the clinical presentation of pyogenic liver abscess

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Br. J. Surg. Vol. 63 (1976) 216219 The clinical presentation of pyogenic liver abscess A. E. YOUNG* SUMMARY The high morfality rate from pyogenic liver abscess is contributed to by delay in diagnosis. The widespread availability of radio-isotopc liver scanning facilitates difignosis once A hepatic abscess is suspected. This retrospectiue study identifies diagnostic features present at the time of admission to hospital in 28 patients who wpr? subszquently found to have a hepatic abscess. PYOGENIC liver abscess is an uncommon disease in the United Kingdom and one that is rarely diagnosed at the time of presentation. Sabbaj et al. (1972) found a delay in diagnosis that averaged 50 days, and in several other series less than 50 per cent of cases were diagnosed in life (Pyrtek and Bartus, 1965; Berke and Pecora, 1966; Joseph et al., 1968). The mortality rate, which in the pre-antibiotic era approached 100 per cent, remains between 30 and 50 per cent (Hoffman et al., 1954; Gainsford and Mark, 1969), and delay in diagnosis must contribute substantially to this poor prognosis. Pyogenic liver abscesses occur at all ages and are equally common in children and in adults (Dehner and Kissane, 1969). In adults they are more common in men than women and there is a higher incidence in diabetics (Holt and Spry, 1966). The commonest infecting agents isolated are Escherichia coli and anaerobic bacteria (Sabbaj et al., 1972; Bateman et al., 1975). The source of infection may be : 1. Portal pyaemia secondary to appendicitis, diverticular disease or other inflammatory disease in the portal drainage area. Only rarely is it a compli- cation of ulcerative colitis or Crohn’s disease (Lee and Block, 1972). 2. Cholangitis secondary to malignant or calculous obstruction of the bile ducts. This is becoming a less common cause of hepatic abscess. There are usually multiple abscesses and the prognosis is poor (Pyrtek and Bartus, 1965). 3. Direct spread from contiguous diseases, e.g. cholecystitis, peptic ulcer, subphrenic and perinephric sepsis. 4. Trauma. Either penetrating or blunt. 5. Infarction after embolism or complicating sickle cell disease. 6. Cryptogenic. With the falling incidence of major intra-abdominal sepsis, the cryptogenic abscess is becoming proportionately more common though no better understood. In 43 per cent of the series reported by Butler and McCarthy (1969) no primary site of sepsis was found. Lee and Block (1972) regarded such cases as occurring after resolved disease in the portal system or as a sequel to spontaneous intrahepatic thrombo-embolism and infarction. In an attempt to identify the clinical and laboratory profile of pyogenic liver abscess at the time of presen- tation, the 26 cases of pyogenic liver abscess admitted to St Thomas’s Hospital, London, between 1936 and 1974 have been studied. To these have been added 2 cases seen by the author at Lewisham Hospital in 1972. Abscesses developing in inpatients have been excluded, Patients Of the 28 patients in this series, 21 were male (75 per cent) and 7 female (25 per cent). Their ages ranged from 9 months to 78 years (mean 46 years). Nine of the patients (32 per cent) were aged between 40 and 50 years. Symptoms Nine patients (32 per cent) gave a history of previous abdominal surgery (3 partial gastrectomies, 2 over- sewings of perforated duodenal ulcer, 2 pancreatico- duodenectomies and 2 appendicectomies), but there was a delay of between 3 months and 2 years (mean 8 months) after these operations before the presen- tation with a liver abscess. Almost all of the operations had been uncomplicated initially. Five patients (I 8 per cent) gave a history of previous medical illness to which the abscess could be attributed, and in the remaining 14 patients (50 per cent) the abscesses were ‘cryptogenic’. Four symptoms were predominant at the time of presentation: pain in 19 patients (68 per cent), nocturnal sweating in 12 (43 per cent), vomiting in 1 I (39 per cent) and malaise in I1 (39 per cent). Pain Pain at the time of presentation was localized to the right upper quadrant of the abdomen in 13 patients (46 per cent), while in 3 (1 1 per cent) it was generalized over the whole abdomen. In one (4 per cent) the pain was located in the right iliac fossa, in one the left upper quadrant and in one the right lower chest. Five (38 per cent) of the patients who complained of right upper quadrant pain at the time of presentation, had previously suffered a generalized abdominal pain of a different character. This generalized pain was reported as being severe, constant and unaffected by movement or coughing. Even untreated, it rarely lasted for more than 3 days and always resolved spontaneously. By contrast, the right upper quadrant pain was usually described as being dull or aching, was persistent but fluctuating in severity and was exacer- bated by coughing, movement or deep inspiration. * St Thomas’s Hospital Medical School, London. 216

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Page 1: The clinical presentation of pyogenic liver abscess

Br. J. Surg. Vol. 63 (1976) 216219

The clinical presentation of pyogenic liver abscess A . E . Y O U N G *

SUMMARY The high morfality rate from pyogenic liver abscess is contributed to by delay in diagnosis. The widespread availability of radio-isotopc liver scanning facilitates difignosis once A hepatic abscess is suspected. This retrospectiue study identifies diagnostic features present at the time of admission to hospital in 28 patients who wpr? subszquently found to have a hepatic abscess.

PYOGENIC liver abscess is an uncommon disease in the United Kingdom and one that is rarely diagnosed at the time of presentation. Sabbaj et al. (1972) found a delay in diagnosis that averaged 50 days, and in several other series less than 50 per cent of cases were diagnosed in life (Pyrtek and Bartus, 1965; Berke and Pecora, 1966; Joseph et al., 1968). The mortality rate, which in the pre-antibiotic era approached 100 per cent, remains between 30 and 50 per cent (Hoffman et al., 1954; Gainsford and Mark, 1969), and delay in diagnosis must contribute substantially to this poor prognosis. Pyogenic liver abscesses occur at all ages and are equally common in children and in adults (Dehner and Kissane, 1969). In adults they are more common in men than women and there is a higher incidence in diabetics (Holt and Spry, 1966). The commonest infecting agents isolated are Escherichia coli and anaerobic bacteria (Sabbaj et al., 1972; Bateman et al., 1975). The source of infection may be :

1. Portal pyaemia secondary to appendicitis, diverticular disease or other inflammatory disease in the portal drainage area. Only rarely is it a compli- cation of ulcerative colitis or Crohn’s disease (Lee and Block, 1972).

2. Cholangitis secondary to malignant or calculous obstruction of the bile ducts. This is becoming a less common cause of hepatic abscess. There are usually multiple abscesses and the prognosis is poor (Pyrtek and Bartus, 1965).

3. Direct spread from contiguous diseases, e.g. cholecystitis, peptic ulcer, subphrenic and perinephric sepsis.

4. Trauma. Either penetrating or blunt. 5. Infarction after embolism or complicating sickle

cell disease. 6. Cryptogenic. With the falling incidence of major

intra-abdominal sepsis, the cryptogenic abscess is becoming proportionately more common though no better understood. In 43 per cent of the series reported by Butler and McCarthy (1969) no primary site of sepsis was found. Lee and Block (1972) regarded such cases as occurring after resolved disease in the portal system or as a sequel to spontaneous intrahepatic thrombo-embolism and infarction.

In an attempt to identify the clinical and laboratory profile of pyogenic liver abscess at the time of presen- tation, the 26 cases of pyogenic liver abscess admitted to St Thomas’s Hospital, London, between 1936 and 1974 have been studied. To these have been added 2 cases seen by the author at Lewisham Hospital in 1972. Abscesses developing in inpatients have been excluded,

Patients Of the 28 patients in this series, 21 were male (75 per cent) and 7 female (25 per cent). Their ages ranged from 9 months to 78 years (mean 46 years). Nine of the patients ( 3 2 per cent) were aged between 40 and 50 years.

Symptoms Nine patients (32 per cent) gave a history of previous abdominal surgery (3 partial gastrectomies, 2 over- sewings of perforated duodenal ulcer, 2 pancreatico- duodenectomies and 2 appendicectomies), but there was a delay of between 3 months and 2 years (mean 8 months) after these operations before the presen- tation with a liver abscess. Almost all of the operations had been uncomplicated initially. Five patients ( I 8 per cent) gave a history of previous medical illness to which the abscess could be attributed, and in the remaining 14 patients (50 per cent) the abscesses were ‘cryptogenic’.

Four symptoms were predominant at the time of presentation: pain in 19 patients (68 per cent), nocturnal sweating in 12 (43 per cent), vomiting in 1 I (39 per cent) and malaise in I 1 (39 per cent).

Pain Pain at the time of presentation was localized to the right upper quadrant of the abdomen in 13 patients (46 per cent), while in 3 (1 1 per cent) it was generalized over the whole abdomen. In one (4 per cent) the pain was located in the right iliac fossa, in one the left upper quadrant and in one the right lower chest.

Five (38 per cent) of the patients who complained of right upper quadrant pain at the time of presentation, had previously suffered a generalized abdominal pain of a different character. This generalized pain was reported as being severe, constant and unaffected by movement or coughing. Even untreated, it rarely lasted for more than 3 days and always resolved spontaneously. By contrast, the right upper quadrant pain was usually described as being dull or aching, was persistent but fluctuating in severity and was exacer- bated by coughing, movement or deep inspiration.

* St Thomas’s Hospital Medical School, London.

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Page 2: The clinical presentation of pyogenic liver abscess

Pyogenic liver abscess

This pain may have lasted for months and in no patient did i t disappear without treatment. Seven of the 28 patients in this study (25 per cent) experienced progression from the generalized type of abdominal pain to the more specific right upper quadrant pain, and in all these there was a pain-free interval between the two types of pain. The shortest such interval was 6 days and the longest was 5 weeks. A case which illustrates this 'silent interval' is described below. Of the 8 patients who never complained of pain, 6 (75 per cent) had experienced night sweats. In the whole series 12 patients (43 per cent) complained of night sweats.

Physical findings Abnormal findings on physical examination were usually few. Pyrexia was noted in 22 patients (79 per cent) at the time of admission, and thereafter usually, but not always, ran a hectic, spiking course. Abdominal tenderness was noted in 21 patients (75 per cent). Those whose pain was felt in the right upper quadrant of the abdomen displayed tenderness well localized to that area, but in patients with general abdominal pain the tenderness was poorly localized. Guarding or rigidity was found in only 9 patients (32 per cent), and enlargement of the liver in 14 (50 per cent). None of the patients was jaundiced at the time of admission.

Investigations The pertinent laboratory findings are recorded in Table 1. The chest X-ray showed the changes of effusion or consolidation at the right base in 15 (58 per cent) of the 26 patients thus examined. Liver scanning was not performed at the time of admission in any of the patients studied.

Diagnosis Twenty-one patients (75 per cent) were diagnosed in life and the remaining 7 at necropsy. The time from admission to hospital to diagnosis ranged from 1 day to 13 months, the overall mean time being 14 days.

Mortality rate The mortality rate in this series was 30 per cent.

Case report A 45-year-old Mauritian man, who had been resident in the United Kingdom for 14 years, presented as an emergency. He had been suffering mild upper abdominal pain for 12 hours and this had suddenly become worse 2 hours prior to admis- sion, a t which time it was felt over the whole upper abdomen. There was no radiation, but the pain was worsened by move- ment. There was no nausea, vomiting, rigors or sweating. The patient had previously been healthy. When examined he was clearly ill and in severe pain. The temperature was 383 "C and he was not jaundiced. There was board-like rigidityand rebound tenderness over the whole abdomen, but the bowel sounds were normal. It was not possible to determine whether there was any hepatomegaly.

Investigations revealed the following: haemoglobin 11.6 g/ 100 ml, white cell count 10 OOO/mm3 (88 per cent neutrophils), alkaline phosphatase 23 King-Armstrong units, bilirubin 0.2 mg/100 ml. Liver enzyme tests were within normal limits and the ESR was 8 6 m m in 1 hour. N o organisms were cultured from the blood.

Table I : LABORATORY INVESTlGATlONS No. of Abnormal . .

Investigation cases Range Mean (%)

Le~~cocytes/mrn~ 28 5100-28 000 16 500 82 Haemoglobin

(g/100 mlt Males 18 7.0-14.9 11.6 75 Females 7 7.6-1 5.5 12.0

ESR (mm/h)* 23 1-136 73 95 Alkaline 14 6-72 25 19

phosphatase (K.-A. units)t

* Only 1 patient's ESR was below 30 mm/h. t King-Armstrong units.

An emergency diagnostic laparotomy was performed and the abdominal viscera were all found to be entirely normal apart from the liver, which was enlarged, but smooth and soft.

The pain faded postoperatively and disappeared within 36 hours without treatment. The temperature returned to normal in 3 days and the white cell count fell to 6000/mm3. The patient, being content with his health, discharged himself 6 days after admission, before further investigations could be arranged.

He was readmitted seriously ill 5 weeks later. On this occasion he complained of night sweats, fever which had been present for 4 days and right upper quadrant pain. The liver was now enlarged down to the umbilicus, being smooth, tense and tender. The haemoglobin was 9.2 g/lOO ml, the white blood count only 7800/mms, ESR 114 mm in 1 hour, alkaline phosphatase 21 King-Armstrong units and bilirubin 1 . 1 mg/ 100 ml. The liver enzymes were again within normal limits. A diagnosis of liver abscess was made and the abscess was confirmed and shown to be solitary by coeliac axis arterio- graphy.

The patient was treated by aspiration of a total of 3900 ml of pus on three occasions with replacement by carbon dioxide, contrast medium and ampicillin, after which he made a complete recovery. Salmonella (Dublin) was cultured from the pus and this organism was also cultured from the blood.

Discussion The average general hospital in the United Kingdom is unlikely to see more than one pyogenic liver abscess each year, though multiple liver abscesses as a complication of terminal disease are not uncommon ; they have been excluded from this series. Unfamiliarity with the condition and the variability of its symptoms confuse diagnosis. In this series the mean time taken to reach a diagnosis was 14 days. This compares favourably with other workers' experience (Pyrtek and Bartus, 1965; Joseph et al., 1968; Sabbaj et al., 1972). Once the diagnosis is suspected, confirmation is now made simpler by the widespread availability of radio-isotopic liver scanning. In a series of 1500 patients reported by Cuaron and Gordon (l970), hepatic scanning was reliable in 95 per cent of cases and was shown to detect lesions as small as 2 cm in diameter. Coeliac axis arteriography and ultrasonics (McCarthy, 1967) offer alternative routes to the diagnosis, and there is a high success rate with blind percutaneous hepatic needling, as most pyogenic abscesses are located in the lateral half of the right lobe (Cuaron and Gordon, 1970).

From the findings of the present study, several important clinical diagnostic pointers have been identified. The incidence of recent abdominal surgery in this series is high enough to suggest a causal

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A. E. Young

relationship to subsequent hepatic abscesses. Previous abdominal surgery need not, however, have been complicated by sepsis or have been performed recently to allow the suspicion of a hepatic abscess. In this series of patients up to 2 years had elapsed after abdominal surgery before the symptoms of a hepatic abscess developed. There may, however, be no history of past disease; half the abscesses in this series were ‘cryptogenic’.

Pain is the most helpful presenting symptom. The classic right subhepatic pain, due to direct peritoneal irritation by the inflammatory process, is not invariably present. Some patients present with a severe generalized abdominal pain, and diagnosis is then more difficult. This generalized pain is probably generated by the stretching of the hepatic capsule and leads to poorly localized foregut pain in a manner similar to that seen when acute hepatitis or cardiac failure produces abdominal pain. A diagnostic laparotomy was performed during this phase in 2 patients and the liver found to be enlarged, pale and soft. The spontaneous disappearance of this generalized pain observed in 25 per cent of the patients in this study has not been recorded in previous reports and is possibly due to a slowing of a cellulitic phase of the abscess formation. The ‘silent period’ that follows may last several weeks and can lull the physician into a false belief that any antibiotics that may have been prescribed have cured the patient. There appears to be no published evidence that established hepatic abscesses can be cured by systemic antibiotics alone. Although some can be treated by repeated percutaneous needle aspiration and the instillation of antibiotics into the abscess cavity (McFadzean et al., 1953), the great majority will need formal surgical drainage. The ‘silent interval’ in the development of a liver abscess may account for those who present without pain.

Night sweating occurred in 43 per cent of the patients, and was noted in a smaller proportion of those presenting with pain than those without. The reason for this is obscure, but it may merely represent an increased likelihood of a patient being asked about this symptom when he is pyrexial but pain-free. If this is so, then the true incidence of night sweating in the group as a whole may be higher.

Perhaps surprisingly, jaundice was not seen at the time of presentation in any of the patients in this study. Where it has been recorded in other series it has probably represented underlying biliary tract pathology rather than being a sign of the abscess itself (Warren and Hardy, 1968; Lazarchick et al., 1973).

Examination of the patient’s abdomen rarely gives sufficient information to allow a diagnosis of liver abscess to be made. Tender hepatomegaly was found in less than half the patients in this group and was usually undramatic. Abdominal tenderness and rigidity, however, can be so marked that early laparotomy is undertaken.

Laboratory investigations disclosed non-specific changes in the majority of the patients studied. Butler and McCarthy (1969) have noted that in the young

patient the serum vitamin B,, levels may be elevated, and Hirschowitz (1952) has found that an isolated rise in the alkaline phosphatase levels is suspicious. In Schraibman’s series (1974), there was a reversal of the albumin : globulin ratio in all the patients in whom it was measured. The most consistently abnormal findings in the present series were anaemia, leuco- cytosis and a raised ESR which was often much higher than would be expected from the clinical state of the patient.

Even in patients where most of the diagnostic pointers were present, the diagnosis was usually that of gallbladder disease or a subphrenic abscess, the true diagnosis being made only at laparotomy. It is suggested, therefore, that more widespread use of radio-isotopic liver scanning in suspicious cases could speed the diagnosis and improve a mortality rate that remains unacceptably high.

Acknowledgement Mr Ivor Smith kindly allowed details of his patient to be reported as the illustrative case.

References BATEMAN N. T., EYKYN s. J. and PHILIPS I. (1975)

Pyogenic liver abscess caused by Streptococcus milleri. Lancet 1, 657-659.

BERKE J. and PECORA c. (1966) Diagnostic problems of pyogenic hepatic abscess. Am. J. Surg. 111,

BUTLER J. J. and MCCARTHY c. F. (1 969) Pyogenic liver abscess. Gut 10, 389-395.

CUARON A. and GORDON F. (1970) Liver scanning: analysis of 2,500 cases of amoebic hepatic abscess . J . Nucl. Med. 11, 4 3 5 4 8 .

DEHNER L. F. and KISSANE J. M. (1969) Pyogenic hepatic abscesses in infancy and childhood. J . Pediatr.

GAINSFORD w. D. and MARK J. B. D. (1969) Surgical management of hepatic abscess. Am. J. Surg. 118, 317-326.

HIRSCHOWITZ B. I. (1 952) Pyogenic liver abscess : review with case report of solitary abscess, caused by Salmonella enteritidis. Gastroenterology 21,

HOFFMAN H. L., PARTINGTON P. F. and DE SANCTIS A. L. (1954) Pylephlebitis and liver abscess. Am. J. Surg. 88, 41 1-416.

HOLT J . M. and SPRY c. J. F. (1966) Solitary pyogenic liver abscess in patients with diabetes mellitus. Lancet 2, 198-200.

JOSEPH w. L., KAHN A. M. and LONGMLRE w. P. (1968) Pyogenic liver abscess. Am. J. Surg. 115, 63-68.

D. R. and WASHINGTON I. A. (1973) Pyogenic liver abscess. Mayo Clin. Proc. 48, 349-355.

LEE J. F. and BLOCK G. E. (1972) The changing clinical pattern of hepatic abscesses. Arch. Surg. 104,

MCCARTHY c. F. (1967) Ultrasonic scanning of the liver. In : READ A. E. (ed.) The Liver. Butterworths, London, pp. 113-121.

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Pyogenic liver abscess

MCFADZEAN A. J. S., C H A N G W . P. S. and W O N G C. C . SABBAJ J., SUTTER V. L. and FINEGOLD S. M. (1972) (1953) Solitary pyogenic abscess of the liver Anaerobic pyogenic liver abscess. Ann. Intern. treated by closed aspiration and antibiotics. Med. 77, 629-638. Br. J. Surg. 41, 141-152. SCHRAIBMAN I. G. (1974) Non-parasitic liver abscess.

New Engl. J. Med. 272, 551-554. WARREN K. w. and HARDY K. J. (1968) Pyogenic hepatic PYRTEK L. J. and BARTUS s. A. (1965) Hepatic pyaemia. Br. J. Suug. 61, 709-712.

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