alarms were blaring, the tidal volumes were low, and the pilot balloon was completely flat. The patient was quickly decompensating with a respiratory rate in the 40’s, heart rate in the 160’s, and MAP (mean arterial pressure) <65. Suddenly, we weren’t just dealing with poor ventilation — this was a new shock state. My mind shifted into resuscitation mode.

We quickly activated the room to begin stabilization with rapid titration of norepinephrine, airway equipment, a STAT CXR on the way.

Rule out the Killers

In the ICU, you have to rule out the worst-case scenarios first. My differential diagnosis split into two major branches:

  • Hypoxia on a Ventilator: is this an equipment failure or is it due to lung physiology?

    • Equipment Failure:

      • Check the Circuit: Thoroughly inspect the entire ventilator circuit for kinks, obstructions, or leaks.

      • Suction: Suction the ETT to ensure patency.

      • Manual Ventilation: Disconnect the patient from the ventilator and manually ventilate using BVM to assess if the problem lies with the ventilator or the patient.

      • Repositioning: If the kink is in the oral cavity, reposition the patient's head and neck to relieve pressure on the tube.

      • Consider Reintubation: In some cases, reintubation (re-inserting the ETT) may be necessary.

      • Consider other causes: If the problem persists, consider other causes of airway obstruction, such as bronchospasm or mucus plugging.

    • Lung Physiology:

      • remember your 5 causes for hypoxemia: hypoventilation, low altitude, V/Q mismatch, diffusion disorder, shunt physiology

        • Cuff leak→ hypoventilation→ hypoxia (again?)

        • acute bronchospasms

        • Mucus plug or tube obstruction with sections/foreign body

        • Pneumothorax/Hemothorax

        • ARDS or evolving pulmonary edema

        • Diffuse Alveolar Hemorrhage (DAH)

  • Acute Shock on a Vent: Why is she crashing?

    • Obstructive shock (Pneumothorax, PE, Tamponade)

    • Distributive shock (Sepsis, anaphylaxis)

    • Hypovolemic shock (Bleeding, volume loss)

    • Cardiogenic shock (MI, massive PE)

Could it be a cuff leak again? Loss of tidal volumes would lead to poor ventilation = hypoxia → sympathetic surge → tachycardia and increased cardiac output → eventual circulatory collapse due to ongoing hypoxia and worsening acidosis.

But I couldn’t ignore the possibility of a pneumothorax. New shock state + ventilator issues? That’s a pneumothorax until proven otherwise.

We called for a chest X-ray. However, it was Sunday, and no X-ray tech was in sight. Time for some point of care ultrasound (POCUS). In a case like this, bedside lung ultrasound can help you distinguish between major causes of respiratory failure, especially when you suspect a pneumothorax.

Lung sliding is the key finding.

In a normal lung, the visceral and parietal pleura slide past each other with each breath, creating a shimmering, back-and-forth motion on ultrasound.

If lung sliding is absent, it means the visceral and parietal pleura are no longer in contact—classic for pneumothorax.

I grabbed the probe and scanned for lung sliding—It’s that shimmering back-and-forth movement of the pleura that assures the absence of a pneumothorax.

Right lung? Sliding present. ✅

Left upper lobe? Sliding present. ✅

Left lower lobe? … No sliding. 🚨

Could this be a left- sided pneumothorax? But before I grabbed a chest tube, I took a breath and thought it through.

What were the ventilator pressures telling me? By looking at the peak and plateau pressures, I could figure out if it was primarily a cardiac or respiratory issue.

Peak Pressure (Ppeak)

Peak pressure is the maximum pressure measured in the airway during the inspiratory phase of a mechanical breath.

  • What It Reflects:

    • Airway resistance

    • Tubing resistance

    • Bronchospasm

    • Mucus plugging

    • Tube kinking

Peak pressure is essentially how much pressure it takes to push air into the lungs. It reflects both the airway resistance and the lung compliance.

  • If peak pressure is elevated while plateau pressure remains normal → It’s likely an airway resistance issue (like a bronchospasm or tube obstruction).

  • If both peak and plateau pressures are elevated → It’s likely a lung compliance issue (like a pneumothorax or pulmonary edema).

Plateau Pressure (Pplat)

Plateau pressure is the pressure measured after the inspiratory phase, when airflow has stopped and the lungs are being held at a constant volume (measured during an inspiratory pause).

  • What It Reflects:

    • Lung compliance

    • Alveolar pressure

    • Chest wall compliance

Plateau pressure tells you about the lung and chest wall compliance—basically, how stiff the lungs are.

  • If plateau pressure is elevated, the problem is at the alveolar level—think lung injury, ARDS, pulmonary edema, or pneumothorax.

  • If peak pressure is high but plateau pressure is normal, the issue is more likely in the airways—like a tube kink, mucus plug, or bronchospasm.

I quickly checked on the ventilator:

  • Peak pressure? Normal.

  • Plateau pressure? Normal.

That meant this wasn’t a pneumothorax. If it was, her plateau pressure would be high due to trapped gas increasing alveolar pressure.

So what was really happening?

That’s when one of the respiratory therapists, bless her sharp eyes, leaned in.

“Hold on,” she said, squinting at the pilot balloon tubing. “I think she bit through it.”

She held up the tubing. Sure enough—there was a clean bite mark. Somehow, despite sedation, the patient had managed to chomp down on the thin pilot tubing, creating a slow leak that deflated the cuff. With each breath, tidal volumes dropped, hypoxia worsened, and the body’s response was to panic—tachypnea, tachycardia, and eventually, hypotension from systemic stress and metabolic acidosis.

The respiratory therapist wrapped a piece of tape tightly over the puncture site, held some light pressure, and reinflated the pilot balloon. This time, the cuff held. Tidal volumes climbed back to normal. The vent alarms went quiet.

We ultimately had to exchange the endotracheal tube again, but this time we secured the pilot balloon tubing next to the endotracheal tube in the ETT holder, with a bite block over the top. No more chewing through the line.

Teaching Points

  1. Don’t overlook the small details (“blown cuff”)

    Male sure to physically inspect the pilot balloon and tubing with each ETT exchange. In this case, a simple oversight contributed to the problem later on.

  2. New shock state on the vent? Work the algorithm.

    New shock state on a vented patient is a big deal. Work through it systematically:

    • Hypoxia – Airway obstruction, cuff issues, pneumothorax.

    • Hypovolemia – Blood loss or third spacing?

    • Cardiogenic – Arrhythmia or myocardial depression?

    • Obstructive – Tension pneumothorax, PE, tamponade?

    • Distributive – Septic or neurogenic shock?

  3. Ventilator pressures are your friend.

    • High peak + high plateau pressures → Pneumothorax, airway obstruction, or poor compliance.

    • High peak + normal plateau → Bronchospasm or tube kink.

    • Normal peak + normal plateau → Cuff issue or tubing leak (like this case).

  4. POCUS is a great adjunct, but must be used in accordance with other objective findings.

    Poor lung sliding in the left lower lobe initially made me think pneumothorax. However, the real problem was left lower lobe atelectasis. If the vent pressures are normal, think twice before you put in a chest tube.

  5. Protect the tubing.

    Once the tube was replaced, we secured the pilot tubing to the ETT with a bite block on top. Simple fix. Big difference.

  6. Teamwork and Communication.

    That RT saved the day. It’s easy to get tunnel vision in the middle of a crisis. Listen to your team—they might see the detail you’ve missed.

In the ICU, things aren’t always what they seem. It’s easy to get caught up in the high-stakes environment and chase the scariest diagnosis. But sometimes, the solution isn’t in a procedure or a scan—it’s in the details.

And sometimes, it’s as simple as a piece of tape.

Further Reading & Resources

  1. El-Orbany M, Salem MR. Endotracheal tube cuff leaks: causes, consequences, and management. Anesth Analg. 2013 Aug;117(2):428-34. ​pubmed.ncbi.nlm.nih.gov

  2. Chen L, Zhang M, Li Y, et al. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Emerg Med J. 2012 Mar;29(3):e88. ​pmc.ncbi.nlm.nih.gov

  3. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008 Jul;134(1):117-25.

  4. Nickson C. Endotracheal tube cuff leak. Life in the Fast Lane [Internet]. 2018 Sep 8. ​litfl.com

  5. Chen L. Bedside ultrasonography for diagnosis of pneumothorax. Quant Imaging Med Surg. 2015 Aug;5(4):618-23. ​qims.amegroups.org


 

ABOUT THE AUTHOR

Lane is a physician assistant in the ICU with a passion for critical care. She kicked off her career in infectious disease before tackling a tough critical care residency at Medical College of Wisconsin in Milwaukee. After completing her training, she made her way to Georgia and has been a valued member of our team since 2022. When she’s not at the hospital, Lane loves biking, hanging out with her two dogs, and spending time with her family.

 

Lane R1 Comment