Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (38 page)
Non-obstetric acute abdominal pain is relatively common in pregnancy, causes being similar to those in non-pregnant patients, and transabdominal US and MRI are the primary imaging modalities. Laparoscopic cholecystectomy is generally a safe therapeutic option in pregnancy.
21
Although traditionally invasive approaches during the first trimester have been avoided, more recent data indicate that minimally invasive surgery can be conducted with relative safety in the first trimester.
22,
23
Biliary imaging may be performed with intraoperative ultrasound, or with limited exposure fluoroscopy and foetal shielding. Management decisions must be based on the efficacy or otherwise of non-operative measures, fully informed consent and with foetal–maternal benefits being considered on an individual basis.
Torsion of the gallbladder is rare, may be partial or complete and can result in gallbladder necrosis. It can present with clinical and radiological features of acute cholecystitis without gallstones. Treatment is by cholecystectomy.
Acute inflammation of the gallbladder can occur in the absence of gallstones and is termed acute acalculous cholecystitis (AAC). Although AAC may present as a complication of a number of clinical conditions, it occurs most frequently in the critically ill or postoperative patient. Despite the fact that AAC is an uncommon entity, it does appears to be increasing in frequency.
24
Observational studies have suggested that AAC occurs in 0.004–0.05% of patients undergoing surgery.
25,
26
Although much less common than gallstone-induced acute cholecystitis, the mortality rate of AAC is significantly higher, in part reflecting the patient population affected.
24
The pathogenetic mechanisms in AAC are not clear. Most recent evidence suggests that AAC is a consequence of microvascular ischaemia resulting in gallbladder inflammation. Studies have demonstrated that the gallbladder arterial and capillary network is reduced and irregular in AAC compared with that in acute cholecystitis.
27
Furthermore, in animal models, the induction of a vasculitic process through the activation of factor XII causes AAC. As indirect evidence, AAC can occur as a consequence of systemic lupus erythematosus, polyarteritis nodosa and antiphospholipid syndrome. In critical illness states, gallbladder microvascular ischaemia probably occurs as a manifestation of the systemic inflammatory response syndrome.
The diagnosis of AAC is often difficult. Because it occurs principally in critically ill patients and in those who have recently had abdominal surgery, the symptoms and signs may be masked by coexisting problems. The critically ill patient may be sedated and/or ventilated, limiting the availability of historical information, and abdominal signs may be masked by sedation or drug-induced paralysis in the critical care setting. In the postoperative patient, abdominal signs may be limited by wound pain, and other more operation-specific complications may be considered as a cause for changes in the clinical condition.
Unfortunately, diagnostic imaging may also be unhelpful. Although US signs of AAC have been described (dilated gallbladder, gallbladder wall thickening, pericholecystic fluid and gallbladder sludge), these are not diagnostic. In a prospective series of 21 critically ill patients, all study subjects had gallbladder abnormalities on at least one occasion during serial US examinations; however, only four patients required intervention for AAC.
28
Similarly, although CT may demonstrate gallbladder abnormalities, these signs may again be non-diagnostic. Cholescintigraphy may be the most accurate method of identifying AAC. In a retrospective study of 27 patients with AAC, cholescintigraphy detected AAC in 9 of 10 patients (90%), whereas CT detected AAC in 8 of 12 (67%) and US detected AAC in 2 of 7 (29%).
29
However, these results must be viewed cautiously as every patient did not undergo all investigations. Moreover, other series have suggested a high incidence of false-positive cholescintigraphy scans in critically ill patients.
30
Because of the inaccuracy of imaging studies, the definitive diagnosis of AAC may only be made at laparotomy or diagnostic laparoscopy.
31
AAC must therefore be considered in all critically ill or postoperative patients with right upper quadrant pain, deranged LFTs or unexplained sepsis. With the difficulty of diagnosis in mind, one prospective study assessed the benefit of percutaneous cholecystostomy in 82 critically ill patients with unexplained sepsis.
32
In 48 patients (59%) there was rapid improvement in the clinical condition within 48 hours but ultrasound did not predict which patients would respond to cholecystostomy.
The optimal therapeutic strategy in AAC is not clear. In all patients, broad-spectrum antibiotic therapy should be instituted as 65% of bile cultures will be positive, with
Escherichia coli
the most common organism. Therapeutic interventions include cholecystostomy with or without interval cholecystectomy, or early cholecystectomy. Several series have demonstrated that percutaneous cholecystostomy is not only an effective immediate intervention but may also constitute definitive treatment as the likelihood of recurrent episodes is small.
33,
34
However, early cholecystectomy has been advocated because necrosis of the gallbladder may occur in up to 63% of cases,
29,
35
with perforation occurring in approximately 15%. It would therefore appear reasonable to manage AAC in critically ill patients with initial percutaneous cholecystostomy, but in the absence of rapid clinical improvement a complication should be presumed and cholecystectomy carried out. In those patients managed successfully by percutaneous cholecystostomy there does not appear to be an absolute requirement for interval cholecystectomy.
A high index of suspicion is required for the diagnosis of AAC in critically ill patients.
32
Percutaneous cholecystostomy under either US or CT guidance is the primary treatment unless there are signs of overt peritonitis when cholecystectomy is indicated. Failure to improve after cholecystostomy is also an indication for cholecystectomy.
Acute cholangitis may be defined as an acute pyogenic infection within the biliary tree. Because of the possibility of rapid disease progression, acute cholangitis is a potentially life-threatening condition that requires urgent therapeutic intervention.
Acute cholangitis arises as a consequence of biliary stasis with subsequent bacterial infection. Although a number of pathological processes may lead to biliary stasis, the most common underlying causes of acute cholangitis are bile duct calculi, malignant bile duct obstruction and biliary stent occlusion. Biliary obstruction need not be complete as acute cholangitis can arise in a partially obstructed biliary system. Under normal conditions bile is sterile; however, in 58% of individuals with asymptomatic ductal calculi, bile cultures will be positive, indicating bacterial colonisation.
36
In those progressing to acute cholangitis, cholangiovenous reflux of bacteria and bacterial products occurs because of increasing hydrostatic pressure within the biliary tree. This cholangiovenous reflux results in bacteraemia and the induction of a systemic inflammatory response, and it is this response, leading to organ dysfunction, that is responsible for the morbidity and mortality in acute cholangitis. Decompression of the biliary tree removes the inflammatory insult.
Aerobic Gram-negative bacilli (
E
.
coli
,
Klebsiella
,
Pseudomonas
species), enterococcus and anaerobes are the most common organisms cultured from the bile of patients with acute cholangitis.
36
In up to 50% of patients, anaerobic organisms may be associated with aerobic organisms. In the elderly, polymicrobial infection is more common than monomicrobial infection, and again concomitant anaerobic infection occurs in the majority. In approximately 35% of patients, blood cultures will be positive for the same organisms that are found in the bile.
37
The route of bacterial biliary colonisation is not clear; however, the types of bacteria involved suggest that they are derived from the intestinal tract.
The presentation of acute cholangitis can be variable, ranging from mild symptoms and signs to overwhelming septic shock. Classically, patients with acute cholangitis present with the symptoms and signs that constitute Charcot's triad: upper abdominal pain, jaundice and pyrexia. However, the complete triad may be present in as few as 22% of patients.
38
In the elderly patient, the presentation may be subtle, with signs of an acute confusional state being common and deranged LFTs being the only pointer to the diagnosis. Similarly, acute cholangitis must be included in the differential diagnosis for any patient presenting with rigors. It is not uncommon for patients who have previously had endoscopic biliary stents to present with a rigor as the major feature of an obstructed and infected stent. At the other end of the spectrum, acute cholangitis can present with signs of septic shock and evidence of multiple organ dysfunction. Because the progression to septic shock can be rapid in patients with biliary obstruction, the diagnosis of acute cholangitis must be considered in any patient presenting with jaundice and signs of sepsis.
Cholestatic LFTs are found in the majority of patients with acute cholangitis, demonstrating elevated bilirubin, alkaline phosphatase and γ-glutamyl transferase. However, serum bilirubin may be normal in acute cholangitis arising in a partly obstructed biliary tree because the remaining unobstructed liver is able to compensate. A neutrophilia is typical and serum amylase may also be raised. Deranged coagulation tests can occur, either as a consequence of prolonged biliary obstruction resulting in vitamin K deficiency, or due to disseminated intravascular coagulation. Blood cultures must be obtained as soon as possible.
The initial radiological investigation of choice is transabdominal US. This may demonstrate signs of bile duct obstruction, although false-negative scans can occur. Ultrasound may also determine the underlying pathology. CT can identify biliary dilatation in 78% of patients with acute cholangitis as well as the level of obstruction in 65% and the cause of the obstruction in 61%;
39
however, the initial information obtained is no greater than with US.
Although the determination of the exact site and nature of the bile duct obstruction may require direct visualisation with either ERCP or percutaneous transhepatic cholangiography (PTC), the true value of these procedures is their potential for therapeutic intervention. For this reason, although MRCP has recently been reported to be accurate in identifying biliary obstruction and the underlying obstructing lesion, it does not have an early role in managing patients with acute cholangitis.
Initial resuscitation aims to achieve adequate oxygen delivery, administration of an appropriate volume of intravenous fluid and appropriate analgesia. Efficacy of therapy is assessed by close monitoring of vital signs and, because of the potential for rapid decompensation, management of the patient in a high-dependency unit is usually required (see also
Chapter 16
).
Aerobic Gram-negative bacilli are the most common organisms in acute cholangitis and therefore empirical therapy with antibiotics covering these bacteria should be commenced. In addition, because anaerobic bacteria, although rarely cultured from blood, are frequently found in bile cultures in association with aerobic bacteria, antibiotic regimens should also have anaerobic activity. Piperacillin is an extended-spectrum penicillin with activity against aerobic Gram-negative bacilli, enterococcus and anaerobes. The addition of the β-lactamase inhibitor tazobactam increases the spectrum of activity.
In a randomised clinical trial involving 96 patients with acute cholangitis, piperacillin had similar efficacy to combination therapy with ampicillin and tobramycin, achieving clinical cure or significant improvement in 70% of patients.
40
Another randomised trial assessing single antibiotic therapy
37
demonstrated that intravenous ciprofloxacin alone improved the clinical condition in 85% of cases and had similar efficacy to a combination of ceftazidime, ampicillin and metronidazole.
Although appropriate antibiotic therapy is important, relief of biliary obstruction is crucial to successful disease resolution. Emergency operative intervention is associated with significant risk, with a reported mortality of 20% and a 50% complication rate for patients with severe acute cholangitis.
41
As a result, the mainstay of treatment now is endoscopic bile duct drainage, with improved results compared with surgical intervention.
42
The benefits of endoscopic therapy over surgery in patients with acute cholangitis were confirmed several years ago in a randomised controlled trial, with significantly fewer complications and lower mortality in those undergoing endoscopic drainage.
42,
43
The method used to achieve non-surgical biliary drainage would appear to be less important than simply achieving adequate drainage. Within the confines of a randomised trial, one study
44
demonstrated that biliary decompression in acute cholangitis with a biliary stent inserted without a sphincterotomy was as efficacious as insertion of a nasobiliary drain. In patients in whom ERCP is unsuccessful, drainage by PTC should be undertaken in the acute situation, even in patients who do not have a dilated intrahepatic biliary tree.
45
Once external drainage has been achieved in the first instance, the placement of a biliary stent can be organised as a staged procedure.
In the case of gallstone-related acute cholangitis, following resolution of the episode of acute cholangitis, adequate clearance of the bile duct should be confirmed by direct cholangiography, ERCP, high-quality MRCP or operative cholangiography. Cholecystectomy should be undertaken if there are no contraindications in order to reduce the risk of further gallstone-related problems.
46,
47