A Flood of Blood in the Airway

During intubation,  any liquid in the mouth that obscures the view of larynx not only hinders visualization, it risks aspiration. We’re used to being able to rapidly suction the mouth clear or secretions, blood, or vomit and then have a clear view of the larynx. But sometimes, either because of continued profuse bleeding or massive emesis, fluid continues to accumulate while we’re watching. How can you manage this situation and successfully intubate?

Case #1

The year was 1982. The patient was an 18 year old girl on the liver transplant list. She had end stage cirrhosis due to what at the time was called “non A- non B” hepatitis. She had been admitted to the ICU that day to be worked up for a stable upper GI bleed. The most likely etiology was her esophageal varices: superficial esophageal veins that have become abnormally distended due to portal hypertension in end stage liver disease. So far she had been rock stable — that was about to change.

When I, the ICU fellow, reached the bedside, the patient was coughing and sputtering blood onto the bed sheets and there was blood everywhere. Her varices were bleeding profusely and she was going to drown in her own blood if we didn’t intubate her now. Her blood pressure was 80/50 and her pulse was 150.

I ordered the crash cart and asked for blood to be brought from the blood bank while we were giving her a bolus of crystalloid. We kept her on her side, in trendelenburg position until the last possible moment to allow the blood to drain out of her mouth. Once ready, I administered an induction dose of ketamine and succinylcholine. Ketamine would help to maintain her blood pressure.

As the drugs took effect we laid her flat, still in steep trendelenburg. This position usually lets the blood pool up and away from the larynx allowing the intubator to see the landmarks. All I could see was a puddle of blood welling up. Sucking the blood through the yankauer catheter could not clear the mouth fast enough to keep it clear.  Intubation was impossible under these conditions; something needed to be changed, quickly.

We turned her onto her left side and placed the open end of the suction tubing itself into her mouth to allow it to suction continuously. The side position allowed the blood to drain out as fast as it entered her mouth and let the tongue fall to the left, where I wanted it to go anyway. I was able to intubate her.

After resuscitation with 9 units of blood, 4 units of FFP and a 6 pack of platelets plus about 5 liters of normal saline, the bleeding slowly stopped and we stabilized her. She eventually went on to successful transplant.

Afterward, I and the entire team went down to employee health for gamma globulin shots because we were covered in her blood and thus exposed to non-A, non-B virus.

Case #2

As I ran into the ICU to intubate during a cardiac arrest resuscitation effort, I knew immediately that this was not going to be easy. The nurses at the head of the bed were suctioning huge volumes of emesis out of the patient’s mouth. The patient was flat on her back and no one at the time was ventilating because they were afraid to stop suctioning to apply the mask.

I took a quick look with my laryngoscope but could see nothing but emesis.

Normally I would turn the patient left side down to let the emesis drain out and intubate with the patient on her side. However, I couldn’t turn the patient lateral without stopping chest compressions. I quickly put the bed into steep trendelenburg to get the emesis to puddle up and  away from the airway as best I could. I then placed the bare suction tubing into the back of the throat where it could suck emesis as soon as it appeared. I turned the patient’s face as far to the left as possible to let things drain.

I gave the patient several breaths with the ventilation bag, satisfied that the liquid was being removed and that little was going down the trachea. These days I often bring the glidescope with me when I go to an airway emergency because you never know if the patient you’ve been called to help has a difficult airway, or is in a difficult position, such as on the floor.  With an emergency intubation, minimizing repeated intubation attempts and rapidly establishing an airway can prevent further loss of patient stability.

With the patient still in steep trendelenberg and with my helper holding the suction catheter, ready to move it or remove it if I needed them to, I quickly used the glidescope to intubate.

We could now ventilate the patient. The hospitalist was ultimately able to establish a rhythm and eventually stabilized the patient.

Managing Blood or Other Secretions In the Airway

Active bleeding in the airway makes intubation very challenging: airway bleeding, in both the acute trauma and postoperative settings, means that the anatomy may be altered and landmarks difficult to identify; hemodynamic instability makes choice of sedative/hypnotic agents and muscle relaxants problematic; and usually, the patient has a stomach full of blood ready to aspirate.

In addition, the patient is at risk of aspiration. Hypoxia and even asphyxiation is possible if the airways are filled with blood and not oxygen. There is risk of inducing shock with induction agents. Finally, the providers are going to be exposed to the risk of any blood born pathogens.

Know how to deal with this dangerous and demanding situation.

  • Consider awake intubation, although that may not be an option. That wasn’t possible in either of the above cases. Also, fiberoptic bronchoscopy with massive fluid in the airway is extremely challenging. However, I have performed awake direct laryngoscopy in a patient in shock.
  • Always pre-oxygenate when you can, especially if you’re patient is awake. Your patient will b better able to tolerate longer periods of apnea.
  • You will need helpers, but they need you to direct their efforts to assist you. Think out loud, don’t make them guess your next move or possibly get in your way! Tell your helpers what you plan to do, what you’re worried about, what you need them to do, and when you need them to do it.
    • Place a helper, each with a suction, on either side of the patient .
    • They need to suction while you are intubating but they also need to avoid hitting your hand or obstructing your view.
  • Consider placing a orogastric or nasogastric tube  before you start and suction it completely if possible
  • Consider placing the bed in steep trendelenburg — this will not interfere with chest compressions if in progress
    • On the positive side, Trendelenburg allows fluid to puddle and drain away from the airway.
    • On the negative side, Trendelenburg  decreases functional residual capacity (the patient’s reserve “oxygen tank”) thereby decreasing how long they can hold their breath. It also shifts the larynx and tongue upward, which may potentially make intubation a bit more challenging.
  • Turn the patient onto the side if you can — left side is optimal since the tongue will shift out of the way of your laryngoscope blade. If you can’t, sometimes turning the face to the left side allows sufficient liquid to drain.
  • SUCTION IS KEY! You must ensure adequate suction. This may mean using unguarded suction tubing. If so,  make sure your assistant keeps it open as it will tend to suck up against the tongue and obstruct
  • Choose your induction medications wisely. Inducing shock is a real potential risk.
  • Be prepared for emergent cricothyrotomy.
    • Have the equipment and your helper ready to go.
    • Know when to stop intubation attempts. Failure to promptly recognize the failed airway leads to disaster!
  • Consider using your video laryngoscope if you have one, however be aware that the camera lens can be easily blocked by secretions. Direct laryngoscopy is often the best method
  • Protect yourself and your crew! Don protective gowns, wear a mask and eye protection. Wash well afterward and consider changing if your clothes are soiled.

What about an LMA?

Could you use an LMA in a can’t-intubate-can’t-ventilate scenario with massive amounts of blood or emesis in the airway?  Its definitely not optimal because of the aspiration risk and it depends on the source of bleeding.

  • If you’re dealing with a massive nose bleed, an LMA, especially if it’s an LMA with a gastric suction port like the LMA Supreme, could be used to protect the airway. In this case the blood is not within the channel of the LMA so ventilation is possible and you can suction the stomach through the gastric port.
  • If the bleeding is pulmonary, obviously the blood is coming from a source inside the LMA and an LMA would not be protective.
  • With bleeding gastric varices or massive emesis you could argue that placing a device like the LMA Supreme would allow you to vent the liquid away from the airway, allowing you to ventilate with some protection and perhaps even use the LMA’s channel to intubate.

Cricothyrotomy would be the more optimal way to proceed in the can’t intubate can’t ventilate scenario with massive airway hemorrhage as it definitively protects the airway. However, cricothyrotomy may or may not be an option depending on the equipment available and the skill set of the providers involved. If the choice is ventilation with a continued risk of aspiration vs. not ventilating at all, then by all means try an LMA.

Patients in shock frequently vomit, sometimes profusely. Trauma, nose bleeds, or esophageal varices can produce massive bleeding in the oropharynx. You need to be prepared at all times to deal with liquid in the airway.

May The Force Be With You!

Christine Whitten MD, author Anyone Can Intubate, 5th Edition

Safe Medication Administration For Our Smallest Patients

For the last 3 months, I’ve been teaching critical event training classes for our OR and Perioperative RNs, Anesthesia MDs and CRNAs, and OR techs in preparation for opening our new hospital in San Diego. Several of the scenarios involved pediatric cases. As part of that process, I’ve been reviewing with my providers ways to avoid the potentially deadly problem of pediatric drug dosing errors as well as ways to avoid them.

Pediatric drug errors are unfortunately common. The literature states that medication errors occur in 5% to 27% of all pediatric medication orders, a very sobering number. Considering that many of these errors occur in the smallest, and therefore most vulnerable, of our little patients, the potential impact is especially great. Let’s discuss some of the ways to make pediatric medication administration safer. Continue reading

Difference in Ventilating With a Self-Inflating Ventilation Bag vs. a Free Flow Inflating Bag

Ventilating with a bag-valve-mask device requires a good mask seal against the face in order to generate the pressure to inflate the lungs. But it also requires knowledge of how to effectively use the ventilation device to deliver a breath. This article will discuss the differences in ventilation technique for self-inflating vs free-flow ventilation bags. Continue reading

Ventilation Perfusion Mismatch

Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered.

When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation/perfusion mismatch is said to exist. The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

What Is The Importance Of Dead Space?

Dead space is the portion of the respiratory system where tidal volume doesn’t participate in gas exchange: it is ventilated but not perfused. There are three types of dead space: anatomic, physiologic, and that dead space belonging to any airway equipment being used to assist ventilation. They all impact how well a patient ventilates.

Anatomic Dead Space

Anatomic deadspace consists of the parts of the respiratory tract that are ventilated but not perfused. It consists of conducting airways such as the trachea, bronchi, and bronchioles —structures that don’t have alveoli. It’s called anatomic because it’s fixed by anatomy and doesn’t change.

About a third of each normal breath we take is anatomic dead space, which means that a third of each breath is essentially wasted. Dead space is age dependent. It’s highest in the infant at 3 ml/kg ideal body weight and is about 2 ml/kg in older children and adults. An adequate tidal volume must include enough volume to also fill the deadspace, otherwise not enough air enters the alveoli and the patient hypoventilates.

A healthy teenage boy weighing 60 kg (132 lb) will have about 360 ml of alveolar ventilation . A healthy infant weighs about 2.7 kg (6 lb) will have about 22 ml alveolar ventilation. In terms of liquid volume, that’s a can of soda vs. about a tablespoon — an impressive difference. Let’s look at an example of how anatomic deadspace impacts adequacy of breathing.

Anatomic dead space is an important concept in determining if tidal volume is adequate.

Anatomic dead space is an important concept in determining if tidal volume is adequate. It’s important to realize that for a particular patient, barring trauma or surgical alteration, anatomic dead space is fixed.

Our teenager will have an anatomic dead space of 120ml (2 ml/kg X 60 kg), which means that of his 480 ml breath, roughly 360 reaches the alveoli and 120 doesn’t participate in exchange gas at all. For our baby, the anatomic dead space is 8 (3 X 2.7). So again that’s 14 ml of air reaching the alveoli and 8 ml being effectively wasted.

Let’s say our baby is sick with nausea, vomiting, and a fever of 101F (38C) . She starts to hypoventilate and is now breathing tidal volumes of 10 ml. She’s still moving 10 ml of gas in and out of her mouth and you can feel her breathing and see her chest move, even though it looks shallow. Her dead space is still 8 so now the amount of gas reaching her alveoli is 2 ml (10 ml – 8 ml). That’s not enough.

Remember, oxygenation and ventilation are different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. If you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Oxygenation mostly changes PaO2. Ventilation mostly changes PaCO2.

If you’re providing our baby with extra oxygen, she may not become hypoxic right away because enough oxygen will still reach her alveoli to maintain her oxygen saturation for a while. However, she is barely moving her dead space gas back and forth so her ventilation is poor. As a result, her carbon dioxide starts to rise. Hypoventilation leads to increased PaCO2.

Acute values above 50 mmHg are significant and require treatment, values above 70 mmHg can be life-threatening because of respiratory acidosis among other things. Each 10 mmHg change in PCO2 roughly changes your pH by 0.1. So all other things being equal,  a PCO2 of 70 is associated with a pH of 7.1. If carbon dioxide rises into the 70–80mmHg range it will also profoundly sedate the patient. This worsens hypoventilation, and increases carbon dioxide even more. Respiratory rate eventually slows and the patient can stop breathing.

It’s important to realize that by providing extra oxygen, a good practice, you delay the onset of hypoxia, but you may also delay the diagnosis of dangerous hypoventilation if you’re not looking for it. For another clinical explanation of how hypoventilation causes hypoxia and the difference between oxygenation and ventilation  click here.

Physiologic Dead Space

A second type of dead space, physiologic dead space, consists of alveoli that are ventilated but lack capillary blood flow to pick up oxygen and drop off carbon dioxide. In other words, they are not perfused.

In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.

In physiologic dead space, alveoli are ventilated but not perfused. Physiologic dead space can change as lung perfusion changes.

However, unlike anatomic dead space, which is fixed, physiologic dead space can change from minute to minute with alterations in cardiac output and pulmonary blood flow. Many things can impair alveolar perfusion and increase physiologic dead space such as:

  • cardiovascular shock (blood flow to the lungs is decreased),
  • emphysema (lots of enlarged alveoli with less surface area and fewer alveolar capillaries)
  • pulmonary embolus (flow is blocked by clot).

Let’s go back to the baby in our clinical scenario. Perhaps the baby is hypoventilating because she is in shock from diarrhea. Now she has two reasons for respiratory failure:

She’s hypoventilating, and barely exceeding her anatomic dead space.

She’s in cardiovascular shock. Hypovolemia and acidosis is decreasing her cardiac output and lung perfusion. Her physiologic dead space has increased and she is not perfusing all of the alveoli that are still getting ventilated. Remember, hypovolemia and shock increases physiologic dead space. And this brings us to the concept of shunt.

What Is Pulmonary Shunt?

The second type of V/Q mismatch is shunt. Shunt is the opposite of dead space and consists of alveoli that are perfused, but not ventilated.

In pulmonary shunt, alveoli are perfused but not ventilated.

In pulmonary shunt, alveoli are perfused but not ventilated.

Blood flowing past poorly ventilated alveoli doesn’t pick up additional oxygen. This poorly oxygenated blood returns to the heart and mixes with oxygenated blood coming from other areas of the lungs that are ventilated. The mixture lowers the total oxygen content of the arterial blood, producing hypoxemia. The larger the shunt, the lower the oxygen content.

Giving a patient with an intrapulmonary shunt 100% oxygen to breathe won’t increase the PaO2 much, if at all, depending on the size of the shunt because the alveoli that are being ventilated are already filled with oxygen and the blood from the non-ventilated alveoli won’t pick up any more.

Common causes of shunt occur in lung tissue disease and include:

  • pneumonia and pulmonary edema: some alveoli filled with fluid
  • tissue trauma: alveolar wall swelling
  • atelectasis: collapse of alveoli from failure to expand, or absorbsion of the air out of the alveoli without replacing it
  • mucous plugging: air can’t get into the alveoli
  • pulmonary arteriovenous fistulas

You can also have certain defects in the heart that cause abnormal mixing of oxygenated and un-oxygenated blood, like a right to left shunt, but that’s a different mechanism from pulmonary shunt.

Many types of shunt can be improved with treatment. The most common example of shunt is atelectasis, which is collapse of alveoli. For example, taking deep breaths or sighs easily treats atelectasis, one of the most common day-to-day causes of shunt. We do this naturally several times an hour, often without even being aware of it. In contrast, patients who take very shallow breaths without sighing often develop atelectasis. Factors that can cause atelectasis to develop are:

  • painful breathing from surgery or trauma
  • depressed levels of consciousness such as from drug,  injury, or illness
  • the disease process itself

Ventilation Perfusion Mismatch

As you can see it’s possible, and quite common, for both deadspace and shunt to be present in the same patient. Looking back at our baby one more time her potential causes of hypoxemia/hypoxia include:

  • Hypoventilation: tidal volumes close to her anatomic dead space volume producing inadequate alveolar ventilation. If you think about it, this is producing poorly ventilated alveoli which are still being perfused- that’s shunt
  • Shock: increasing her physiologic dead space.
  • Fever of 101 which will increase her metabolic rate and cause her to need even more oxygen than normal

V/Q mismatch can lead easily lead to hypoxemia and hypercarbia.

May The /Force Be With You

Christine Whitten MD, Author Anyone Can Intubate 5th Edition

all illustrations copyright Christine Whitten MD

 

Intubation With A Curved Blade

Direct laryngoscopy depends on being able to bring the 3 axes of the airway into alignment to see the larynx. Curved blades are commonly used, especially by beginners because they are more forgiving of less than optimal placement and provide more room to pass the tube. However, it’s important to use them correctly. This article will discuss intubation technique using a curved blade. Straight and curved blades use different techniques for bringing the larynx into view. For a discussion of how to use a straight blade click here. Continue reading

Help! My Anesthesia Machine’s Not Working!

There is nothing quite as scary as being in the middle of administering an anesthetic and having your anesthesia machine fail. In my 36 years of anesthesia practice I’ve had this happen to me a few times. Knowing how to quickly troubleshoot your machine, and knowing how to protect your patient are important, potentially life-saving skills. It helps to have thought through the steps to rescue the situation before it happens to you. Continue reading

Codeine Can Be Risky In Small Children, Especially Those With Sleep Apnea

Although the initial FDA warnings about potentially fatal codeine overdose in children were released in 2012, I’m recently discovered that a few of my surgeon and nursing colleagues were still unaware of the potential risks. Therefore I thought it might be helpful to bring up the topic so people can remind their own colleagues of the risks. Continue reading