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Tropical splenomegaly: surgical aspects
877 TRANSACTIONS OF THE ROYALSOCIETY
OP TROPICAL
Tropical
MEDICINE
AND HYGIENE,
splenomegaly
VOL.
75, No.
: surgical
G. AJAO College Hospital,
6, 1981
aspects
OLUWOLE
Dept. of Surgery,
University
Summary At the University College Hospital, Ibadan, Nigeria, in a 22-month period from January 1975 to September 1976, nine splenectomies were electively performed for unruptured spleens. The diagnoses were either tropical splenomegaly syndrome (when no obvious cause was found to be responsible for, or associated with, the splenomegaly) or splenic abscess in various stages of formation. The weights of the spleens removed ranged from 160 g in a 1%year-old girl to 5080 g in a 39-year-old male. One death due to uncontrollable bleeding from the solenic bed occurred. Histology of td spleens afier removal showed lymphosarcoma in one, non-specific changes in another, and thickened fibrous capsule, perisplenitis, haemorrhagic infarcts, pockets of chocolate-coloured fluid and inflammatory processes in various stages in the other seven. In the tropics, enlarged spleens with no obvious cause or associated condition are often best treated by splenectomy for histological diagnosis, definitive treatment and the prevention of rupture caused by minor trauma. There are, as yet, no convincing data which show that splenectomy in the tropics causes a significant diminution of immunity to malaria (or other diseases) and it does not, therefore, predispose to the development of cerebral malaria, Introduction Splenomegaly with no clear-cut aetiology and usually not associated with other obvious disease is endemic in tropical Africa. This condition, usually referred to as tropical splenomegaly syndrome, is diagnosed after exclusion of the other known causes of an enlarged spleen. The spleen is the organ most commonly injured in blunt abdominal trauma in Ibadan, Nigeria (ADEKUNLE, 1976) and in Accra, Ghana (ARCHAMPONG, 1976). At the University College Hospital, Ibadan, in a 22-month period (January 1975 to September 1976), 27 patients suffering from a ruptured spleen were operated upon and, in one case, splenectomy was necessitated by trauma sustained during vagotomy and pyloroplasty. It has been suggested that removing spleens from people resident in the tropics may lead to depression of the natural immunity to diseases, especially malaria, thus leading to the development of cerebral malaria. Up to the time of writing, there has been no well documented scientific data to justify this claim. In cases where immunity to malaria has been depressed as a result of many vears of urotection from reoeated attacks. a malaria prophylactic drug, such ai proguanil (I’aludrine), administered weekly is effective. This drug is cheap and easily available.
Ibadan,
Nigeria
Sagoe reported 43 cases of tropical splenomegaly syndrome from the medical service of the University College Hospital, Ibadan, Nigeria (SAGOE, 1970). 32 of these cases responded to proguanil 100 mg daily and 11 did not. The duration of response ranged from a few months to over two years. From the surgical point of view, this period is sufficiently long to risk rupture of an enlarged spleen from relatively minor trauma, with fatal consequences. The purpose of this paper is to stress the importance of splenectomy for the treatment, pathological diagnosis and prevention of the risk of a ruptured spleen in cases of enlarged spleen in which no obvious cause can be found by current laboratory methods. Experience with nine cases of enlarged spleen electively removed is also described. Materials and Methods In a 22-month period (January 1975 to September 1976), nine elective splenectomies were performed by the surgical service of the University College Hospital, Ibadan, Nigeria. The pre-operative diagnosis in all cases was either tropical splenomegaly or splenic abscess. The age and sex of each patient were recorded and the duration of symptoms and the presentations noted. The packed cell volumes of all the patients were estimated and the genotypes of four patients were determined. Splenic aspirates were cultured from patients with proven splenic abscess or haematoma. In each case, the removed spleen was weighed and measured. The measurements considered were the longitudinal axis, the transverse diameter and the height at the hilum. The histological picture of each spleen removed was carefully studied. Cases of traumatic ruptured spleen were not included in this study. Results Patients were between 15 and 55 years old; five were males and four were females. The spleens removed weighed between 160 g in a 15-year-old girl and 5080 g in a 39-year-old man. The duration of presentations ranged from a 24-hour to a threeyear history. The most common presentations were abdominal mass and left upper quadrant pain. Only one patient, an Hausa herdsman mauled by a bull four months before admission, gave a history of trauma. His spleen weighed 5080 g on removal and contained 3.5 litres of chocolate-coloured fluid in a splenic cavity of 22 cm x 13 cm. Blood smears for malaria parasites were taken from two patients and were negative. The uacked cell volume ranged * from 16% to40%. The patient that had a PCV of 16% had no obvious cause other than hypersplenism to explain
15
38
394245
EHOPD
M.S.
E.A.
F
25
25
39
374537
384159
369037
T.C.
A.J.
F.S.
M
M
2860 2610
M F
OHOPD 414740
5080
245
2413
1110
M
160
360
F
36
393967
L.F.
F
770
M
55
Spleen weight (grams)
505948
Initials
Sex
splenectomies
A.A.
of nine elective
Age
I-Details
Hosp. No.
Table
23 x 50 x 8
14.5 x 10 x 6.3
34 x 23 x 21
37 x 29 x 28 30 x 14 x 14
17 x 11.5 x 9.5
15X9X3
17 x 12.5 x 3.3
18 x 10 x 4
College
1 month
9 days
1 year
2 years 3 years
2 years
1 week
1 year
24 hours
Duration of symptoms
at University
Spleen measurements (4
performed
Pathology
Ibadan
Pockets of chocolatecoloured fluid; perisplenitis, multiple haemorrhagic infarcts splenic congestion Fibrous capsule, perisplenitis, haemorrhagic infarcts, congested pulp Soft, cystic spleen, thickened capsule, focal subcapsular necrosis Areas of focal haemorrhages, congestion, lymphoid aggregates, poorly formed germinal centres. Non-specific changes Lymphosarcoma Areas of splenic infarction, capsular fibrosis, Gamma-Gandy bodies, no sickle cells. Hypersplenism Perisplenitis, pockets of chocolate-coloured fluid, congestion; haemorrhagic infarcts Perisplenitis, fibrous capsulitis, congestion 3.5 litres of chocolatecoloured fluid. Haematoma cavity of 25 x 13 cm. Fibrous capsule 0.5 cm
Hospital,
28
37
16
28 30
28
37
35
40
PCV
AA
AS
AA
AA
Genotype
-
-
-
+
-
-
-
-
Mortality
0.
G. AJAO
her anaemia. Her genotype was AS and her stools were negative for hookworm ova. Her spleen weighed 2413 g. The histology showed haemorrhagic fluid, infarcts, perisplenitis and pockets of chocolatecoloured fluid. The genotypes of four patients were determined : three had haemoglobin-AA and one haemoglobin -AS. There was one death from uncontrollable oozing of blood from the raw surface of the diaphragm and left upper abdominal wall where the spleen had been practically fused to these areas by severe degree of perisplenitis. This spleen weighed 2160 g. The histological diagnoses made from slides of the spleens were lymphosarcoma, splenic abscesses, splenic haematomata, splenic infarcts, splenic congestion and non-specific changes (see Table I). Most of these were diagnosed before surgery as tropical splenomegaly. It is significant that no malaria parasites were found in any of the spleens removed. Culture from those specimens with a suggestion of abscess or haematoma proved negative. This may have been due to the fact that these patients were treated with antibiotics before surgery. Discussion Since seven of the nine cases presented had splenic haematoma, infarcts and abscesses, this discussion is focused primarily on splenic cysts and solenic abscesses, which are usually diagnosed before surgery as-tropical splenomegaly. Sulenic cvst was first recognized in 1829 by An&al and splenectomy for this condition was first performed by Pean in 1867 (KING et al., 1968; QURESHI et al., 1964). One of the aetiological factors in the pathogenesis of splenic abscess is splenic infarction. In six of the spleens removed in this series definite areas of splenic infarcts and necrosis were present. Splenic infarction is relatively common in people with haemoglobinopathies. Genotypes were determined in only four of our patients and only one was a carrier of the S-gene. In sickle cell disease, the sickling of the red blood cells when there is a reduction in oxygen tension often leads to blockage of capillaries causing multiple infarctions in the affected viscera. Five of six cases of splenic abscess reported from this institution in 1962 (COCKSHOTT & WEAVER, 1962) were carriers of the S-gene. ZATZKIN et al. (1964) also claimed that, in Africa, the increased incidence of sickle cell disease parallels the increased incidence of splenic abscess. The mode of splenic abscess formation can be explained by the fact that infarction in any organ may eventually lead to liquefactive necrosis resulting in abscess formation from secondary infection. Unrecognized splenic trauma is probably a common cause of splenic abscess in the tropics where splenomegaly is endemic. History of abdominal trauma may be as short as two weeks or as long as four months. In this type of splenic trauma, laceration occurs within the substance of the spleen and not through the hilum or the capsule as hilar and capsular splenic tears are invariably fatal unless surgical intervention is immediate. In cases of
879
splenic abscess resulting from trauma, a haematoma is first formed within the splenic substance. Systemic bacteraemia then leads to secondary infection and suppuration in the haematoma, resulting in abscess formation (MCSHERRY & DINEE, 1962). The splenic capsule becomes thickened and fibrotic and severe perisplenitis occurs. COCKSHOTT & WEAVER (1962) have shown that the so-called “idiopathic primary” splenic abscess is due to infarction of the spleen. In some of these cases they found that the splenic vessels between the hilum and the capsule were thrombosed. Mycotic emboli or metastatic abscess (ZOOK et d., 1970) originating from different sites may cause splenic abscess even in the absence of infection. Salmonella choraesuis gastro-enteritis and Escherichia coli disseminated from a prostatic needle biopsy procedure have been shown to cause splenic abscess (ZOOK et al., 1970). It is claimed that splenic abscess may be the cause or the result of bacterial endocarditis in certain cases. In the earlier reports on splenic abscess, malaria was implicated as the cause in many cases (MCSHERRY & DINEE, 1962). Hydatid cyst of the spleen (QURESHI et al., 1964) and amoebiasis (WHELAN, 1957) are also possible causes of splenic abscess, especially in the tropics. The most common symptoms of splenic abscess are upper abdominal pain, dragging sensation in the abdomen, presence of an abdominal mass, post-prandial discomfort and anorexia. Clinical findings include moderate tenderness in the left upper quadrant of the abdomen, a mass extending down from the left upper quadrant towards the right lower quadrant for a variable distance, low-grade fever and anaemia.
Fig. 1. Barium meal showing displacement of the and anteriorly by an enlarged spleen.
medially
880
TROPICAL SI’LENOMEGALY : SURGICAL ASPECTS
Fig. 2. Barium meal showing displacement downward displacement of the jejunum and enlarged spleen.
Fig. 3. Angiography of a splenic mass.
of the splenic
stomach and flexure by an
Plain chest X-ray may show elevation of the left hemi-diaphragm due to the enlarged spleen. Atelectasis of the left lower lobe (KING et aZ., 1968) and a reactive left pleural effusion may also be nresent (ZATZKIN et ~2.. 1964). Plain abdominal X-ray may show a soft tissue mass in the left upper quadrant, a gas bubble or bubbles (COCKSHOTT & WEAVER, 1962) outside the alimentary tract in the left unoer auadrant. and an air-fluid level (ZATZKIN et al.: -1964) if liquefaction necrosis has occurred. Calcification in the wall of the abscess or cyst may also be noted (QURESHI et al., 1964). An excretory urogram may show downward displacement of the left kidney by the enlarged spleen (DOWSE, 1962; FORDE et al., 1960). A barium meal X-ray may show displacement of the stomach medially and anteriorly (Fig. 1) and downward displacement of the jejunum and splenic flexure (WHELAN, 1957) (Fig. 2). Selective angiography is a more direct and accurate means of diagnosing splenic abscess (KING et al., 1968) (Fig. 3). The initial management consists of improving the nutritional state, correction of anaemia and treatment for malaria. Broad spectrum antibiotics are indicated, especially if splenic abscess is suspected. The use of antibiotics should be regarded as a prelude to surgical intervention and not as definitive treatment. Direct needle puncture and aspiration of a splenic mass is to be discouraged, because aspiration of purulent material from the left upper quadrant does not necessarily differentiate a splenic cyst from an adrena or a renal cyst. Also, there is.a danger of splenic or renal laceration during the procedure which may result in fatal haemorrhage. Splenectomy is recommended as the definitive treatment for undiagnosed splenic enlargement after a failure of proguanil trial. Failure of surgical intervention may result in rupture, either spontaneously or as a result of minor trauma to the abdomen, especially during pregnancy, with greatly increased morbiditv and mortalitv. Untreated splenic abscess may rupture through ihe diaphragm or into the peritoneal cavity. Three common incisions used for the removal of enlarged spleens are thoraco-abdominal incision, midline or left paramedian with a left subcostal extension (“T-incision”), and left subcostal incision with an extension to the right subcostal area (bilateral subcostal or “bucket-handle” incision). Whereas a thoraco-abdominal incision provides good exposure, the thoracotomy increases postoperative morbiditv. A midline or left naramedian incision with a left subcostal extension also gives a good exposure. The junction of the two incisions, however, may fail to heal properly and on time. The left subcostal incision that may be extended by a right subcostal incision is preferred by the present author. This incision provides excellent exposure, especially if the spleen enlarges to the right lower Quadrant and, being a transverse incision, healing is good and there is l&s chance of wound dehisceice. Troublesome bleeding from the severe oerisolenitis and the numerous daated splenic veins make the surgery very hazardous. In two cases, the splenic veins were almost the size of a normal inferior vena cava. The single death in this series (J. 0. Hosp. No.
0.
414740) was due to persistent oozing of blood from the snlenic bed. Insertion of a bie tube drain into the sblenic bed monitors post-operative bleeding from it. Conclusion Splenic enlargement in the tropics without any obvious cause is best treated by splenectomy for histological diagnosis (most will be abscesses in various stages of formation), for prevention of anaemia and traumatic rupture, and for definitive treatment. There are no up-to-date scientific data to support the view that splenectomy depresses immunity to malaria in endemic areas thus increasing the danger of cerebral malaria. In cases of tropical splenomegaly syndrome, the alternative to surgical removal is the use of proguanil. Not all cases will respond to this treatment and? in those that do, the response is obvious from perrods of a few months to over two years. References Adekunle, 0. 0. (1976). Abdominal injuries in Nigeria. Paper presented at the West African College of Surgeons Meeting “Symposium on Care of the Injured”. Archampong, E. Q. (1976). Closed abdominal injuries in Ghana. Paper presented at the West African College of Surgeons Meeting “Symposium on Care of the Injured”. Cockshott, W. I?. & Weaver, E. J. M. (1962). Primary tropical splenic abscess: a misnomer. British Journal of Surgery, 49, 665-669. Dowse, J. L. (1962). Left renal displacement due to splenomegaly. British Journal of Surgery, 50, 114-116.
881
G. AJAO
Forde, W. J., Ostrolenk, D. G. & Finby, H. (1960). Renal disnlacement associated with enlarnement of spleen: American Journal of Roentge%ology, Radium Therapy and Nuclear Medicine, 94, 889-897. King, M. C., Glick, B. W. & Treed, A. (1968). The diagnosis of splenic cyst. Surgery, Gynecology and Obstetrics, 127, 509-512. Lemmon, W. T. & Paschal, G. W., Jr. (1948). Splenic abscess with drainage and recovery. American Journal of Surgery, 56, 641-646. McSherry, C. K. & Dinee, I’. (1962). The significance of splenic abscesses. American Journal of Surgery,
103, 618-623.
Qureshi, M. A., Hafner, C. D. & Dorchak, J. R. (1964). Non-parasitic cyst of the spleen. Archives of Surgery, 89, 570-574. Sagoe, A.-S. (1970). Tropical splenomegaly syndrome. Long-term proguanil therapy correlated with spleen size, serum IgM and lymphocyte transformation. British Medical Journal, iii, 378-382. Whelan, T. J., Jr. (1957). Abscess of the spleen. American Journal of Surgery, 94, 945-950. Zatzkin, H. R., Drazan, A. D. & Irwin, G. A. (1964). Roentgenographic diagnosis of splenic abscess. American Journal of Roentgenology, Radium Therapy and Nuclear Medicine, _ 91., 896-899. -Zook, E. G., Bolivar, J. C. & Epstein, L. I. (1970). The value of scintiscans in the diagnosis of splenic abscess. Surgery, Gynecology and Obstetrics, 131, 1125-1129.
Accepted for publication 5th March,
1981,
OP TROPICAL
Tropical
MEDICINE
AND HYGIENE,
splenomegaly
VOL.
75, No.
: surgical
G. AJAO College Hospital,
6, 1981
aspects
OLUWOLE
Dept. of Surgery,
University
Summary At the University College Hospital, Ibadan, Nigeria, in a 22-month period from January 1975 to September 1976, nine splenectomies were electively performed for unruptured spleens. The diagnoses were either tropical splenomegaly syndrome (when no obvious cause was found to be responsible for, or associated with, the splenomegaly) or splenic abscess in various stages of formation. The weights of the spleens removed ranged from 160 g in a 1%year-old girl to 5080 g in a 39-year-old male. One death due to uncontrollable bleeding from the solenic bed occurred. Histology of td spleens afier removal showed lymphosarcoma in one, non-specific changes in another, and thickened fibrous capsule, perisplenitis, haemorrhagic infarcts, pockets of chocolate-coloured fluid and inflammatory processes in various stages in the other seven. In the tropics, enlarged spleens with no obvious cause or associated condition are often best treated by splenectomy for histological diagnosis, definitive treatment and the prevention of rupture caused by minor trauma. There are, as yet, no convincing data which show that splenectomy in the tropics causes a significant diminution of immunity to malaria (or other diseases) and it does not, therefore, predispose to the development of cerebral malaria, Introduction Splenomegaly with no clear-cut aetiology and usually not associated with other obvious disease is endemic in tropical Africa. This condition, usually referred to as tropical splenomegaly syndrome, is diagnosed after exclusion of the other known causes of an enlarged spleen. The spleen is the organ most commonly injured in blunt abdominal trauma in Ibadan, Nigeria (ADEKUNLE, 1976) and in Accra, Ghana (ARCHAMPONG, 1976). At the University College Hospital, Ibadan, in a 22-month period (January 1975 to September 1976), 27 patients suffering from a ruptured spleen were operated upon and, in one case, splenectomy was necessitated by trauma sustained during vagotomy and pyloroplasty. It has been suggested that removing spleens from people resident in the tropics may lead to depression of the natural immunity to diseases, especially malaria, thus leading to the development of cerebral malaria. Up to the time of writing, there has been no well documented scientific data to justify this claim. In cases where immunity to malaria has been depressed as a result of many vears of urotection from reoeated attacks. a malaria prophylactic drug, such ai proguanil (I’aludrine), administered weekly is effective. This drug is cheap and easily available.
Ibadan,
Nigeria
Sagoe reported 43 cases of tropical splenomegaly syndrome from the medical service of the University College Hospital, Ibadan, Nigeria (SAGOE, 1970). 32 of these cases responded to proguanil 100 mg daily and 11 did not. The duration of response ranged from a few months to over two years. From the surgical point of view, this period is sufficiently long to risk rupture of an enlarged spleen from relatively minor trauma, with fatal consequences. The purpose of this paper is to stress the importance of splenectomy for the treatment, pathological diagnosis and prevention of the risk of a ruptured spleen in cases of enlarged spleen in which no obvious cause can be found by current laboratory methods. Experience with nine cases of enlarged spleen electively removed is also described. Materials and Methods In a 22-month period (January 1975 to September 1976), nine elective splenectomies were performed by the surgical service of the University College Hospital, Ibadan, Nigeria. The pre-operative diagnosis in all cases was either tropical splenomegaly or splenic abscess. The age and sex of each patient were recorded and the duration of symptoms and the presentations noted. The packed cell volumes of all the patients were estimated and the genotypes of four patients were determined. Splenic aspirates were cultured from patients with proven splenic abscess or haematoma. In each case, the removed spleen was weighed and measured. The measurements considered were the longitudinal axis, the transverse diameter and the height at the hilum. The histological picture of each spleen removed was carefully studied. Cases of traumatic ruptured spleen were not included in this study. Results Patients were between 15 and 55 years old; five were males and four were females. The spleens removed weighed between 160 g in a 15-year-old girl and 5080 g in a 39-year-old man. The duration of presentations ranged from a 24-hour to a threeyear history. The most common presentations were abdominal mass and left upper quadrant pain. Only one patient, an Hausa herdsman mauled by a bull four months before admission, gave a history of trauma. His spleen weighed 5080 g on removal and contained 3.5 litres of chocolate-coloured fluid in a splenic cavity of 22 cm x 13 cm. Blood smears for malaria parasites were taken from two patients and were negative. The uacked cell volume ranged * from 16% to40%. The patient that had a PCV of 16% had no obvious cause other than hypersplenism to explain
15
38
394245
EHOPD
M.S.
E.A.
F
25
25
39
374537
384159
369037
T.C.
A.J.
F.S.
M
M
2860 2610
M F
OHOPD 414740
5080
245
2413
1110
M
160
360
F
36
393967
L.F.
F
770
M
55
Spleen weight (grams)
505948
Initials
Sex
splenectomies
A.A.
of nine elective
Age
I-Details
Hosp. No.
Table
23 x 50 x 8
14.5 x 10 x 6.3
34 x 23 x 21
37 x 29 x 28 30 x 14 x 14
17 x 11.5 x 9.5
15X9X3
17 x 12.5 x 3.3
18 x 10 x 4
College
1 month
9 days
1 year
2 years 3 years
2 years
1 week
1 year
24 hours
Duration of symptoms
at University
Spleen measurements (4
performed
Pathology
Ibadan
Pockets of chocolatecoloured fluid; perisplenitis, multiple haemorrhagic infarcts splenic congestion Fibrous capsule, perisplenitis, haemorrhagic infarcts, congested pulp Soft, cystic spleen, thickened capsule, focal subcapsular necrosis Areas of focal haemorrhages, congestion, lymphoid aggregates, poorly formed germinal centres. Non-specific changes Lymphosarcoma Areas of splenic infarction, capsular fibrosis, Gamma-Gandy bodies, no sickle cells. Hypersplenism Perisplenitis, pockets of chocolate-coloured fluid, congestion; haemorrhagic infarcts Perisplenitis, fibrous capsulitis, congestion 3.5 litres of chocolatecoloured fluid. Haematoma cavity of 25 x 13 cm. Fibrous capsule 0.5 cm
Hospital,
28
37
16
28 30
28
37
35
40
PCV
AA
AS
AA
AA
Genotype
-
-
-
+
-
-
-
-
Mortality
0.
G. AJAO
her anaemia. Her genotype was AS and her stools were negative for hookworm ova. Her spleen weighed 2413 g. The histology showed haemorrhagic fluid, infarcts, perisplenitis and pockets of chocolatecoloured fluid. The genotypes of four patients were determined : three had haemoglobin-AA and one haemoglobin -AS. There was one death from uncontrollable oozing of blood from the raw surface of the diaphragm and left upper abdominal wall where the spleen had been practically fused to these areas by severe degree of perisplenitis. This spleen weighed 2160 g. The histological diagnoses made from slides of the spleens were lymphosarcoma, splenic abscesses, splenic haematomata, splenic infarcts, splenic congestion and non-specific changes (see Table I). Most of these were diagnosed before surgery as tropical splenomegaly. It is significant that no malaria parasites were found in any of the spleens removed. Culture from those specimens with a suggestion of abscess or haematoma proved negative. This may have been due to the fact that these patients were treated with antibiotics before surgery. Discussion Since seven of the nine cases presented had splenic haematoma, infarcts and abscesses, this discussion is focused primarily on splenic cysts and solenic abscesses, which are usually diagnosed before surgery as-tropical splenomegaly. Sulenic cvst was first recognized in 1829 by An&al and splenectomy for this condition was first performed by Pean in 1867 (KING et al., 1968; QURESHI et al., 1964). One of the aetiological factors in the pathogenesis of splenic abscess is splenic infarction. In six of the spleens removed in this series definite areas of splenic infarcts and necrosis were present. Splenic infarction is relatively common in people with haemoglobinopathies. Genotypes were determined in only four of our patients and only one was a carrier of the S-gene. In sickle cell disease, the sickling of the red blood cells when there is a reduction in oxygen tension often leads to blockage of capillaries causing multiple infarctions in the affected viscera. Five of six cases of splenic abscess reported from this institution in 1962 (COCKSHOTT & WEAVER, 1962) were carriers of the S-gene. ZATZKIN et al. (1964) also claimed that, in Africa, the increased incidence of sickle cell disease parallels the increased incidence of splenic abscess. The mode of splenic abscess formation can be explained by the fact that infarction in any organ may eventually lead to liquefactive necrosis resulting in abscess formation from secondary infection. Unrecognized splenic trauma is probably a common cause of splenic abscess in the tropics where splenomegaly is endemic. History of abdominal trauma may be as short as two weeks or as long as four months. In this type of splenic trauma, laceration occurs within the substance of the spleen and not through the hilum or the capsule as hilar and capsular splenic tears are invariably fatal unless surgical intervention is immediate. In cases of
879
splenic abscess resulting from trauma, a haematoma is first formed within the splenic substance. Systemic bacteraemia then leads to secondary infection and suppuration in the haematoma, resulting in abscess formation (MCSHERRY & DINEE, 1962). The splenic capsule becomes thickened and fibrotic and severe perisplenitis occurs. COCKSHOTT & WEAVER (1962) have shown that the so-called “idiopathic primary” splenic abscess is due to infarction of the spleen. In some of these cases they found that the splenic vessels between the hilum and the capsule were thrombosed. Mycotic emboli or metastatic abscess (ZOOK et d., 1970) originating from different sites may cause splenic abscess even in the absence of infection. Salmonella choraesuis gastro-enteritis and Escherichia coli disseminated from a prostatic needle biopsy procedure have been shown to cause splenic abscess (ZOOK et al., 1970). It is claimed that splenic abscess may be the cause or the result of bacterial endocarditis in certain cases. In the earlier reports on splenic abscess, malaria was implicated as the cause in many cases (MCSHERRY & DINEE, 1962). Hydatid cyst of the spleen (QURESHI et al., 1964) and amoebiasis (WHELAN, 1957) are also possible causes of splenic abscess, especially in the tropics. The most common symptoms of splenic abscess are upper abdominal pain, dragging sensation in the abdomen, presence of an abdominal mass, post-prandial discomfort and anorexia. Clinical findings include moderate tenderness in the left upper quadrant of the abdomen, a mass extending down from the left upper quadrant towards the right lower quadrant for a variable distance, low-grade fever and anaemia.
Fig. 1. Barium meal showing displacement of the and anteriorly by an enlarged spleen.
medially
880
TROPICAL SI’LENOMEGALY : SURGICAL ASPECTS
Fig. 2. Barium meal showing displacement downward displacement of the jejunum and enlarged spleen.
Fig. 3. Angiography of a splenic mass.
of the splenic
stomach and flexure by an
Plain chest X-ray may show elevation of the left hemi-diaphragm due to the enlarged spleen. Atelectasis of the left lower lobe (KING et aZ., 1968) and a reactive left pleural effusion may also be nresent (ZATZKIN et ~2.. 1964). Plain abdominal X-ray may show a soft tissue mass in the left upper quadrant, a gas bubble or bubbles (COCKSHOTT & WEAVER, 1962) outside the alimentary tract in the left unoer auadrant. and an air-fluid level (ZATZKIN et al.: -1964) if liquefaction necrosis has occurred. Calcification in the wall of the abscess or cyst may also be noted (QURESHI et al., 1964). An excretory urogram may show downward displacement of the left kidney by the enlarged spleen (DOWSE, 1962; FORDE et al., 1960). A barium meal X-ray may show displacement of the stomach medially and anteriorly (Fig. 1) and downward displacement of the jejunum and splenic flexure (WHELAN, 1957) (Fig. 2). Selective angiography is a more direct and accurate means of diagnosing splenic abscess (KING et al., 1968) (Fig. 3). The initial management consists of improving the nutritional state, correction of anaemia and treatment for malaria. Broad spectrum antibiotics are indicated, especially if splenic abscess is suspected. The use of antibiotics should be regarded as a prelude to surgical intervention and not as definitive treatment. Direct needle puncture and aspiration of a splenic mass is to be discouraged, because aspiration of purulent material from the left upper quadrant does not necessarily differentiate a splenic cyst from an adrena or a renal cyst. Also, there is.a danger of splenic or renal laceration during the procedure which may result in fatal haemorrhage. Splenectomy is recommended as the definitive treatment for undiagnosed splenic enlargement after a failure of proguanil trial. Failure of surgical intervention may result in rupture, either spontaneously or as a result of minor trauma to the abdomen, especially during pregnancy, with greatly increased morbiditv and mortalitv. Untreated splenic abscess may rupture through ihe diaphragm or into the peritoneal cavity. Three common incisions used for the removal of enlarged spleens are thoraco-abdominal incision, midline or left paramedian with a left subcostal extension (“T-incision”), and left subcostal incision with an extension to the right subcostal area (bilateral subcostal or “bucket-handle” incision). Whereas a thoraco-abdominal incision provides good exposure, the thoracotomy increases postoperative morbiditv. A midline or left naramedian incision with a left subcostal extension also gives a good exposure. The junction of the two incisions, however, may fail to heal properly and on time. The left subcostal incision that may be extended by a right subcostal incision is preferred by the present author. This incision provides excellent exposure, especially if the spleen enlarges to the right lower Quadrant and, being a transverse incision, healing is good and there is l&s chance of wound dehisceice. Troublesome bleeding from the severe oerisolenitis and the numerous daated splenic veins make the surgery very hazardous. In two cases, the splenic veins were almost the size of a normal inferior vena cava. The single death in this series (J. 0. Hosp. No.
0.
414740) was due to persistent oozing of blood from the snlenic bed. Insertion of a bie tube drain into the sblenic bed monitors post-operative bleeding from it. Conclusion Splenic enlargement in the tropics without any obvious cause is best treated by splenectomy for histological diagnosis (most will be abscesses in various stages of formation), for prevention of anaemia and traumatic rupture, and for definitive treatment. There are no up-to-date scientific data to support the view that splenectomy depresses immunity to malaria in endemic areas thus increasing the danger of cerebral malaria. In cases of tropical splenomegaly syndrome, the alternative to surgical removal is the use of proguanil. Not all cases will respond to this treatment and? in those that do, the response is obvious from perrods of a few months to over two years. References Adekunle, 0. 0. (1976). Abdominal injuries in Nigeria. Paper presented at the West African College of Surgeons Meeting “Symposium on Care of the Injured”. Archampong, E. Q. (1976). Closed abdominal injuries in Ghana. Paper presented at the West African College of Surgeons Meeting “Symposium on Care of the Injured”. Cockshott, W. I?. & Weaver, E. J. M. (1962). Primary tropical splenic abscess: a misnomer. British Journal of Surgery, 49, 665-669. Dowse, J. L. (1962). Left renal displacement due to splenomegaly. British Journal of Surgery, 50, 114-116.
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Forde, W. J., Ostrolenk, D. G. & Finby, H. (1960). Renal disnlacement associated with enlarnement of spleen: American Journal of Roentge%ology, Radium Therapy and Nuclear Medicine, 94, 889-897. King, M. C., Glick, B. W. & Treed, A. (1968). The diagnosis of splenic cyst. Surgery, Gynecology and Obstetrics, 127, 509-512. Lemmon, W. T. & Paschal, G. W., Jr. (1948). Splenic abscess with drainage and recovery. American Journal of Surgery, 56, 641-646. McSherry, C. K. & Dinee, I’. (1962). The significance of splenic abscesses. American Journal of Surgery,
103, 618-623.
Qureshi, M. A., Hafner, C. D. & Dorchak, J. R. (1964). Non-parasitic cyst of the spleen. Archives of Surgery, 89, 570-574. Sagoe, A.-S. (1970). Tropical splenomegaly syndrome. Long-term proguanil therapy correlated with spleen size, serum IgM and lymphocyte transformation. British Medical Journal, iii, 378-382. Whelan, T. J., Jr. (1957). Abscess of the spleen. American Journal of Surgery, 94, 945-950. Zatzkin, H. R., Drazan, A. D. & Irwin, G. A. (1964). Roentgenographic diagnosis of splenic abscess. American Journal of Roentgenology, Radium Therapy and Nuclear Medicine, _ 91., 896-899. -Zook, E. G., Bolivar, J. C. & Epstein, L. I. (1970). The value of scintiscans in the diagnosis of splenic abscess. Surgery, Gynecology and Obstetrics, 131, 1125-1129.
Accepted for publication 5th March,
1981,