Postoperative cervical hemorrhage is a rare but life-threatening complication that can cause severe morbidity. Different mechanisms leading to asphyxia have been described based only on clinical observation.Methods:
We performed a series of in vivo animal studies simulating post-thyroidectomy hemorrhage and its effect on respiratory drive. Three series of tests were carried out in 12 German domestic pigs under general anesthesia. The pigs were breathing spontaneously with secured airways. An additional series using functional magnetic resonance imaging of the pigs’ brainstem was also conducted.Results:
The first experimental series carried out on 2 animals revealed an obvious difference between the effects of cervical hemorrhage and external bleeding with development of hemorrhagic shock. An experimental setting for the repeated simulation of cervical hemorrhage was established. A pressure-dependent mechanism was discovered that led to apnea in every animal despite the secured airway. In 8 of 10 animals, relief of cervical pressure led to complete respiratory recovery. The test was repeated up to 6 times per pig. Apnea was induced in 25 of 25 test procedures (100%) and was followed by respiratory recovery in 22 of 25 tests (88%). The threshold pressure at which the respiratory rate started to decrease was 47 ± 14 Torr when blood was used to increase the cervical compartment pressure. When silicone oil was used in a further experimental series, the threshold pressure was similar at 44 ± 21 Torr. The cervical compartment pressure needed to induce apnea was 74 ± 18 Torr using blood and 74 ± 39 Torr using silicone oil, both of which exceeded the mean arterial pressure by 28 Torr during apnea. Functional magnetic resonance imaging revealed a decrease in brainstem activity during phases of increased cervical compartment pressure, which suggests a possible role for cerebral vascular perfusion.Conclusion:
Respiratory drive can be suppressed by increased pressure in the cervical compartment, possibly because of a pressure-dependent impairment in cerebral perfusion through a form of cervical compartment phenomenon or, less likely, a pressure-dependent reflex (nervous) mechanism.