Acute pancreatitis
Update:
This chapter has been very substantially updated, in particular with regard to grading of disease severity, and indications for and techniques of surgical intervention.
Essentials
Acute pancreatitis affects 300 to 600 new patients per million population per year and is most commonly caused by gallstones or alcohol, but there are many other causes and associations. Careful imaging reveals that most so-called idiopathic acute pancreatitis is due to small (1–3 mm diameter) gallstones. Diagnosis is made by a combination of a typical presentation (upper abdominal pain and vomiting) in conjunction with raised serum amylase (> × 3 upper limit of normal) and/or lipase (> × 2 upper limit of normal). Several acute abdominal emergencies can mimic acute pancreatitis and may be associated with a raised serum amylase. These include perforated peptic ulcer (particularly perforated posterior gastric ulcer) and acute mesenteric ischaemia. In equivocal cases, a CT scan is indicated in order to exclude other causes and confirm the diagnosis.
Initial management is with (1) analgesia, (2) ensuring adequate oxygenation, (3) the early restoration of circulating volume through intravenous fluid administration. The revision of the Atlanta classification separates patients clinically into (1) mild—with early resolution without complications, (2) moderate—local complications without organ failure, and (3) severe—complications associated with organ failure.
Mild acute pancreatitis responds to analgesia and intravenous fluids, and patients rarely need to be in hospital beyond a few days. If gallstones have been identified, then cholecystectomy (or endoscopic retrograde cholangiopancreatography (ERCP) sphincterotomy where clinically appropriate) should be performed during the same admission, or at least within 2 to 4 weeks to prevent recurrent attacks. Severe acute pancreatitis carries a high mortality (up to 20%). Management in the early stages is centred on organ support (respiratory, circulatory, and renal failure). Later management involves surgical or radiological intervention for sepsis, usually within a specialist pancreatic unit.
With regard to some specific aspects of management: (1) There is no indication for an NG tube or starvation. In patients with a prolonged illness nutrition support will be required—enteral feeding is associated with fewer risks and side effects than total parenteral nutrition. (2) Antibiotics should not be given until and unless a specific indication arises; there is no benefit to early initiation of prophylactic antibiotics. (3) ERCP—occasionally cholangitis (abdominal pain, jaundice, and fever) may be associated with hyperamylasaemia, in which case urgent biliary decompression at ERCP is indicated. In the absence of cholangitis or jaundice, the evidence to support early ERCP is weak. (4) There are no pharmacological agents that benefit any form of acute pancreatitis. (5) The case for decompressive laparotomy for abdominal compartment syndrome remains unproven.
Epidemiology
The incidence of acute pancreatitis varies between populations. In large population studies from Scotland and Finland the incidence of the disease has risen steadily to the current 400 patients/million per year. A population-based study from England showed the incidence is increasing at 3.1% per year, mainly in young women. The disease is most prevalent in those with poorer socioeconomic status, especially where alcohol is the cause. Overall mortality is from 2.0 to 7.5%, highest in those who are over 70 years, obese individuals, and those with comorbidity at the time of onset. Prospective and retrospective studies record 45 to 50% of deaths as occurring in the initial week of the illness secondary to fulminant multiple organ failure.
Aetiology
Aetiological factors and rare associations of acute pancreatitis are listed in Boxes 15.24.1.1 and 15.24.1.2.
Major factors
Biliary disease and alcohol abuse together account for over 80% of patients with acute pancreatitis in most prospective studies.
Gallstones
Gallstones are the predominant cause of acute pancreatitis and all patients should have abdominal ultrasound carried out to identify these, even where there is a history of alcohol excess. Endoscopic ultrasound (EUS) is more sensitive than transabdominal ultrasound in identifying small gallstones (microlithiasis) and results in many cases of so-called idiopathic acute pancreatitis being identified as due to stones. The mechanism by which gallstones induce acute pancreatitis is not certain, but increased back pressure in the pancreatic duct following transient impaction of a migrating gallstone at the ampulla of Vater is considered to be the likely initiating event. Subsequent intracellular events lead to activation of proteases within acinar cells, acinar cell injury, and a local inflammatory response.
Alcohol
The proportion of patients in whom pancreatitis is due to alcohol abuse is dependent on the population under study. Alcohol has been implicated in acute pancreatitis probably through intracellular lysosomal release modulated through elevations in cytosolic and mitochondrial ionized Ca2+ concentration. Rates may be as high as 70 to 80% in New York (United States of America) and Helsinki (Finland). The risk of alcohol-induced pancreatitis is highest in young males who drink in excess of 80 g alcohol per day. Smoking is a cofactor in the development of both acute and chronic pancreatitis. Many patients with a possible alcohol history also have gallstones and the diagnosis should be one of exclusion.
Minor factors
Drugs
The drugs most commonly implicated in causing acute pancreatitis are valproic acid, azathioprine, l-asparaginase, and corticosteroids. There is equivocal evidence regarding thiazide and other diuretics. However, unless viral titres have been determined, together with adequate biliary investigations including endoscopic examination of the ampulla of Vater, it is unwise to ascribe acute pancreatitis to a particular drug. Repeat exposure to the same drug again causing acute pancreatitis is the strongest evidence of a direct association.
Viral infection
Viral infection, particularly mumps, Coxsackie B, and viral hepatitis, can cause acute pancreatitis. One clinical feature that may prove useful is prodromal diarrhoea, which is rare in all other types of acute pancreatitis. Of increasing importance in endemic areas are the effects of HIV infection. There are also concerns that some antiretroviral therapy may cause acute pancreatitis.
Benign pancreatic duct stricture
A focal area of pancreatic necrosis in a primary attack of acute pancreatitis can cause secondary fibrosis with main duct stricture formation, with segmental ‘upstream’ recurrent attacks of pancreatitis as a consequence. Stricture dilatation or occasionally surgical decompression or distal pancreatectomy may be required.
Congenital or developmental anatomical abnormalities can present with pancreatitis (choledochal cyst, duodenal duplication, anomalous pancreaticobiliary junction). Pancreas divisum (nonunion of main and accessory ducts) occurs in 3 to 5% of people and is not usually a primary cause of pancreatitis.
Periampullary or obstructive pancreatic tumours
Periampullary adenoma or carcinoma resulting in upstream obstruction is an important association. Ampullary tumours are best diagnosed by endoscopic biopsy. With the increase in this approach to diagnosis, tumours at or close to the ampulla have been shown to have a greater association (0.4%) with acute pancreatitis than hyperparathyroidism. Effective treatment of the tumour abolishes recurrent attacks. This usually involves surgical resection, but endoscopic laser therapy or endoscopic papillectomy can be effective in older and less fit patients. Carcinoma of pancreas can occasionally present with clinical acute pancreatitis and other primary tumours (such as neuroendocrine tumours) or tumours metastasizing to the pancreas (such as renal carcinoma) may present in this way, probably by causing pancreatic duct obstruction.
Carcinoma of pancreas can occasionally present with clinical acute pancreatitis and other primary tumours metastasizing to the pancreas may present in this way.
Hyperparathyroidism
Hypercalcaemia secondary to hyperparathyroidism is now recognized to be an uncommon cause of acute pancreatitis. Removal of a parathyroid adenoma usually prevents further acute pancreatitis since persistent hypercalcaemia appears to be the provoking factor.
Hyperlipidaemia
Patients with type I or type V hyperlipoproteinaemia may develop acute pancreatitis. Both subtypes are associated with chylomicrons, of which more than 90% are triglycerides. These patients are prone to attacks of acute pancreatitis in the absence of alcohol ingestion. Dietary restriction of lipids and various lipid-lowering drugs are valuable in therapy. Hyperlipidaemia of any cause where triglyceride levels reach in excess of 2000 mg/dl may cause acute pancreatitis, and acute pancreatitis may rarely complicate hyperlipidaemia of pregnancy or diabetic ketoacidosis.
Hypothermia
This is an important association, for example in elderly people living in a cold, unheated house. In younger patients, alcohol abuse may be linked, particularly if patients fall asleep out of doors. Management is directed at gradual warming and supportive measures for organ compromise.
Hereditary
This condition is increasingly being studied since the 1996 discovery of genetic mutations of the cationic trypsinogen gene (PRSS1), which shed light on the mechanism of acute pancreatitis. A Europe-wide study (EUROPAC) has tracked multiple families in the United Kingdom, Germany, and France, and similar work in Japan and the United States of America is ongoing. The two most common mutations are R122H and N291. An autosomal dominant pattern of inheritance is seen. Severe acute inflammatory changes are rare and diagnosis is often delayed. Patients usually have a long history of recurrent abdominal pain from childhood or adolescence. Changes of chronic fibrosis may be present at diagnosis. Typically chronic pancreatitis is evident by the age of 20 to 40 years, and the risk of pancreatic carcinoma over 60 years is significantly increased. Mutations in the cystic fibrosis transmembrane conductance regulator gene (CTFR) and the pancreatic secretory trypsinogen inhibitor gene (SPINK1) are also linked to pancreatitis.
Trauma
Hyperamylasaemia may occur after blunt abdominal trauma, usually from a crush injury to the body of the pancreas against the vertebral column. The risk of associated injuries to surrounding organs is high, and in the acute phase are usually more significant than the pancreatic injury. The identification of a pancreatic injury during a trauma laparotomy should be managed by simple drainage in most cases. When there is transection of the main pancreatic duct, therapeutic options include endoscopic trans-papillary stenting and distal pancreatectomy. Late presentation is associated with pseudocyst formation due to leakage from the damaged pancreatic duct.
Iatrogenic
Surgical or endoscopic procedures involving the ampulla of Vater can induce pancreatitis. In recent years, the significant decrease in the use of diagnostic ERCP (1% risk of acute pancreatitis) as a result of noninvasive imaging modalities (EUS and magnetic resonance cholangiopancreatography (MRCP)) has reduced the overall incidence of postprocedural acute pancreatitis. The risk of acute pancreatitis increases to 3% where a therapeutic endoscopic sphincterotomy has been performed, and may be as high as 20% in high-risk patients (sphincter of Oddi dysfunction). The potential of iatrogenic perforation should be considered in all patients who develop pancreatitis after therapeutic ERCP.
Autoimmune pancreatitis
This is a rare condition, which is considered part of the IgG4-related autoimmune disease spectrum and associated with other autoimmune diseases (polyarteritis nodosa, systemic lupus erythematosus, other vasculitides) and inflammatory bowel disease (Crohn’s disease and ulcerative colitis). It may present as abdominal pain with obstructive jaundice more typical of chronic than acute pancreatitis. Other features may include: (1) an increased IgG4/IgG ratio in serum; (2) homogeneous gland enlargement with a well-defined halo on CT; (3) EUS revealing characteristic diffuse abnormality, and (4) periductal lymphoplasmocytic infiltrate on biopsy, which may also be associated with abnormalities in the extrahepatic biliary tree resembling sclerosing cholangitis. Focal autoimmune pancreatitis may prove difficult to differentiate from carcinoma. A good response to steroids is diagnostic.
Worm infestation
Ascaris lumbricoidis within the ampullary area may manifest as acute pancreatitis clinically, and other worms stuck in this area can produce the same effect.
Scorpion bites
The Trinidad scorpion (Tityus trinitatis) bite can be associated with the production of a clinical episode of acute pancreatitis soon after the victim is bitten. Patients customarily bring the dead scorpion to show the doctor.
Sphincter of Oddi dyskinesia
Rarely, sphincter of Oddi dyskinesia can present with acute abdominal pain, although the more common presentation is one of chronic relapsing abdominal discomfort. The attacks associated with hyperamylasaemia are usually mild (except where pancreatitis follows an ERCP). Recently, a symposium on functional disorders of the pancreas and biliary tree established the Rome II diagnostic criteria for sphincter of Oddi dyskinesia. The benefit of sphincterotomy in the prevention of further attacks is variable.
Pathology
The initial phase of acute pancreatitis is characterized by oedema and the development of an acute inflammatory infiltrate, rich in neutrophils, with tiny spots of fatty tissue necrosis, mainly on the surface but also in the intralobular fatty tissue. In mild cases, the changes are most marked in the peripancreatic tissue, but because the initial pancreatic histological change is within the intralobular fat, there is a relationship between extent of necrosis and the amount of fat within the pancreas. In severe disease intravascular thrombosis and local enzymic necrosis lead to confluent areas of fat necrosis, which extends beyond the pancreas into the peripancreatic fat. Within the pancreas disseminated ductal and periductal necrosis may be evident.
Clinical features
Sudden onset of severe upper abdominal pain, focused in the epigastrium and with vomiting, is the most common presentation. This tends to lessen in severity progressively over the first 48 to 72 h, and it is not usually a significant factor beyond this time. There may be upper abdominal tenderness and guarding, but these signs are often less marked than might be suspected from the severity of the pain. Bowel sounds are usually absent in the early stages. Vomiting is prevalent in the first 12 h of illness, contributing to hypovolaemia and hypotension. Clinical jaundice is rare on admission, although minor abnormalities of biochemical liver blood tests occur in 80% of patients with a biliary aetiology. Occasionally hyperamylasaemia occurs in association with cholangitis, which if overlooked may result in irreversible multiple organ failure. The presence of jaundice and pyrexia on the day of admission is therefore an indication for urgent ERCP and biliary decompression.
Diagnosis
The diagnosis is usually made from the clinical presentation of upper abdominal pain and vomiting associated with an elevation of serum amylase or lipase. Where doubt exists, a CT scan should be performed, typically revealing pancreatic swelling, fluid collection, and change in density of the gland (Figure 15.24.1.1). Occasionally the diagnosis may first be made at laparotomy, when simple washout and closure is all that should be done. The differential diagnosis is that of an acute abdomen (Box 15.24.1.3). A raised amylase may be associated with a number of these conditions, but CT scanning (if available) has greatly simplified diagnosis when doubt exists.
Biochemical abnormalities
A multitude of biochemical phenomena are found in acute pancreatitis. Various pancreatic enzymes are released that are useful as diagnostic markers. Acinar cell disruption leads to high serum levels of amylase, lipase, trypsin, chymotrypsin, phospholipase, elastase, trypsinogen activation peptide, and phospholipase activation peptide, and these are also elevated in peritoneal and retroperitoneal tissues as well as lymph. C-reactive protein (CRP), an acute phase reactant, is of most use for longitudinal monitoring of progress (Figure 15.24.1.2). Very high concentrations of circulating cytokines occur in the blood at an early stage in the disease, including tumour necrosis factor α (TNFα), platelet activating factor (PAF), and interleukin 6 (IL-6), with maximal levels in those with severe pancreatitis, but these are of research interest rather than clinical value.
(From the British Journal of Surgery, with permission).
Grading disease severity
Multiple biochemical scoring systems, including the Glasgow and Ranson scoring systems, attempt to objectively grade severity of an attack of acute pancreatitis. Whilst there is value in directing less experienced clinicians to the multisystem organ dysfunction associated with a severe attack, none is sufficiently accurate to direct treatment. The APACHE II system has been shown to be useful in the stratification of severity of acute pancreatitis within trials. CT scanning can be useful in demarcating location and extent of pancreatic damage, and a CT severity index has been developed. CT is, however, more commonly used to monitor the development of evolving complications. In practice, sequential physiological scoring systems (e.g. Medical Early Warning Score (MEWS)) can assist the identification of clinical deterioration and are in common use in most surgical units.
Organ failure scoring
Quantification of the clinical assessment by scoring 0 to 4 points for each of several organ systems using the modified Marshall Critical Illness Scoring System (Table 15.24.1.1) has revealed that 44% of patients with an APACHE II score of 6 or more will show an organ failure score of 2 or more at admission. Many patients improve fairly rapidly with intensive supportive intravenous fluids and oxygen: they are regarded having low risk transient organ failure with mortality of less than 1%. By contrast, those who continue with a minimum modified Marshall score of 2 have persistent organ failure and high mortality (35–55%). This dynamic aspect of organ failure demands regular clinical review and reassessment of treatment priorities where appropriate (Table 15.24.1.2).
Table 15.24.1.1 Modified Marshall Critical Illness Scoring System (excludes hepatic index)
|
Score |
0 |
1 |
2 |
3 |
4 |
|---|---|---|---|---|---|
|
Systolic BP (mm Hg) PO2/Fio2 ratio |
>90 |
<90 responds to fluid |
<90 poor response to fluid |
<90 (pH<7.3) |
<90 (pH<7.2) |
|
>400 |
301–400 |
201–300 |
101–200 |
<101 |
|
|
Glasgow Coma Score |
15 |
13–14 |
10–12 |
6–9 |
<6 |
|
Platelet count × 109/litre |
>120 |
81–120 |
51–80 |
21–50 |
<21 |
|
Creatinine (µmol/litre) |
<134 |
134–169 |
170–310 |
311–439 |
>439 |
Fio2, fraction of inspired oxygen; PO2, partial pressure of oxygen.
Clinical progress and outcome
The revision of the Atlanta classification separates patients clinically into (1) mild—with early resolution without complications, (2) moderate—local complications without organ failure, and (3) severe—complications associated with organ failure.
Mild acute pancreatitis
Mild acute pancreatitis is associated with a low mortality (maximum 2%) and rarely requires prolonged hospitalization. In those with a gallstone aetiology, cholecystectomy should be performed in the same admission or within 2 to 4 weeks to prevent a recurrent attack. In those with significant comorbidity, ERCP with sphincterotomy is considered a satisfactory alternative.
Moderate acute pancreatitis
The mortality in this group should again be low and management is determined by any complications and not by the acute inflammation. Any procedure should be discussed with a specialist team prior to intervention, and delayed until the acute episode has resolved.
Severe acute pancreatitis
The principles of organ support should be followed, as for any critical illness, ensuring reversal of hypoxaemia, restoration of circulating volume, maintenance of tissue perfusion, and organ support, ideally within a critical care environment. Early restoration of circulating blood volume is associated with improved outcome. The combination of fluid lost from vomiting and loss of capillary integrity can be very substantial. The introduction of catecholamines should only be considered after it is established that adequate fluid restoration has been achieved. Hypoxaemia reflects disease severity in acute pancreatitis, and although most patients can be managed with supplemental humidified oxygen, assisted ventilation may be required in more severe cases.
After immediate resuscitation, intravenous fluid should be given at sufficient rate to produce 0.5 mL/kg of urine per hour. Renal replacement therapy by haemodialysis or haemofiltration may be required if renal failure becomes established. High fever within the first 24 h is rare and, if associated with jaundice, is suspicious of ascending cholangitis. The more severe cases of acute pancreatitis are characterized by the development and persistence of a systemic inflammatory response syndrome, one aspect being the development of a swinging pyrexia. This is often incorrectly taken as evidence of sepsis, but is usually a reflection of the inflammatory cascade and the presence of devitalized tissue in the retroperitoneum rather than bacterial infection.
Specific aspects of management of severe acute pancreatitis
ERCP
The one group of patients with an unequivocal indication for ERCP and biliary decompression are those with hyperamylasaemia associated with cholangitis (jaundice and pyrexia), where the cholangitis, rather than any pancreatic inflammation, is driving organ dysfunction. The role of ERCP remains controversial in other circumstances. There is no role for early ERCP in mild disease. Several randomized studies and cohort series have looked at the role of early ERCP with endoscopic sphincterotomy, compared with conservative management in acute gallstone pancreatitis. A number of meta-analyses have failed to demonstrate a definite benefit, and early ERCP is difficult to justify in patients who are not jaundiced.
Antibiotics
The dual peak in mortality in acute pancreatitis is well recognized, the late peak being associated with complications associated with necrosis, including the development of pancreatic or peripancreatic infection. The consensus of the most recent systemic reviews and meta-analyses is that there is no evidence supporting the use of prophylactic antibiotics in either mild or severe acute pancreatitis, and the recommendation is to avoid their use, using targeted antibiotic therapy for episodes of proven infection.
Nutrition support
There is no benefit from enteral feeding in mild pancreatitis, and these patients need have no dietary restrictions, but artificial feeding may be used in cases of complicated moderate or severe and prolonged acute pancreatitis to provide long-term nutritional support. In addition to the requirement to maintain nutritional integrity, it has been suggested that nutritional support may also help to preserve mucosal function and limit the stimulus to the inflammatory response. The experimental evidence supporting this has not been confirmed in clinical practice, and there is no evidence that the mode of feeding alters disease progression. Randomized studies have shown that enteral nutritional support is cheaper and associated with fewer side effects than total parenteral nutrition, also that there is no difference in outcome with nasogastric compared to nasojejunal feeding. In clinical practice, therefore, the mode of nutrition support does not appear to affect the disease process, and the choice of delivery relates to tolerance and minimizing morbidity associated with the delivery system. Probiotics may be detrimental in acute pancreatitis and specifically supplemented nutrition should only be administered in the context of clinical trials.
Other approaches
Large randomized studies have failed to provide sufficient evidence to recommend the use of antiprotease, antisecretory, or anti-inflammatory agents in patients with acute pancreatitis. More recent randomized trials of antioxidant therapy have shown similarly disappointing results. There remains no proven pharmacological therapy for the treatment of acute pancreatitis.
Surgical intervention
The role of surgery in acute pancreatitis has evolved significantly in the last 20 years. The trend is toward delaying (or avoiding) intervention, and towards minimally invasive approaches to the management of complications. The only indications for early surgical intervention are the management of early haemorrhagic or visceral complications. In patients with mild attacks, gallstones (when relevant) should be removed, ideally within the same hospital admission. In those with severe disease, the role of surgery is aimed at the control of sepsis, usually several weeks after disease onset. Most sterile collections can be managed conservatively and late drainage achieved with low morbidity once the acute phase has passed.
Because the issues surrounding surgical intervention are complex, this should be undertaken within, or following discussion with, a specialist unit. The most common indication is the development of infection within an acute necrotic collection, which is normally heralded by a deterioration in biochemical and haematological markers, coupled with clinical signs of sepsis. Conventional management demanded complete debridement of any devitalized tissue at the earliest opportunity through open surgical debridement, but it is now clear that maintaining adequate drainage is more important than eradication of necrosis, and minimally invasive options for intervention are now preferred, the choice of procedure determined by local expertise and preference.
Aggressive percutaneous drainage, retroperitoneal necrosectomy, endoscopic debridement, and the video-assisted retroperitoneal debridement approach have all been shown to be options in cohort series, but there is insufficient evidence to promote the use of one method over another and in practical terms achieving continued sepsis control is probably more important than the method used (Fig. 15.24.1.3).
Specific complications of acute pancreatitis
Acute pancreatic pseudocyst
It is rare that an acute inflammatory collection persists beyond 4 weeks and contains little or no debris (as required by the Atlanta definitions). Unfortunately, necrosis is poorly demonstrated by CT (MRI is more sensitive), and an acute fluid collection on CT may appear homogeneous. Pancreatic pseudocyst most commonly occurs in the lesser sac and often represents a closed pancreatic fistula, as a breach in the main or major pancreatic duct can frequently be demonstrated at ERCP. Transpapillary duct stenting and ERCP should be avoided if possible, as this leads to the introduction of infection in more than 10% of patients. In the absence of sepsis, fluid-predominant acute fluid collections may be adequately drained as a one-step procedure by EUS-guided endoscopic transmural procedures, although repeated tract dilatation is often required. By contrast, solid-predominant acute fluid collections, especially in younger, fit patients, may be best dealt with by internal surgical drainage to the stomach or to a defunctioned Roux loop of jejunum. This procedure can be done either laparoscopically or at open surgery, depending on local expertise, and can also be combined with a cholecystectomy.
Haemorrhage
Poorly controlled sepsis within a collection can present with acute internal haemorrhage into the collection, or bleeding from a drain site (Fig. 15.24.1.4). Venous bleeding can be controlled by tamponade, but arterial haemorrhage requires urgent CT angiography, proceeding to angiographic embolization where appropriate. The prognosis is grave where this is unsuccessful and surgical intervention required, as the bleed is usually associated with a combined hypovolaemic and septic deterioration and associated multiple organ dysfunction.
(From the British Journal of Surgery, with permission).
Visceral fistulation
Spontaneous discharge of a postacute collection into the gastrointestinal tract is not uncommon and can decompress the collection and result in clinical improvement. Fistulation into the lower gastrointestinal tract (Fig. 15.24.1.4) often results in poorly drained collection and defunctioning ileostomy or resection of the affected segment then required.
Pancreatic ascites
This condition rarely occurs in association with acute pancreatitis, but when it does it is due to spontaneous decompression of a pancreatic pseudocyst, with escape of pancreatic juice into the peritoneal cavity. Amylase-rich fistula fluid is common after percutaneous drainage and internal control can often be successfully achieved by endoscopic transpapillary drainage.
Splenic and portal vein thrombosis
The use of CT to monitor progress has resulted in more frequent detection of splenic and segmental portal vein thrombosis. Splenic vein thrombosis does not usually require treatment, but thrombosis or thrombus in the portal or superior mesenteric vein requires anticoagulation either with low molecular weight heparin or warfarin (Fig. 15.24.1.4).
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