“You don’t get another chance, life is no Nintendo game!”
-Eminem, “Love the Way You Lie”
I once had a patient with polycystic kidney disease. The autosomal dominant disease is caused by mutations in cell signaling genes PKD1, PKD2, and PKD3 genes- named for the disease in which the mutations occur (PKD=polycystic kidney disease). When the genes are defective it causes widespread cyst formation in organs such as the kidneys, liver, and pancreas. It also causes aneurysms in blood vessels. The most recognized sign is enlarged, cystic, non-functional kidneys. If the kidneys become large enough they can cause abdominal pain, acid reflux, and shortness of breath. My patient was a young guy in his 30s with these exact problems. He was scheduled for robotic resection.
Robotic urologic procedures are ominous for anesthesiologists. Most of the time they have no complications and the patients do well. Once in a while a major blood vessel is injured, the bleeding cannot be controlled with the robotic arms, and the patient can bleed out before the robot can be removed from the surgical field for an open surgical exploration. Large blood vessels like the renal artery, renal vein, inferior vena cava, and abdominal aorta can hemorrhage 1L of blood per minute. For perspective the blood volume of a 70kg person is about 5.5L. Sometimes the difference between a successful surgery and massive hemorrhage is measured in millimeters. I’m always impressed my surgical colleagues don’t injure MORE blood vessels. Their results are a testament to their precision.
On the morning of surgery anesthesia was induced and the patient intubated uneventfully. The robot was docked then the urologists carefully dissected the fascial planes around the massive, cystic kidneys. Considering two patients died the previous year from vascular injuries during robotic urological surgery my eyes were glued to the video screen of the surgery. Hundreds of these procedures are done every year- the overall mortality rate is very low. I hoped this case would be in the uneventful 99%. Then I saw pulsating red liquid.
In the next 5 minutes I gave him a liter of IV fluids. The surgeons quickly ligated the bleeding artery. I breathed a sigh of relief as my sphincters relaxed. The rest of the surgery proceeded uneventfully. I extubated him in the OR then transported him to the post-anesthesia care unit (PACU), one floor below. At that time he was breathing spontaneously without support. Upon arrival the PACU about 3 minutes later a nurse plugged in his pulse oximeter- his oxygen saturation was 10%. I immediately ran to the bedside. He wasn’t breathing. I quickly asked for an ambu-bag. As I watched his lips turn blue I bagged oxygen into his lungs. His saturation slowly rose to 100% as the oxygen diffused from his lungs into his blood and circulated around his body.
The next 30 minutes were the scariest of my life. Even though he was breathing on his own and only 3 minutes had passed since traveling from the OR to the PACU I was still nervous. Hypoxic brain injury also only takes minutes. The only thing left to do was wait- as the anesthesia wore off we would know if he had brain damage or not. After what seemed like an eternity he woke up neurologically intact. I went into the hallway and paradoxically laughed with my head in my hands. I almost gave my patient brain damage.
As I talked with my attending (and several other attendings) we reviewed everything I did so I could learn from the adverse event. I confirmed my patient was breathing before leaving the operating room, but looking back I did a few things differently. The operating nurse had a trainee so I let her drive the bed to the PACU- I usually drive to watch my patient’s breathing. I asked the OR nurse if there was oxygen in the tank, she said yes- I should have verified it for myself.
Perhaps he obstructed- the soft tissue of the mouth and pharynx loses its tone under anesthesia- sometimes it can prevent proper adequate ventilation. But my patient was breathing appropriately when he left the OR! Perhaps there was no oxygen in the O2 tank? Perhaps it wasn’t turned on? Perhaps he simply obstructed and I did not catch it because I didn’t drive the bed? I have taken thousands of patients to the PACU without this complication. Some I watched, some I didn’t. Some I checked the O2 tank myself, some I didn’t. Most I drove, some I let my medical student or a nursing student drive. What is the lesson?
Anesthesiology has changed significantly since the 1940s. Before pulse oximetry and capnography anesthesiologists would literally watch their patients breath. Small barely perceptive changes in their chest excursion and breathing patterns were the only differences between adequate and inadequate ventilation. Modern anesthesia is safer than anesthesia in the 1940s due to better technology, monitors, and drugs- and anesthesiologists who know how to apply those complex tools to ambiguous clinical situations. Some days I feel like a modern anesthesiologist doing dangerous cases on complex patients without complications. And some days I feel like an anesthesiologist in the 1940s, watching my patient breathe, praying he will wake up without brain damage.
The next day I did a cardiac catheterization case on a pleasant man in his 80s. He was calm, kind, and grateful for the doctors and nurses- the ideal patient. The case was uneventful. He was extubated in the same manner as my polycystic kidney disease patient. He was also breathing on his own. The nurses and I moved him from the OR bed to the gurney before transport to the PACU. I checked the oxygen tank. It was empty.