A 1992 study of laparoscopic surgery found the incidence rate of subcutaneous emphysema ranges from 0.45 to 2.3% [3]. The incidence of subcutaneous emphysema due to robotic surgery is less understood, yet it can be assumed to be higher due to known risk factors of subcutaneous emphysema and the nature of robotic surgeries including more than five cannulas used, more torque used in the robotic arms leading to pressure on the incisions, increased intraabdominal pressure, and often longer procedure times greater than 3.5 hours [1]. \({\text{C}\text{O}}_{2}\) insufflation is known to cause respiratory acidosis, yet usually can be countered with use of increasing minute ventilation.
In this case, our patient had respiratory acidosis despite increase in minute ventilation, with mild metabolic acidosis, resulting in hyperkalemia. The hyperkalemia was treated intraoperatively, yet hypercarbia remained a notable problem throughout the surgery. The hypercarbia likely contributed to the delayed awakening from anesthesia. Other factors on the differential diagnosis were residual anesthetics, including ketamine given throughout the surgery for pain control, as the patient had nystagmus in the post anesthesia care unit.
The findings of subcutaneous emphysema on the chest xray, high \(\text{E}\text{t}{\text{C}\text{O}}_{2}\) intraoperatively, combined respiratory and metabolic acidosis and resulting hyperkalemia, point towards the significance of better understanding the consequences of \({\text{C}\text{O}}_{2}\) insufflation during robotic surgery.
A patient’s \({\text{C}\text{O}}_{2}\) production (\({\dot{\text{V}}\text{C}\text{O}}_{2}\)) is normally around 200 ml per minute under anesthesia, which would increase about 30% during a robot assisted laparoscopic surgery secondary to \({\text{C}\text{O}}_{2}\) absorption from \({\text{C}\text{O}}_{2}\) pneumoperitoneum [1, 4]. A patient’s current \({\text{C}\text{O}}_{2}\) production can be estimated by the following equation that includes two other variables: \({\text{P}\text{a}\text{C}\text{O}}_{2}\) and minute alveolar ventilation (\({\text{V}}_{\text{A}}\)) [5].
$$Pa{CO}_{2}=k\frac{\dot{V}{CO}_{2}}{{V}_{A}}$$
Equation 1. \(\text{P}\text{a}{\text{C}\text{O}}_{2}\) as a function of \({\text{C}\text{O}}_{2}\) production (\(\dot{\text{V}}\text{C}\text{O}2\)) and minute alveolar ventilation (\({\text{V}}_{\text{A}}\)). K is a constant.
Since \({\text{V}}_{\text{A}}\) equals to respiratory rate (\(\text{R}\text{R}\)) multiplying the difference of tidal volume and dead space (\({\text{V}}_{\text{t}}{\text{V}}_{\text{d}}\)) [6], Eq. 1 becomes Eq. 2:
$$Pa{CO}_{2}=k\frac{\dot{V}CO2}{RR({V}_{t}{V}_{d})}$$
Equation 2. \(\text{P}\text{a}{\text{C}\text{O}}_{2}\) as a function of \({\text{C}\text{O}}_{2}\) production (\(\dot{\text{V}}{\text{C}\text{O}}_{2}\)), respiratory rate (RR), tidal volume (\({\text{V}}_{\text{t}}\)) and dead space volume (\({\text{V}}_{\text{d}}\)). K is a constant.
If we move this term, RR, to the left of the equation, we get:
$$Pa{CO}_{2}\times RR=k\frac{\dot{V}{CO}_{2}}{({V}_{t}{V}_{d})}$$
Suppose k, tidal volume and dead space remain the same throughout surgery. Then we can simplify the previous equation and derive\(PaCO2\times RR=k{\prime }\times \dot{V}{CO}_{2}\)
$$Let \frac{k}{({V}_{t}{V}_{d})}={k}^{{\prime }}$$
$$Then Pa{CO}_{2}\times RR=k{\prime }\times \dot{V}{CO}_{2}$$
From the last equation, it is easy to see that the product of \(\text{P}\text{a}{\text{C}\text{O}}_{2}\) and \(\text{R}\text{R}\) is positively related to \(\dot{\text{V}}{\text{C}\text{O}}_{2}\). The higher the product, the higher the \({\text{C}\text{O}}_{2}\) production.
The following table is constructed with our patient’s data, listing the product of \(\text{P}\text{a}{\text{C}\text{O}}_{2}\) and \(\text{R}\text{R}\) at each time point.
Table 1
The product of \(\text{P}\text{a}\text{C}\text{O}2 \text{a}\text{n}\text{d} \text{R}\text{R}\) at each time point.
Time

\(\text{E}\text{t}{\text{C}\text{O}}_{2}\)

\({\text{P}\text{a}\text{C}\text{O}}_{2}\)

RR

\({\text{P}\text{a}\text{C}\text{O}}_{2}\) x RR

\({\text{V}}_{\text{t}}\)

8:00

30

39

12

468

584

9:00

32

41

10

410

521

10:00

39

48

16

768

538

11:00

44

53

18

954

602

12:10

45

54

18

972

585

12:40

41

50

23

1150

616

13:00

42

51

22

1122

550

14:05

36

45

19

855

561

15:00

31

40

11

440

596

16:25

41

51

16

816

460

From Table 1, we see the gradual increase in the products of PaCO2 and RR, and, therefore, \(\dot{\text{V}}{\text{C}\text{O}}_{2}\). It starts at 468, peaks at 1150 and drops to 816 before extubation. (When there is no ABG, \(\text{P}\text{a}{\text{C}\text{O}}_{2}\) is estimated with endtidal \({\text{C}\text{O}}_{2}\) plus 9 mmHg, a difference that is inferred from the ABGs drawn later.)
Of note, from the beginning of 456 to the peak of 1150, the product of PaCO2 and RR increases by about 2 and 1/2 times, suggesting \({\text{C}\text{O}}_{2}\) production has increased by the same degree. Since the \({\text{C}\text{O}}_{2}\) production during a typical robotic surgery only increase by 30% due to \({\text{C}\text{O}}_{2}\) pneumoperitoneum, quantitative analysis reveals that the only plausible explanation for excessive \({\text{C}\text{O}}_{2}\) production is subcutaneous emphysema [1, 3, 4].
For practical purpose, when the respiratory rate is more than two times as fast as the baseline (in order to maintain normal \({\text{E}\text{t}\text{C}\text{O}}_{2}\)) during a robotic surgery, the presence of subcutaneous emphysema is highly suspected.