Post-operative outcomes
Time elapsed from recent MI
Cholecystectomy (%)
30-day MI
0–30 days
28.8b
31–60 days
17.8b
61–90 days
6.5b
91–180 days
5.7b
181–365 days
3.9b
No Recent MI
0.9
30-day mortality
0–30 days
10.5b
31–60 day
6.9b
61–90 days
5.9b
91–180 days
4.8b
181–365 days
5.9b
No recent MI
2.3
1-year mortality
0–30 days
28.0b
31–60 days
26.4b
61–90 days
19.9b
91–180 days
18.7b
181–365 days
19.2b
No recent MI
8.0
Table 13.2
Odds ratio of repeat myocardial infarction (MI) or mortality after cholecystectomy
30-day MI [RR (95 % confidence interval)] | |
---|---|
0–30 days | 26.59 (15.37-34.73) |
31–60 days | 21.95 (13.13–32.54) |
61–90 days | 7.15 (2.46–14.14) |
91–180 days | 4.74 (1.97–7.97) |
181–365 days | 4.71 (2.43–7.60) |
30-day mortality [RR (95 % confidence interval)] | |
0–30 days | 3.84 (2.06–6.38) |
31–60 days | 2.08 (0.86–3.93) |
61–90 days | 1.56 (0.41–4.34) |
91–180 days | 1.58 (0.68–3.05) |
181–365 days | 2.23 (1.25–3.38) |
Cholecystectomy Following Stroke
The time to perform elective surgery after a major cerebrovascular event has been controversial. After a stroke, the brain must recover sufficiently from the insult before further ischemia can be tolerated. From a cellular standpoint, the past ischemia and inflammation need to be resolved fully before the brain can withstand any new hemodynamic stressors from surgery and anesthesia. Cerebral autoregulation is also impaired following a stroke [48, 49]. This alteration in normal cerebral physiology allows the brain to be more vulnerable to subsequent ischemic events for an indeterminate time course. Aries et al. studied this phenomenon by examining transcranial Doppler studies after an ischemic stroke and found a progressive deterioration of cerebral autoregulation in the first 5 days after stroke. The authors also concluded that a full recovery back to baseline of cerebral autoregulation required at least 3 months and possibly more [49].
Unfortunately, concrete recommendations regarding the safety of elective surgery following stroke are largely nonspecific and based largely on opinion. A recent investigation of the association between prior stroke and further risk of adverse cardiovascular events found that prior ischemic stroke was associated with an adjusted 1.8 and 4.8-fold increased relative risk of 30-day mortality and 30-day major adverse cardiovascular events, respectively, compared to those without prior stroke [50]. An interpretation of these findings can be that the risk for stroke parallels the recovery of the brain’s cerebral autoregulation as patients in this study with strokes were particularly at morbidity for the first 3 months after the stroke and the risks did not fully decrease until about 9 months after the stroke (Table 13.3). The increased risk did not differentiate between low- and high-risk surgeries. Based on these data, a logical recommendation is that elective surgery should be delayed for at least 3 months and preferably 9 months following a major cerebrovascular event.
Table 13.3
Adjusted Odds Ratios of 30-Day Major Adverse Cardiac Events Stratified by Stroke Prior to Surgery and Time Elapsed Between Stroke and Surgery
Crude events,No. | Sample size,No. | Odds ratio (95 % CI) | ||
---|---|---|---|---|
30-day MACE | ||||
No prior stroke | 1923 | 474,046 | 1 [Reference] | |
Prior stroke anytime | 389 | 7137 | 4.03 (3.55–4.57) | |
Stroke <3 months prior | 153 | 862 | 14.23 (11.61–17.45) | |
Stroke 3 to <6 months prior | 34 | 469 | 4.85 (3.32–7.08) | |
Stroke 6 to <12 months prior | 37 | 898 | 3.04 (2.13–4.34) | |
Stroke ≥12 months prior | 165 | 4908 | 2.47 (2.07–2.95) | |
30-day all-cause mortality | ||||
No prior stroke | 2914 | 474,046 | 1 [Reference] | |
Prior stroke anytime | 254 | 7137 | 1.75 (1.51–2.03) | |
Stroke <3 months prior | 66 | 862 | 3.07 (2.30–4.09) | |
Stroke 3 to <6 months prior | 21 | 469 | 1.97 (1.22–3.19) | |
Stroke 6 to <12 months prior | 29 | 898 | 1.45 (0.95–2.20) | |
Stroke ≥12 months prior | 138 | 4908 | 1.46 (1.21–1.77) | |
30-day ischemic stroke | ||||
No prior stroke | 368 | 474,046 | 1 [Reference] | |
Prior stroke anytime | 210 | 7137 | 16.24 (13.23–19.94) | |
Stroke <3 months prior | 103 | 862 | 67.60 (52.27–87.42) | |
Stroke 3 to <6 months prior | 21 | 469 | 24.02 (15.03–38.39) | |
Stroke 6 to <12 months prior | 16 | 898 | 10.39 (6.18–17.44) | |
Stroke ≥12 months prior | 70 | 4908 | 8.17 (6.19–10.80) |
Acute Acalculous Cholecystitis
The utility and necessity of cholecystectomy after acute acalculous cholecystitis (AAC) has been debated for some time. The disease most often occurs in patients with more overall illnesses and comorbidities who cannot tolerate surgery at the time of diagnosis. The main populations for AAC include hospitalized patients, those with long-term illnesses, and those with chronic diseases. Other frequently cited groups with AAC include patients with trauma, burns, recent surgery, abdominal infection [38], diabetes mellitus [38], abdominal vasculitis [51], end stage renal disease [52], congestive heart failure, and recent resuscitation from cardiogenic or hemorrhagic shock [53]. Other groups for this disease include cancer patients with severe metastatic disease [54], acute myelogenous leukemia [55], and bone marrow transplant patients [56].
The risk factors and causes of AAC are generally present in the most severely ill hospitalized patients. Overall, AAC appears to be a result of failure of the gallbladder microcirculation with cellular hypoxia. Bile stasis and gallbladder ischemia have been generally implicated in the initial pathogenesis of AAC. Volume depletion, use of opioid analgesics, total parenteral nutrition, and even mechanical ventilation with positive end-expiratory pressure may facilitate the progression to AAC [38]. Gallbladder mucosal perfusion can be further decreased by hypotension, or the administration of vasoactive drugs. Reperfusion injury which can result in a variety of hospitalized settings has also been shown to contribute to AAC [38].
These observations may explain the high rates of gallbladder necrosis and perforation in patients with AAC compared to calculous cholecystitis [51, 57–59]. The differences in arterial perfusion patterns between acute calculous cholecystitis and AAC further supports the finding that AAC results from ischemia [60]. Gallbladders with gallstone disease were noted to have arterial dilatation and extensive venous filling consistent with acute inflammation, while AAC gallbladders have multiple arterial occlusions and minimal to absent venous filling.
As mentioned, many clinicians feel the obstruction of the cystic duct must be resolved before considering removal of the percutaneous drain in patients with AAC. Either tube cholangiography or clamp trials of the percutaneous tube are recommended after resolution of symptoms to determine whether the cystic duct is indeed patent and to confirm the absence of gallstones. If these criteria are met, the percutaneous drain may be safely removed and a cholecystectomy may not be required.
If the patient has persistent obstruction of the cystic duct, consideration for delayed cholecystectomy is required. Patients with AAC in whom death from underlying disease is expected in the near term should be considered for continued nonoperative management for their gallbladder disease. The timing of death in patients with terminal cancer, Gold stage IV COPD, NYHA class IV heart failure, or end stage hepatic failure is impossible to predict. The risk and benefits of surgery must be weighed against the risk of recurrent biliary tract disease. Although laparoscopic cholecystectomy appears to be better tolerated, laparoscopic gallbladder removal may require conversion into an open procedure. Risks of surgery in patients with multiple comorbidities are difficult to quantify and require frank conversations between physicians and patients. Although age does not pose an absolute indication for nonoperative management, patients older than 70 who require emergent abdominal surgery with ASA scores of 3 or 4 have reported mortalities of 31 % and 57 % respectively. Morbidity rates for ASA 3 or 4 have been reported as 63 % and 100 % [61]. Again, the aforementioned risk calculators may be beneficial in assistance to patient and family counseling.
Summary
Early cholecystectomy is the treatment of choice for acute cholecystitis. When patients are considered to have unacceptable risk for anesthesia and surgery, other nonoperative approaches may be considered including antibiotics with or without percutaneous drainage as shown in Fig. 13.1. If the patient’s comorbidities can be successfully treated and the patient medically optimized, then surgery may become an option. For those in whom the risk of surgery remains high for acute calculous or acalculous cholecystitis, continued percutaneous drainage may be necessary. In some cases, removal of the drain can be performed when the cystic duct becomes patent in asymptomatic, stable patients.