pyogenicliver abscess · century a common cause of liver abscess was undiagnosed appendicitis. this...

Gut, 1969, 10, 389-399

Pyogenic liver abscessT. J. BUTLER AND C. F. McCARTHY

From the Department of Gastroenterology, Frenchay Hospital, and the Department of Medicine,University of Bristol, Southmead Hospital, Bristol

At the turn of the century, the mortality from liverabscess was 100%. Surgical drainage reduced themortality to 50 to 75% by 1930. Antibiotics led toa further reduction but there was little change in themortality during the next 25 years until recentlywhen the adoption of special localization techniquespromised a great improvement. In the nineteenthcentury a common cause of liver abscess wasundiagnosed appendicitis. This has been corrected,so eliminating deaths in the young age groups. Thecondition now affects predominantly the aged andenfeebled but it remains a condition with a highmortality and morbidity despite diagnostic aware-ness and therapeutic improvements. Liver abscess issometimes only one manifestation of severe infectionelsewhere. The initial features of the disease may benon-specific and the fully developed picture is latein appearing. Consequently there may be delay orfailure in diagnosis. Inadequate drainage of multi-loculated abscesses or failure to drain secondaryabscesses adds to the problem. Few see many casesand this stresses the need for a continual review ofthe condition in all its aspects.

MATERIAL

During the 10-year period 1957-66, 48 patients withliver abscess were admitted to two Bristol hospitals,and have been classified as follows:

TYPE 1 (17 PATIENTS) In this group presentationwas acute in immediate continuity with some otheracute abdominal pathology. The abscesses wereusually multiple, but in general there was nodiagnostic problem. Table I summarizes the cases inthis group.

TYPE 2 (31 PATIENTS) This group constituted themain problem and forms the basis of the paper. Theabscesses were usually solitary with a 'chronic'presentation. There was no such time relationshipas in type 1 and a prolonged search, often fruitless,was needed to determine a primary source ofinfection. The essential features of patients in thisgroup are given in Table II. This type of abscessoccurred twice as frequently as the acute variety.

389

TABLE ISUMMARY OF PATIENTS WITH LIVER ABSCESS

(TYPE 1)ResultNo. Sex Age Source

(yr)

234567891011121314151617

FFFFFFMMMMMMMMFFM

8668466188532434246146553022766847

Gallstones-cholangitisGallstones-cholangitisGallstones-cholangitisGallstones-cholangitisGallstones-cholangitisGallstones-cholangitisPostappendicularPostappendicularPostappendicularDiverticulitisDiverticulitisPostoperative, gastrectomy (DU)Trauma (via chest)Trauma (via chest)Acute Gram-negative bacteraemiaAcute Gram-negative bacteraemiaPostoperative, splenectomy (trauma)

DiedDiedDiedDiedSurvivedSurvivedSurvivedSurvivedDiedDiedDiedSurvivedSurvivedSurvivedDiedDiedSurvived

Six patients were excluded from the review: twopatients with infected metastases from carcinoma ofthe rectum and one with carcinoma of the stomach,two with non-specific granulomata of the liver, andone patient with a liver abscess due to empyema of anintrahepatic gall bladder. There were two cases ofamnoebiasis of the liver during the period underreview.

In type 1 liver abscess, the most acute form wasseen in patients nos. 15 and 16, who had multipleliver abscesses with jaundice, anuria, convulsions,and coma due to Gram-negative bacteraemia. Thesedied within one week of onset.

In type 2 liver abscess, the preliminary diagnosis inhospital was correct in 26 of the 31 patients. In theremaining five patients, the initial diagnosis wasbrucellosis (2), perinephric abscess (1), and reticu-losis (2).

ANALYSIS

This is largely confined to patients with type 2abscess as these presented the main difficulty.

AGE INCIDENCE This is illustrated in Fig. 1, togetherwith an indication of mortality. The increasingincidence with age is shown, 50% of the patientsbeing over the age of 60 years.

on January 11, 2020 by guest. Protected by copyright.

http://gut.bmj.com

/G

ut: first published as 10.1136/gut.10.5.389 on 1 May 1969. D

ownloaded from

http://gut.bmj.com/

T. J. Butler and C. F. McCarthy

TABLE IISUMMARY OF PATIENTS WITH LIVER ABSCESS (TYPE 2)

No. Sex Age Pain Jaundice Fever Rigors Enlarged(yr) Liver

+±+

+

++

_ +

_- +

+

+

+

+

+

+ +

+

+

_+

_+

+ +

+ +

-+

-+

+ +

++

+ +

-+

+

+

8

,,, 6c)

(00.

- 40

0)

-o

Z 2D

D

D

D

D

D

D

0 1 2 3 4 5 6Age in decades

D

D

D

D

of the abscesses occurring in this lobe alone. Therewere abscesses in both lobes in seven of the 31patients. The largest abscess in the series was25 cm in diameter and the smallest 6 cm in diameter.

D

DD

DD

7 8

FIG. 1. Age incidence of liver abscess.

SEX RATIO There were 18 men and 13 women in thegroup.SITE OF ABSCESS A marked prediliction for the rightlobe of the liver was observed, more than two-thirds

METASTATIC ABSCESSES IN OTHER ORGANS Abscessesother than in the liver were found in 14 patients, ie,in nearly half of the cases. In 10 patients, the secondabscess was in the lungs, in two in the brain, andtwo patients had abscesses in both lung and brain.

CLINICAL PRESENTATION Table III shows the widevariety of presentation and clinical problem onthe patient's admission to hospital.The majority of patients were referred to medical

units in the first instance, but it is important torefer patients with metastatic abscesses at once tothoracic and neurosurgical units. In the past, 30 to40 years ago, brain abscesses were usually of the'neighbourhood' variety secondary to middle ear orfrontal sinus disease and carried a reasonableprognosis. Now an increasing frequency of metastaticbrain abscess is evident; the liver, as well as the lung,must be borne in mind in searching for the source.Of the three patients with unsuspected liver abscesses,two were admitted from the waiting list with herniae,whilst the third was a diabetic with a large liverabscess.

390

+

Leucocytosis Site inLiver

2345678910111213141516171819202122232425262728293031

+±+

+

A-

+

MMMFFMFMMFMFMFMMMFMFMFM

F

MFMFM

56344963775577666553417360544866764441613665373868767341477761

+

+

++

+

+

+

+

+

+

+

LRRR and LR and LRR and LR and LRRRR and LR and LRRRRRRRRRRR and LLRRRRRR

++

+++

A 5*

9


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

Pyogenic liver abscess

TABLE II-continuedSUMMARY OF PATIENTS WITH LIVER ABSCESS (TYPE 2)

ess Surgical Treatment Primar

Pyrexia of unknown originPUOPUOPUO'Cardiac failure'UnsuspectedAbdominal massLung sepsisComa'Cardiac failure'CollapsePUOComaCollapseAbdominal painLung sepsisAbdominal painUnsuspectedComaPUOPUOAbdominal massUnsuspectedPUOAbdominal massPUOComaPUOAbdominal painPUODiarrhoeaPUO

Lung abscessBilateral lung abscess

Lung abscess

Lung abscess

Brain abscessBrain and lung abscess

Lung abscess

Brain abscessBrain and lung abscessLung abscessLung abscess

Lung abscess

Lung abscess

Lung abscess

DrainageDrainage (liver and lung)Drainage (liver and lung)

Drainage

DrainageDrainage (brain)

Drainage (liver and lung)Drainage

Drainage (liver and brain)Drainage (liver and brain)Drainage (liver and lung)

DrainageDrainageDrainageResection L lobe of liverDrainageDrainageDrainageDrainage (liver and lung)DrainageDrainage

TABLE IIICLINICAL PRESENTATION IN 31 PATIENTS WITH

LIVER ABSCESS (TYPE 2)Case Presentation No. of AbscessesNo.

Pyrexia of unknown 11origin

Coma 4 (1 hepatic, 1 diabetic, 2 brain sepsis)Abdominal pain 3Abdominal mass 3Lung abscess 2'Cardiac failure' 2Collapse 2Unsuspected 3Diarrhoea 1

Total 3 1

CLINICAL FEATURES The frequency of importantclinical features appearing during the course of thedisease is shown in Table IV. The striking feature inthe series was the insidious onset of the diseaseprocess, so much so that many patients were

uncertain of the beginning of the illness. The lengthof such a history ranged from three months to threeyears, and formed a background even in those whoseadmission to hospital was precipitated by a suddenincrease in severity of the condition. In only one

patient (no. 30) was the duration of the symptoms

short. The significance of symptoms and thtirduration may not be appreciated by the elderly andare attributed simply to their age.

TABLE IVFREQUENCY OF CLINICAL FEATURES IN 30 PATIENTS

WITH LIVER ABSCESS (TYPE 2)

Weight loss (31)Anaemia (31)Hepatomegaly (23)Fever (21)Leucocytosis (21)Pain (18)Rigors (12)Jaundice (8)

100 °'.

100%

23-3%40%

5666%

66-6%66-6%

73-3

The onset was usually painless with little else butmalaise. When pain appeared it was either centrallydisposed in the abdomen or in the right hypo-chondrium. Liver tenderness was common, butlocalized tenderness over the liver was late inappearing. Liver enlargement was the commonestphysical sign.

Rigors did not occur daily, as in patients in theacute group, but only once or twice weekly, andthere was no history of these in the majority. Whenpresent, they were interpreted as being indicative ofthrombophlebitis in the portal radicles with spreadof the abscess or of episodes of bacteraemia.

Presentation Metastatic Absct

391

ry Source Result

LungCryptogenicCryptogenicCryptogenicCholangitisActinomycosisLungPostoperativeDiverticulitisCholangitisCryptogenicPancreasCryptogenicCholangitisCryptogenicCryptogenicCryptogenicCryptogenicCryptogenicCryptogenicActinomycosisCholangitisCholangitisCrohn's diseaseDiverticulitisCryptogenicCryptogenicCholangitisPostoperativeDiverticulitisDiverticulitis

SurvivedSurvivedSurvivedDiedDiedDiedDiedDiedDiedDiedDiedDiedDiedDiedSurvivedSurvivedDiedDiedDiedSurvivedDiedSurvivedSurvivedDiedSurvivedDiedSurvivedSurvivedSui vivedSurvivedSurvived

23456789


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/


Whereas all the patients in the acute group(type 1) had jaundice, only approximately one infour had this feature in the main group. Usually itwas not severe until the terminal stages, but in twopatients it was a transient feature for a day or so

occurring several months before admission. Thesehad been labelled as attacks of viral hepatitis.Although anaemia was present in all patients at

some time, it was the original feature that causedthe patient to seek medical advice in two cases, andwas treated symptomatically only. Oedema occurredin those with low serum protein levels, especially inthose with a fatal outcome. Local oedema over thechest wall alone, as seen in subphrenic abscess, wasnot common and was recorded in only three (10%)patients. Perhaps the most significant item requiringcomment is the presence or absence of leucocytosis.The white cell count was raised in 21 of the 31patients to a level ranging from 16,000 to 28,000per c mm. One third of the series, however, did nothave any leucocyte response during their stay inhospital. Among the fatal cases, nearly 50%(eight) did not have a leucocytosis. This observationneeds to be stressed: a leucocytosis may not beevident in many cases of liver abscess, and its absenceis of sinister import.Although liver abscess may present with a variety

of clinical patterns, the termination of the conditionin fatal cases reveals a more restricted picture. Of17 such patients, eight were in coma, seven hadprofound hypotension lasting from 24 hours to sixdays, one died from peritonitis due to rupture of theliver abscess, and one had terminal pulmonaryfibrosis from an old actinomycotic infection of thelungs. In the patients in coma, this was hepatic infour, diabetic in one, and due to brain sepsis in three.All three patients in the series with coincidentdiabetes died.

METHODS OF INVESTIGATION All patients had plainradiographs of the abdomen and chest which demon-strated the large soft tissue shadow of the enlargedliver in the upper right quadrant of the abdomen.The right leaf of the diaphragm was raised and itsrespiratory excursion reduced. In about 25% of thecases, the base of the right lung had collapsed, with

TABRESULTS OF LIVER FUNCTI

Test

5

4E

D2

:3-02

E

1U)

0

0

:0 \

\\ 0

10 0\

\\ * :0 * \\**\\\\* \ Deaths

\\ *-*0~ 0

4%

0

15 30 45Serum Alkaline Phosphatase (KA. units)

60

FIG. 2. Relationship of serum alkaline phosphatase toserum albumin.

pleural effusion; in one of these the effusionamounted to an empyema. Evidence of fluid levelsin abscesses was not seen. Cholecystography andbarium studies (meal and enema) were used in thesearch for sources of the abscesses.

Haematological studies The occurrence ofanaemia and leucocytosis has already beenmentioned. Those patients with rigors (12) hadblood cultures done, but none were positive.

Liver function tests These were done in all cases

and the results are summarized in Table V. Therelationship of the raised serum alkaline phosphataselevel and the falling level of the serum albumin isillustrated in Figure 2. The fatal cases had levels ofserum albumin below 2g/100 ml. Of the liver functiontests, the rapidly falling serum albumin level is themost important index of liver abscess. The trans-aminases are used as an index of hepatocellulardamage whilst serum alkaline phosphatase esti-mation is dependent on liver excretion(Fig. 3.) Serialstudies of these in patients with liver abscess mayshow a degree of parallelism as illustrated inFigure 4.

Liver biopsy This method of investigation wasused in 12 patients. In two, repeated biopsy over a

;LE VION TESTS IN LIVER ABSCESS

Values

1 Serum bilirubin (normal <0 5 mg/100 ml) (23)' Without jaundice O5-18 mg/100 ml(8) With jaundice 3.5, 3-8, 4-1, 4 5, 4.9, 5 0, 7-3, 13-5 mg/100 ml

2 Serum alkaline phosphatase (normal < 12 King-Armstrong units/lOOml) 8-56 K-A units/100 ml (raised)3 Serum albumin (normal 4 g/100 ml or more) 1-114-2 g/100 ml (reduced)4 Serum globulin Increased, especially gamma fraction5 Serum transaminase (SGPT) (normal 22-95 King units/100 ml) 99-306 units/100 ml (raised)'No. of cases.

1 a

392


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

Pyogenic liver abscess 39

40 r 400

Cl.

2MN0 200

0 1 2 3 4Months after operation

FIG. 3. Alterations in liver function tests with healing of i-G. 5a.Iiver abscess.

period of six months revealed no abnormality. Theabscess cavity was entered in one patient, confirmingthe diagnosis. In the remaining nine cases, the tissueobtained showed a non-spedific hepatitis withinflammatory cells, but no focal necrosis and wasinterpreted as being in the neighbourhood of anabscess or tumour.Serum vitamin B12 estimations Six patients had

these studies. Grossly raised levels (2,000 to 4,000juiug/ml) were found in five cases. The last patient,although she had an abscess some 9 cm in diameter,had a vitamin B12 level of 140 jigg/ml. It may bethat the liver stores of vitamin B12 are alreadydepleted in the elderly so that the serum levelcannot be raised when liver tissue is destroyed.

_. .......5 -i50

I FIC. 5b.F 4 Fr140< FIG. 5. Ultra.onic scan (compound B scan) in liver

0 | / | _ abscess (a) and (b) radiographic appearance of abscess\ /̂ | a) ~~~~~~~~~~cavity.

-3t / 30 0)

2 20

EI X

(o 1 r N--- i 1 2

0)

0 1 2 3 4 5Months after operation

FIG. 4. Improvement in serum albumin and alkalinephosphatase levels after drainage of liver abscess. FIG. 6. Ultrasonic scan of amoebic liver abscess.


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

T. J. Butler and C.TF. McCarthy

TABLE VISOURCE OF INFECTION IN LIVER ABSCESS

IN 31 CASES

Source of Infection No. of Cases

Cryptogenic-no source foundGallstones/cholangitisDiverticulitisPostoperative (abdominal)Actinomycosis (abdominal)PancreatitisCrohn's diseaseLung

FIG.''7. Isotope liver scanin .live.as s

FIG. 7. Isotope liver scan in liver abscess.

Ultrasonic scan Ultrasonic B scans (McCarthy,Read, Ross, and Wells, 1967) were carried out ontwo patients (case 17, Table I, case 31, Table II). Ineach instance it was possible to say confidently thatan abscess or abscesses were present. Scans on apatient with amoebic abscess were equally helpful.Figure 5 shows the ultrasonic liver scan of case 31,and Fig. 5a the appearance of the abscess cavityafter drainage. Figure 6 shows the appearance of thepatient with amoebic liver abscess.

Isotope scans These were performed on twopatients, cases 17 and 31, and showed the presenceof localized areas of low count rate. Figure 7indicates the type of appearance. The isotope usedwas techetium 99m tagged to a sulphur colloid(Paton, 1966). Scans of a patient with multipleamoebic abscesses also showed localized areas of lowuptake.Of the commonly used investigations, most help

in diagnosis was afforded by the falling albuminlevel and the increased vitamin B12 level, especiallyin view of the fact that there may be no increase inthe leucocyte count. The ultrasonic and isotopescans were diagnostic when used.With reference to the return of liver function tests

to normal after an abscess has been drained, this maytake from three months to one year, and is illustratedin Figure 3. It is important to stress that the serumalbumin level may continue to fall for a period afteroperation, due to impaired liver function, loss in theexudate, and the catabolic effect of the procedure.

PRIMARY SOURCE OF INFECTION This is the mostdifficult part of the analysis: although there must bea source in every case, prolonged search may notreveal it. The immediate task of treating the abscesstakes priority and in most patients the search for theprimary focus follows later. This source may be verysmall and may have healed before the liver abscesshas become manifest. Table VI indicates the probablesource in this series.

13 (43.3%)6(200%)4212 (30% source in portal area)111J2 (67% systemic, source outside

portal area)

The cryptogenic group may be regarded as 'notproven' but consideration of the bacteriology ofthese, chiefly coliform organisms, would indicatethat they probably have an origin in the portal area.The patients with postoperative abscesses had gastricoperations one and four years previously. Followingpancreatitis, the liver abscess became apparent afteran interval of nine months. In the patients with thesource in the lungs, both had proven pneumoniaone and three years previously.

ORGANISMS Bacteriological studies in liver abscessare of twofold importance: (1) to control antibiotictherapy by sensitivity tests, and (2) as an aid inidentifying the source of the infection. Unusualorganisms, not coliform in origin, may point to thebiliary tract as the culprit.

Table VII shows the organisms identified in thisseries. The findings indicate the importance of doinganaerobic and aerobic cultures for bacteria andfungi. It is perhaps of interest to note that only theanaerobic actinomyces are found as commensals inman. In the acute abscesses (type 1) additionalorganisms were found in one fourth of the patients:Cl. welchii, haemolytic streptococci, and coagulase-positive staphylococci.

TABLE VIIBACTERIOLOGY OF LIVER ABSCESSES IN 31 CASES

Escherichia coli alone or with Strep. faecalisAnaerobic streptococci ..

Actinomyces (anaerobic) ..Nocardia (aerobic) ..Sterile. .

168214

MORTALITY This is influenced by the fact that nosurgical intervention can be contemplated in nearlyone third of the patients, so grave is their condition.It is evident that the only chance of survival lies indrainage of the abscess. Table VIII gives an analysisof the mortality for the acute (type 1) and the morechronic (type 2), the latter being analysed in moredetail. It should be stressed that one in five patientsrequired repeated drainage procedures.

394


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/


TABLE VIIIMORTALITY IN CASES OF LIVER ABSCESS

Group No. of Deaths MortalityCases (%)

Type 1 17 9 52-9Type 2 31 17 53-1Type 2 onlyNo drainage 9 9 100Drainage 22 8 37-3Drainage and without metastatic

abscesses 12 3 25

At this point, it is worth recapitulating thosefeatures of liver abscess which seem to indicate asinister prognosis: features of gross liver destructionand poor defence mechanisms, severe jaundice,coma, hypotension, and associated diabetes (allthree patients with this died), laboratory testsshowing serum albumin level below 2 g/100 ml, noleucocytosis, low blood urea (three patients withlevels below 12 mg/100 ml all died).

OBSERVATIONS ON TREATMENT

All patients had broad-spectrum antibiotics (tetra-cycline or penicillin and streptomycin), which weremodified when bacterial sensitivity was known.Infusions of blood and triple strength plasma wereused when necessary, in particular as a preparationfor surgery. On three occasions, mannitol was givenduring or after operation.Nine patients were never fit for surgery. Drainage

operations, including resection of part of the left lobeof the liver, were performed on 22 patients, seven ofwhom required drainage of metastatic abscesses.Repeated drainage was necessary in four patientsowing to inaccurate siting of the drain and thepresence of loculi. All but two were drained via anabdominal approach, the two with thoracic ap-proaches needed further drainage through theabdomen. There was very little choice about themethod of approach because localization in the liverhad not been determined and there was a need toexplore the abdominal viscera. A thoracic approachin the absence of localization does not permitadequate inspection of the liver.At operation, there may be no visual evidence of

the site of the abscess in the liver, but an alteredconsistency may be palpable. Needle aspiration isusually necessary. In three patients localization wasdetermined before operation, one in whom theabscess was tapped during liver biopsy, and two byultrasonic and isotope scans. After aspiration,Lipiodol was introduced into the cavity and wasfollowed by x-ray studies in different places andpositions to reveal the site and dimensions of thecavity.

FIG. 8a.

FlCi. 8b1.FIG. 8. Anteroposterior sinogram on which the abscesscavity is not clearly seen (a) and lateral view on whichthe cavity is clearly visible (b).

395


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/


When the drainage tube was introduced into theabscess cavity at operation and carefully positionedfor dependent drainage, it was left in situ untilrepeated sinograms showed no cavity but only thetube track. It is important that sinography shouldbe done in two planes (anteroposterior and lateral)to be certain that the cavity has been obliterated(Figs. 8a and 8b). Chemotherapeutic cover wascontinued in this series until drainage was completeand the liver function tests were improving.

DISCUSSION

The classification of liver abscesses adopted in thispaper is not the usual one. It is submitted as usefulbecause it stresses two distinct clinical presentations.In type 1, acute multiple abscesses associated withjaundice follow directly on some other primaryrecognizable pathological process, ie, the source isusually obvious from the beginning. Type 2 abscesses,oni the other hand, have a more chronic presentationand the cause is obscure at the onset. These abscessesmay present a major problem and the main dis-cussion is centred around them. The salient featuresof this group of abscesses in this series are as follows:The onset is insidious. The abscess is solitary, andhas a predilection for the right lobe of the liver.Jaundice is not common. There is a high incidenceof metastatic abscesses elsewhere. Often there is noleucocytic response.The localization of an abscess in the liver is related

to its function as a bacterial filter. The predilectionfor the right lobe is less easily understood on thebasis of 'streaming' of blood in the portal system.Nevertheless, a greater volume of blood goes to theright lobe compared with the left and this must playa part in localization. It is of interest to observe thatliver abscess is a rarity in cases of ulcerative colitisdespite the frequency of bacterial insult that occursvia the portal vein (Brooke and Slaney, 1958). Theoccurrence of liver abscess in the aged and enfeebled,the frequency of bacteraemic shock and metastaticabscesses, and the lack of leucocytic respenseindicate a failure in defence mechanisms.The number of patients in this series is similar to

that in most reviews in the literature.Most series indicated slight preponderances of

males compared withfemales. Rothenberg and Linder(1934), however, recorded a sex ratio M/F of2.5/1, whilst May et al (1967) found an almost equalincidence in men and women. With the exception ofthe series reported from Hong Kong (McFadzeanet al 1953), which had a high incidence in young agegroups, all the remaining authors recorded a maximalincidence in older people.The relative frequency of solitary and multiple

SUMMARY OF REPORTED SERIES

Series No. of Period ofCases Observation

(yr)

Rothenberg and Linden (1934)Ochsner, DeBakey, and Murray (1938)McFadzean, Chang, and Wong (1953)Stokes (1960)Diffenbaugh, Strohl, and De Padua (1960)Cronin (1961)Block, Schuman, Eyler, Truant, DuSault

(1964)Pyrtek and Bartus (1965)Berke and Pecora (1966)May, Lehmann, and Sanford (1967)Present series

24421489

2768

42102146

202010

10

40

2042010

abscesses seems to vary. Cronin (1961) and May et al(1967) found multiple abscesses to be commoner,whereas Block et al (1964) and Pyrtek and Bartus(1965) recorded equal numbers of solitary andmultiple abscesses. The latter authors observed that90% of liver abscesses associated with biliaryobstruction were likely to be multiple whilst some95% of abscesses due to systemic or portal invasionwere usually solitary. It has been frequently reportedthat the solitary liver abscess differs from multipleabscesses in that the source of the former was usuallyobscure (Beaver, 1931; Bourne, 1954; Davidson,1964; Matheson et al, 1964). The present reviewreinforces these observations.The preference of solitary abscesses for the right

lobe of the liver is well documented. Rothenburgand Linder (1934) and Berke and Pecora (1966)found that all the solitary abscesses were so situated.McFadzean et al (1953) reported 13 of a series of11 abscesses to be in the right lobe. Pyrtek andBartus (1965) recorded 17 abscesses in the right lobeand five in the left in 22 cases. Diffenbaugh et al(1960) considered the right lobe to be involved eighttimes more frequently than the left, whilstHirschowitz (1952) indicated that abscesses arelikely to be situated in the right lobe when thesource was unknown. According to Pyrtek andBartus (1965), abscesses following gastric operationsare usually in the left lobe, although the examplesin the present series were in the right lobe.The high incidence of metastatic abscesses in lungs

and brain-nearly 50% in this series-is an import-ant finding because of its influence on presentationand prognosis. It is also indicative of ready blooddissemination. Block et al (1964) reported the needfor drainage of abscesses elsewhere, especially inthe brain and kidneys, in one third of their patients.In the review by Diffenbaugh et al (1960), empyema,abscesses of the lungs and brain, and subphrenicabscesses were reported. Some 10% of cases ofsubphrenic abscess have intercurrent liver abscesses

396


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/


(Harley, 1955). Other complications reported includeinvolvement of the pericardium (Azan, 1932;Zodikoff, 1947) and invasion of the inferior venacava (McKnight, 1928) and of the hepatic veins(Webber and Coe, 1950). A persistent complication,'haemobilia', due to haemorrhage into the abscesscavity, has been described by Karam and Jacobs(1961) and by Urschel, Skinner, and McDermott(1963). Its importance lies in the fact that resectionof the appropriate lobe may be necessary afterprecise localization. One wonders if this feature ismore common than is generally thought by virtueof the severe anaemia, the colour of the pus, and theoccurrence of hypotension seen in patients withliver abscess.With regard to clinical presentation, Rothenberg

and Linder (1934) believed liver abscess to be a welldefined entity, amenable to surgery and associatedwith a reasonable prognosis. This is probably truefor those very familiar with the problem asexemplified by the report of McFadzean et al (1953).The present review, however, is indicative of theopposite point of view and more in keeping with thefindings of Cronin (1961) and Block et al (1964). Itis important to recall the somewhat chasteningobservations of Ogden et al (1961) and Pyrtek andBartus (1965) that the diagnosis may not be estab-lished in more than 60% of patients until necropsy.The non-specific early symptoms and the variedclinical pattern of presentation seen in the presentseries must be stressed.The insidious onset is well recognized (Rothenberg

and Linder, 1934; McFadzean et al, 1953). Thefrequency of pain varies considerably in reportedcases from one in seven of patients (McFadzeanet al, 1953) to almost two-thirds (Cronin, 1961).There is no doubt that pain is a much more regularand persistent feature of acute multiple abscessesthan of solitary ones. A particular observation thatis confirmed by the present review is that the pain isnot usually accompanied by vomiting (McFadzeanet al, 1953; Cronin, 1961).

Jaundice occurred in all the patients with type 1abscess, and in 25% of the 31 patients with type 2abscess. Cronin (1961) observed jaundice in one of10 solitary abscesses and in half of the patients withmultiple abscesses. Diffenbaugh et al (1960) alsofound it to be a feature of multiple abscesses. Ingeneral, it may be said that jaundice is indicative ofmultiple abscesses, of biliary obstruction, or ofdiffuse and severe liver destruction. Hepatomegalyhas been observed as the commonest physical sign,and it should be noted that the enlargement may besudden and dramatic (Wyndham, 1945; Diffenbaughet al, 1960).The investigation of patients with possible liver

abscess needs special comment. In particular, theobservation that 30% of all the cases, and 50% ofthe fatal cases, never had a leucocytosis is important.Although indicative of the overpowering nature ofthe infection, it must be stressed that a normalleucocyte count does not exclude a liver abscess.Abnormalities of the liver function tests in a patientwith sepsis do not necessarily incriminate the liverfor, as Neale, Caughey, Mollin, and Booth (1966)have shown, general infective processes may alterseveral of the usual liver function tests. If thefunction of the liver is depressed by an abscess, thenalbumin synthesis suffers early and if, furthermore,a large area of liver is occupied or 'knocked out' bythe abscess, this leads to a sustained fall in serumalbumin levels. If it drops below 2 g per 100 ml, theprognosis is grave. Elevation of the serum levels ofvitamin B12, due to liberation of liver stores ashepatocellular destruction proceeds, is probably themost important feature of liver abscess, but levelsmay not be raised in the very old if the liver storesare already depleted. Low blood urea levels havebeen mentioned as indices of a poor prognosis.The radiological findings in this series correspond

with those reported in the literature, ie, one third toone quarter of the patients may have signs ofinvolvement of the right lung with effusion.

It will be appreciated already that in patientswith the chronic type 2 abscess, where the source isnot immediately obvious, the abscess will probablybe solitary and in the right lobe. Even so, there is nodoubt that the great need at the moment is theadoption of special localization techniques, essentialfor both early diagnosis and accurate drainage.Photo scanning of the liver following the admin-istration of radioactive substances, eg, Rose Bengal1311, radioactive gold (198Au) or Tehnetium-m 99,has been done with promising results (Wagner et al,1961; Nagler, Bender, and Blau, 1963); Block et al,1964; Schuman, Block, Eyler, and DuSault, 1964;Pyrtek and Bartus, 1965). The smallest defect detect-able is about 2 cm diameter but nevertheless theoverall accuracy is about 77% (Gollin, Sims, andCameron, 1964). If isotope scanning had been used inall patients in the present series it is likely that mostof the abscesses would have been detected as thesmallest was 6 cm in diameter. In the two patientsin whom the investigation was carried out an earlydiagnosis was made. Ultrasonic scanning of theliver used on two patients in this series has a majoradvantage over the isotope scanning in that it canclearly distinguish between solid and fluid-filledlesions thus separating abscess from tumour. Theequipment necessary to perform an ultrasonic Bscan of the liver is not portable but the A scanequipment is, and this latter equipment is adequate

397


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

398 T. J. Butler and C. F. McCarthy

for the diagnosis of abscess provided that theoperator is experienced. Although we have usedthese techniques in a small number of patientswith abscess, in five other patients abscess wasexcluded by the scan, although clinical suspicionwas high.

Transaortic hepatic arteriography and spleno-portography have also been used (Urschel et al,1963; Gollin et al, 1964) and may be indicated ifscanning is not successful. When these techniqueshave been used, the mortality from liver abscess hasbeen reduced to negligible proportions in a smallseries of patients.The probable route of infection is shown in

Table VI: 20% via the biliary tract, 30% by theportal vein, and 6.7% by the systemic circulation.In nearly half the series, the source, and hence theroute, was uncertain but probably in the portal vein.The high incidence of 'cryptogenic' abscess has beenfrequently recorded.

It is surprising that cases occurring afterabdominal operations are not more common in viewof Wilkie's (1911) demonstration of the frequentoccurrence of infarcts in the liver after ligature ofmesenteric vessels. Liver abscess following infarctiondue to polyarteritis nodosa has not been seen, butBrittain et al (1966) have reported an abscess follow-ing liver infarcts due to sickle cell disease.The bacteriological studies require little comment.

All reports show frequent infection by Esch. coli,but some authors have stressed the importance ofanaerobic infection (Stokes, 1960). Block et al (1964)found an approximately equal incidence of aerobicand anaerobic infection. The present series stressesthe necessity ofboth types ofculture on all occasions.Sterile cultures, frequently reported, may be a reflec-tion of failure to observe this rule.The experience of treatment in this series has

already been reviewed briefly, with special referenceto the operative approach and management of tubes.Early diagnosis and localization by ultrasonic orisotope techniques and the use of the appropriateantibiotic are likely to cause a reduction in thepresent mortality due to liver abscess. Surgicaldrainage is probably necessary but the superb resultsobtained by McFadzean and his colleagues (1953)using aspiration and instillation of antibiotics mustbe remembered. 'Septic shock', often due to a Gram-negative bacteraemia, must be treated with theappropriate antibiotics and expansion of plasmavolume with continuous monitoring of the centralvenous pressure by means of a polythene catheterin the superior vena cava or right atrium. Hyper-tensive agents will often be necessary. Isoprenalinemay be the drug of choice as it causes increasedcardiac output and peripheral vasodilatation thus

increasing tissue perfusion (Weinstein and Klainer,1966). Metaraminol (Aramine) is sometimes helpful.Careful control of acid base balance is necessary.In most reported series, the mortality remains highand corresponds with that found in this review,25%, even when the liver abscess is uncomplicated.It will be recalled that the initial diagnosis wascorrect in about 83% of the patients in this series.This is evidence of awareness of the disease andindicates that the critical question in liver abscessmay be not so much, 'What is it?' but 'Where is it?'

SUMMARY

A retrospective analysis of 48 patients with liverabscess abmitted to Bristol hospitals in the 10-yearperiod 1957-66 is presented. In view of the highmortality in cases of pyogenic liver abscess, aidsto diagnosis are stressed, eg, falling serum albuminlevels and raised serum levels of B12. Drainage offersthe only chance of survival but accurate localizationof the abscess by isotopic or ultrasonic scanning isneeded.

REFERENCES

Azan, A. J. (1932). Large spontaneous abscess of liver with ruptureinto pericardium. Illinois med. J., 61, 428-429.

Beaver, D. C. (1931). Granulomatous abscess of the liver of pyogenicorigin. Amer. J. Path., 1, 259-276.

Berke, J., and Pecora, C. (1966). Diagnostic problems of pyogenichepatic abscess. Amer. J. Surg., 111, 678-682.

Block, M. A., Schuman, B. M., Eyler, W. R., Truant, J. P., DuSault,L. A. (1964). Surgery of liver abscess. Arch. Surg., 88, 602-610.

Bourne, W. A. (1954). The diagnosis of pyogenic liver abscess.Lancet, 2, 1093-1094.

Brittain, H. P., De la Torre, A., and Willey, E. N. (1966). A case ofsickle cell disease with an abscess arising in an infarct of theliver. Ann. Intern. Med., 65, 560-563.

Brooke, B. N., and Slaney, G. (1958). Portal bacteraemia in ulcerativecolitis. Lancet, 1, 1206-1207.

Cronin, K. (1961). Pyogenic abscess of the liver. Gut, 2, 53-59.Davidson, J. S. (1964). Solitary pyogenic liver abscess. Brit. med. J.,

2, 613-615.Diffenbaugh, W. G., Strohl, E. L., and De Padua, C. (1960). Pyogenic

abscess of the liver. Arch. Surg., 81, 934-941.Gollin, F. F., Sims, J. L., and Cameron, J. R. (1964). Liver scanning

and liver function tests. J. Amer. med. Ass., 187, 111-116.Harley, H. R. S. (1955). Subphrenic abscess, with particular reference

to the spread of infection. Ann. roy. Coll. Surg. Engl., 17,201-224.

Hirschowitz, B. I. (1952). Pyogenic liver abscess: a review with a casereport of a solitary abscess caused by Salmonella enteriditis.Gastroenterology, 21, 291-299.

Karam, J. H., and Jacobs, T. (1961). Hemobilia: report of a case ofmassive gastrointestinal bleeding originating from a hepaticabscess. Ann. intern. Med., 54, 319-326.

Matheson, N. A., Gardner, D. L., and Dudley, H. A. F. (1964).Liver sepsis. Brit. J. Surg., 51, 363-367.

May, R. P., Lehmann, J. D., and Sanford, J. P. (1961). Difficulties indifferentiating amebic from pyogenic liver abscess. Arch. intern.Med., 119, 69-74.

McCarthy, C. F., Read, A. E. A., Ross, F. G. M., and Wells, P. N. T.(1967). Ultrasonic scanning of the liver. Quart. J. Med., 36,517-524.

McFadzean, A. J. S., Chang, K. P. S., and Wong, C. C. (1953).Solitary pyogenic abscess of the liver treated by closedaspiration and antibiotics. Brit. J. Surg., 41, 141-152.

McKnight, R. B. (1928). Rupture of hepatic abscess into theabdominal cavity and inferior vena cava. J. Amer. med. Ass.,90, 1929-1930.


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

Pyogenic liver abscess 399

Nagler, W., Bender, M. A., and Blau, M. (1963). Radioisotopephotoscanning of the liver. Gastroenterology, 44, 36-43.

Neale, G., Caughey, D. E., Mollin, D. L., and Booth, C. C. (1966).Effects of intrahepatic and extrahepatic infection on liverfunction. Brit. med. J., 1, 382-387.

Ochsner, A., DeBakey, M., and Murray, S. (1938). Pyogenic abscessof the liver. II. An analysis of 47 cases with review of theliterature. Amer. J. Surg., 40, 292-319.

Ogden, W. W., Hunter, P. R., and Rives, J. D. (1961). Liver abscess.Postgrad. Med., 30, 11-19.

Pyrtek, L. J., and Bartus, S. A. (1965). Hepatic pyemia. New Engl. J.Med., 272, 551-554.

Rothenberg, R. E., and Linder, W. (1934). The single pyogenic liverabscess. Surg. Gynec. Obstet., 59, 31-40.

Schuman, B. M., Block, M. A., Eyler, W. R., and DuSault, L. (1964).Liver abscess: Rose Bengal 1131 hepatic photoscan in diagnosisand management. J. Amer. med. Ass., 187, 708-71 1.

Stokes, J. F. (1960). Cryptogenic liver abscess. Lancet, 1, 355-358.Urschel, H. C., Jr, Skinner, D. B., and McDermott, W. V., Jr (1963).

Hemobilia secondary to liver abscess. J. Amer. med. Ass.,186, 797-799.

Wagner, H. N., Jr, McAfee, J. G., and Mozley, J. M. (1961).Diagnosis of liver disease by radioisotope scanning. Arch.intern. Med., 107, 324-334.

Webber, R. J., and Coe, J. I. (1950). Rupture of pyogenic hepaticabscess into hepatic vein. Surgery, 27, 907-910.

Weinstein, L., and Klainer, A. S. (1966). Septic shock: pathogenesisand treatment. New Engi. J. Med., 274,950-953.

Wilkie, D. P. D. (1911). Retrograde venous embolism as a cause ofacute gastric and duodenal ulcer. Edinb. med. J., 6, 391-402.

Wyndham, N. (1945). Liver abscess with especial reference to systemicinfections. Med. J. Aust., 1, 252-254.

Zodikoff, R. (1947). Multiple liver abscesses with rupture into thepericardium. Amer. Heart J., 33, 375-384.

The April 1969 IssueTHE APRIL 1969 ISSUE CONTAINS THE FOLLOWING PAPERS

Signposts

Bilirubin metabolism BARBARA H. BILLING and MARTINBLACK

Skin lesions in ulcerative colitis M. L. JOHNSON andH. T. H. WILSON

Osteomyelitis complicating regional enteritis M. j.GOLDSTEIN, K. NASR, H. C. SINGER, J. G. D. ANDERSON,and J. B. KIRSNER

Small intestinal histochemical and histological changesin ulcerative colitis N. JANKEY and L. A. PRICE

Aetiology of ulcerative colitis. A review of past andpresent hypotheses F. T. DE DOMBAL, P. R. J. BURCH,and G. WATKINSON

Aetiology of ulcerative colitis. A new hypothesis P. R. J.BURCH, F. T. DE DOMBAL, and G. WATKINSON

Sclerodermatous involvement of the stomach and thesmall and large bowel R. D. G. PEACHEY, B. CREAMER,and J. W. PIERCE

Role of parasites in the pathogenesis of intestinal malab-sorption in hookworm disease B. N. TANDON, R. K.KOHLI, A. K. SARAYA, K. RAMACHANDRAN, and OM PRAKASH

Clinical trial of deglycyrrhizinized liquorice in gastriculcer A. G. G. TURPIE, J. RUNCIE, and T. J. THOMSON

Peptic activity after the administration of Pentagastrinand in gastroduodenal disease M. H. PRITCHARD andA. M. CONNELL

Differences between males and females in the Hollanderinsulin test J. SPENCER, G. P. BURNS, F. C. Y. CHENG,A. G. COX, and R. B. WELBOURN

Lactose malabsorption and postgastrectomy milkintolerance, dumping, and diarrhoea JOHN R. CONDON,PETER WESTERHOLM, and NORMAN C. TANNER

Treatment of overt and subclinical malabsorption inHaiti F. A. KLIPSTEIN, I. M. SAMLOFF, G. SMARTH, andE. A. SCHENK

Transduodenal endoscopy SEAN O'BEIRN

Notes and activitiesCopies are still available and may be obained from the PUBLISHING MANAGER,

BRITISH MEDICAL ASSOCIATION, TAVISTOCK SQUARE w.c. 1. price 18s. 6D.


http://gut.bmj.com

/G


ownloaded from

http://gut.bmj.com/

pyogenicliver abscess · century a common cause of liver abscess was undiagnosed appendicitis. this...

Documents