British Journal of Radiology (2006) 79, e145-e147
© 2006 British Institute of Radiology
doi: 10.1259/bjr/46185784
CT findings of malarial spleen
K Bae, MD
and
K-N Jeon, MD
Department of Diagnostic Radiology, Gyeongsang National University Hospital, Jinju, Republic of Korea
Correspondence: Dr K-N Jeon, Department of Diagnostic Radiology, Gyeongsang National University Hospital, 90 Chilam-dong, Jinju, Republic of Korea, 660-702. E-mail: knjeon{at}nongae.gsnu.ac.kr.
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Abstract
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Malaria is one of the most frequent causes of fever among travellers to tropical countries. We report the CT imaging findings of poor contrast enhancement of the spleen on arterial phase in a case of malaria presenting as splenomegaly. To the best of our knowledge, this is the first report of malarial spleen diagnosed by these CT results.
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Introduction
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Malaria is still a major medical problem in many parts of the world due to increased travel to areas with widespread malaria and due to the development of resistance to antimalarial drugs. Each year, up to three million deaths and close to five billion episodes of clinical illness result from malaria throughout the world [1]. We report a case of malaria diagnosed by CT findings not previously described in the literature.
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Case report
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A 23-year-old man presented with a 5 day history of fever, malaise, headache and diffuse abdominal pain. He had served in the military in mid-east Korea from 2002 to 2004, until 4 months prior to admission. On admission, the patient reported he had not travelled abroad, received a blood transfusion or used parenteral drugs.
The physical examination revealed that the patient had a high fever (39°C), tachycardia and diffuse upper abdominal tenderness with a tender, palpable splenic tip. Laboratory studies showed a white blood cell count of 3.8x109 l–1, a haemoglobin level of 145 g l–1, a haematocrit of 42%, a platelet count of 42x109 l–1 and a normal concentration of electrolytes.
An abdominal ultrasound scan revealed a diffusely enlarged spleen 14 cm long at the greatest axis. There was no significant para-aortic lymphadenopathy and no ascites. The liver, pancreas and kidneys were normal. Dynamic CT of the abdomen was performed to exclude an intra-abdominal source of infection. The pre-contrast phase scans showed an enlarged spleen. The mean pre-contrast attenuation value of the spleen and liver parenchyma were 45 HU and 55 HU, respectively. The spleen was not enhanced significantly in the arterial phase and was only mildly enhanced in the portal venous phase (Figure 1a,b
). Mean post-contrast attenuation measurements of the arterial and portal venous phase gave values of 59 HU and 81 HU, respectively, for the spleen and 71 HU and 125 HU, respectively, for the liver. Several small sized lymph nodes were seen in the abdominal nodal chains.
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Figure 1. Malarial spleen in a 23-year-old man. (a) Arterial phase CT scan shows lack of parenchymal enhancement of the enlarged spleen and several small lymph nodes in the perihepatic space. The cortex of the left kidney is markedly enhanced. (b) Portal phase CT scan shows mild enhancement of the spleen. The attenuation value of the spleen (81 HU) is much lower than that of the liver (125 HU). (c) Stained peripheral blood smear shows a ring form trophozoite (arrow) and a gametocyte (arrowhead) within enlarged red blood cells, which is consistent with P. vivax. (Wright-Geimsa, x1000). (d) Arterial phase CT scan obtained 3 months after treatment shows an intense striped enhancement of the normal sized spleen.
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A blood smear showed trophozoites and gametocytes in normocytic erythrocytes (Figure 1c
). The morphology of the parasites was consistent with that of Plasmodium vivax. After confirming the diagnosis, the patient was treated with chloroquine and primaquine. He was discharged after 10 days of hospitalization. The follow up blood smears revealed that the malaria parasites had gone.
At the outpatient clinic follow up 3 months later, the patient had remained well and asymptomatic, and the splenomegaly had resolved. A repeat abdominal CT scan showed the spleen had diminished in size and the enhancement pattern was normal (Figure 1d).
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Discussion
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Malaria is a protozoan disease transmitted by the bite of infected Anopheles mosquitoes. Malarial transmission is possible in tropical regions where humans and mosquitoes co-exist. Today, malaria remains an overwhelming problem in tropical developing countries and is a potentially life-threatening complication for non-immune travellers to the tropics. Malaria undoubtedly existed before the mid-20th century in Europe, especially in Italy, as well as in northern parts of Asia [2, 3]. South Korea is considered free from malaria as a case has not been reported there since 1984, although it was previously known as a P. vivax endemic area. Recently, however, several cases of P. vivax infection have been reported in Korean soldiers who had never been abroad.
The spleen plays an integral role in host defence against malaria and other intravascular parasites. Spleen enlargement occurs in 95–100% of individuals with acute malaria. During acute and chronic malaria, altered splenic structure and function results in mild to moderate enlargement of the spleen. Within days to weeks after treatment, the spleen generally regresses in size [4, 5]. Gross examination reveals that acute malarial spleen is dark red due to congestion, hyperaemia and deposition of haemozoin. Microscopic examination of malarial spleen demonstrates haemozoin, parasitized and uninfected erythrocytes, as well as a massive proliferation of macrophages throughout the capillaries, venous sinuses and pulp spaces. In addition, congestion and dilatation of sinuses and scattered thrombosis, with focal necrosis in the capillaries and splenic pulp, are observed in the spleen. These changes can lead to an occlusion and infarction of the vessels and splenic tissue [4–8].
The dynamic CT findings of malarial spleen are not adequately described in the literature. Normal splenic parenchyma generally shows an inhomogeneous, striking striped contrast enhancement on arterial phase CT scans. It is well known that normal splenic enhancement is greater than the hepatic enhancement of the arterial phase, and that peak contrast enhancement of the spleen occurs between 0 s and 20 s after peak contrast enhancement of the aorta [9–11]. In the case presented here, the spleen lacked such enhancement in the arterial phase and the splenic enhancement was not greater than the hepatic enhancement at any phase during the scans.
Although histological analysis was not performed in this case, previous reports of splenic complications in malaria may help explain the pathophysiologically abnormal enhancement pattern of the spleen [5, 12]. The pattern probably foremost results from congestion and microthrombosis of sinuses and from focal necrosis in the capillaries and pulp of the spleen. Second, red cell lysis within capillaries may release vasoactive factors that constrict splenic capillaries.
CT findings similar to those reported for this case of malarial spleen could be observed in diffuse infiltrative diseases of the spleen such as amyloidosis, lymphoma and leukaemia [13, 14].
In conclusion, although malaria is a rare cause of fever in developed countries, it should be considered in the differential diagnosis of fever in cases in which CT reveals lack of contrast enhancement of enlarged spleen on arterial phase, particularly when exposure to malaria is possible.
Received for publication August 1, 2005.
Revision received December 6, 2005.
Accepted for publication January 3, 2006.
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References
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Abstract
Introduction
