High End-Tidal CO2 During Tonsillectomy
A 4 y/o 15 kg male is undergoing tonsillectomies & adenoidectomy + bilateral myringotomy tubes for recurrent otitis media. No history of sleep apnea. Child had temp 99.6 -100 F preop (temporal artery scanner). Preop exam: without cough or abnormal chest auscultation. Sevoflurane induction. Easy intubation (uncuffed 4.5 tube) without muscle relaxant. Initial spontaneous ventilation 60-70 cc tidal volumes. ETCO2 rose to >80 mm despite manually controlled ventilation of 30 breaths/min and TV 70-100 cc. Heart Rate was 130-140's with no observed increase in HR with the hypercarbia. Child is not rigid and rectal temperature is 36.8 C.
1. Which of the following might explain the severe hypercarbia?
a. Right mainstem intubation
b. Insufficient minute ventilation (Tidal volume X respiratory rate)
c. Malignant hyperthermia
d. Carbon dioxide rebreathing
e. Tube kinked or partially obstructed with blood or secretions
2. True or False: The absence of rigidity rules out MH as the cause of hypercarbia
No increase in Peak Inflation Pressure (PIP) after mouth gag placement. Breath sounds equal bilaterally. SpO2100% intraoperatively. Maximum temp 37.9 C. The hypercarbia resolved during emergence prior to extubation; operating time was 15 minutes.
3. True or False: The anesthetic was too short to trigger an MH episode.
Other intraoperative medications included 1 mg morphine and 8 mg Decadron. An ABG was not obtained in the OR.
Endotracheal tube removed without secretions or clot in tube. In PACU, heart rate continued to be 130-140, no rigidity. SpO2 low 90's on room air, respiratory rate in 20's. HR decreased to 110-120. The MH Hotline was called. An ABG performed in the PACU did not show any acidosis. CK 128 at 8 hours postop, no hyperkalemia (K+ 3.6 mEq/L). Dantrolene was not administered.
CXR in PACU showed mildly increased perihilar markings (possible viral bronchiolitis), WBC 8.6K. Child discharged home following day. Subsequent recovery was uneventful.
While certainly not typical MH, the Hotline consultant suggested that this might have been an abortive episode, given the unexplained hypercarbia, which persisted despite increased ventilation, and the limited duration of sevoflurane exposure. The lack of any other signs of MH (e.g. increase in HR, spontaneous hyperventilation, rigidity, increase CK and/or myoglobin) did not support the diagnosis.
The Hotline consultant spoke with the patient’s anesthesiologist several days later. He noted that, 3 days later, another patient in the same operating room had unanticipated hypercarbia with no other abnormalities, and the ETCO2dropped 20-25 mm after changing the condensation trap. The Inspired CO2 was less than 10. They were planning to have the gas analyzer and anesthetic machine inspected by their biomedical engineer. Interestingly, the case that followed the 1st patient did not have a high ETCO2.
In light of the isolated "hypercarbia" without an accompanying increase in heart rate or evidence of muscle injury, we agreed to re-classify this as due to monitor error. The anesthesiologist contacted the family to inform and reassure them that their child did not have an MH episode.
Answers:
- C,D
While hypercarbia, by definition, implies insufficient alveolar ventilation, if the tidal volumes were actually delivered to the patient, as opposed to merely intended, the child’s minute ventilation should have been sufficient to maintain normocarbia. If the tube was either kinked or partially occluded with secretions or blood, the peak inflation pressure would have increased and the tidal volume would have decreased. Equipment malfunction causing CO2rebreathing may result in increased inspired CO2and severe hypercarbia. Malignant hyperthermia may also result in severe hypercarbia, but inspired CO2should not be elevated at the onset of the episode. Right mainstem bronchus intubation does not result in hypercarbia unless minute ventilation is decreased, and even so, would not be expected to result in severe hypercarbia.
2) False: Life-threatening episodes of MH may occur without rigidity.
3) False: Larach et al analyzed data from MH episodes reported to the North American MH Registry. Patients aged 19 years and younger had a shorter time than older patients from induction to volatile anesthetic discontinuation (median 45 minutes with a first quartile of 19.0 minutes and a 3rd quartile of 90.0 minutes.)
Discussion: The Hotline consultant was puzzled by the reported severe hypercarbia measured by capnography in the absence of other signs of MH. The HR did not increase, and there was no laboratory evidence of muscle injury. There was also no evidence that supported the most common cause of intraoperative hypercarbia – hypoventilation. While the postoperative CXR suggested a respiratory infection, the child did not have clinical evidence (fever, sputum, increased respiratory rate, abnormal physical exam) consistent with a bronchitis or pneumonitis severe enough to result in severe hypercarbia. Persistence in follow-up was the key factor in uncovering that the hypercarbia was associated with erroneous carbon dioxide measurement. The intermittent nature of the problem is still unexplained – it is not clear why the problem did not recur in the case the immediately followed the reported case, but did recur several days later. It is also unclear why the measured hypercarbia resolved prior to extubation. Other troubleshooting measures that may be employed included briefly disconnecting the sampling line from the connector and breathe into it; one should see an ETCO2 ~40 mm. If the inspired CO2is increased (should be near 0), possibilities include exhausted or bypassed CO2absorbent, absence of CO2 absorbent (possible with newer Drager machines, though obvious on inspection), or an incompetent unidirectional valve. An incompetent unidirectional valve will result in significant hypercarbia that persists despite increasing ventilation and fresh gas flow.
Harvey Rosenbaum, MD
UCLA Medical Center
Los Angeles, CA
