Splenic Infarction Caused by Vivax Malaria

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					대한외과학회지:제 75 권            제3호
Vol. 75, No. 3, September, 2008
                                                                                                                          □ 증 례 □

                             Splenic Infarction Caused by Vivax Malaria
                                   Department of Surgery, Uijeongbu St. Mary's Hospital,
                           The Catholic University of Korea College of Medicine, Uijeongbu, Korea

        Hang Joo Cho, M.D., Ki Hwan Kim, M.D., Ji Il Kim, M.D., Chang Hyuck Ahn, M.D.,
                Seung Jin Yoo, M.D., Keun Woo Lim, M.D., Jeung Soo Kim, M.D.

    Splenic infarction caused by malaria is a rare complication and this is mostly caused by plasmodium falciparum.
    We report here on a 38 year-old female patient who developed symptomatic splenic infarction that was caused
    by vivax malaria. She presented with fever and left upper quadrant pain. Computed tomography showed multiple
    low density areas in the spleen, and the peripheral blood smear revealed plasmodium vivax infestation. We
    examined for other causes of splenic infarction, but all were negative. This is just the second report of symptomatic
    splenic infarction that was caused by vivax malaria only. Unlike the previous case, the levels of D-dimer and
    fibrinogen degradation factor were elevated. This may be related with the hypercoagulable state caused by malaria.
    Treatment was conservative and the further course was uneventful. (J Korean Surg Soc 2008;75:213-215)
    Key Words: Splenic infarction, Vivax malaria, Hypercoagulable state

                                                                             Physical examination showed left upper quadrant mild
                      INTRODUCTION                                           tenderness and splenomegaly and fever (38.1oC). Labora-
                                                                             tory test revealed normocytic normochromic anemia (Hb
  Splenic infarction caused by malaria is very rare and                      7.5 g/dl), thrombocytopenia (99×109/L) and normal liver
there are only 10 reports in the literature which had                        enzyme level. Other laboratory test revealed increased levels
clinically evident splenic infarction occurring with malaria.                of fibrinogen degradation factor (FDP)(11.4 ug/ml), D-
With the exception of one case, all patients were found                      dimer (835 ug/L), and normal levels of fibrinogen and
to have been infected by plasmodium falciparum or                            anti-thrombin III. The diagnosis was confirmed by peri-
co-infected by plasmodium vivax.(1)                                          pheral blood smear with only P. vivax at a density of
  We report a case of woman who presented with                               2.440×109/L. Computed tomography (CT) of the abdomen
symptomatic splenic infarction and vivax malaria which is                    showed splenomegaly (19 cm long along the greatest axis)
a rare cause of splenic infarction.                                          and multiple infarcted zones of low attenuated density in
                                                                             the enlarged spleen (Fig. 1).
                       CASE REPORT                                             We started treatment with oral hydroxychlorquine (800
                                                                             mg, 400 mg, 400 mg, 400 mg at 0, 6, 24, 48 hrs) and
    A 38-year-old Korean woman visited the hospital                          2 days after her admission, serum malaria level fell to
complaining with a periodic fever and left upper quadrant                    0.756×109/L and 3 days after her admission, no more
abdominal pain for 3 weeks. She was a hepatitis B carrier.                   malaria was found on peripheral blood smear. Fever was
                                                                             subsided 1 day after admission and after 48 hours of
Corresponding to: Jeung Soo Kim, Department of Surgery, Uijeongbu            hydroxychlorquine therapy, we started oral primaquine (15
    St. Mary's Hospital, The Catholic University of Korea College of
    Medicine, 65-1, Geumo-dong, Uijeongbu 480-130, Korea. Tel: 031-          mg/day). Vital sign remained stable during the admission
    820-3048, Fax: 031-847-2717, E-mail: drbreast@catholic.ac.kr             and anemia resolved without transfusion (Hb 9.9 g/dl at
Received January 24, 2008, Accepted May 13, 2008

214 J Korean Surg Soc. Vol. 75, No. 3

Fig. 1. Computed tomography of the abdomen shows low density
                                                                 Fig. 2. Follow up computed tomography acquired about 2 weeks
        area in enlarged spleen (arrow).
                                                                         later shows slightly reduced size of spleen and regression
                                                                         of infarcted area.
  We studied other possible causes of splenic infarction         infarction included CT and ultrasonography. CT scanning
including salmonellosis, coagulation disorder (Protein C, S      showed well-defined low attenuated areas within the splenic
deficiency, Leyden mutation, antiphospholipid antibody)          parenchyma without contrast enhancement. Ultrasono-
and infective endocarditis and all were negative. After 8        graphy showed rounded or wedge-shaped, echo-free, hypo-
days of admission, She discharged from the hospital with         echoic, and hyperechoic lesions and these findings changed
primaquine without any complications. One week later, the        over a period of time.(3,4)
patient visited outpatient clinic with improved pain and           True incidence rate of splenic infarction may be
follow up CT revealed slightly reduced size of spleen and        underestimated because the diagnosis is difficult and the
regression of infarction (Fig. 2).                               infarction often goes unnoticed.(1) Symptoms develop in
                                                                 about 60∼70 percent of the patients and the most
                      DISCUSSION                                 common presenting symptom is left upper quadrant
                                                                 abdominal pain. Other symptoms include fever, pleuritic
  The causes of splenic infarction are various. Most             chest pain, back pain and left shoulder pain. In our case,
common causes include infiltrative hematologic disease           the patient also had left upper quadrant abdominal pain
with congestion of the splenic circulation by abnormal cells     and fever.
and thromboembolic conditions which produce obstruction            Pathophysiological mechanism of splenic infarction in
of large vessels.(2) Splenic artery embolization has been        malaria infection is poorly known. Capillary microthrom-
associated with diverse cardiovascular conditions including      bus formation could lead to vascular disturbances and
atherosclerosis, acute myocardial infarction, atrial fibrilla-   downstream necrosis and red cell lysis within capillary
tion and bacterial endocarditis, we ruled out this causes        could release vasoactive factors.(2) There are lots of articles
through electrocardiography and echocardiography. After          about coagulation profile in malaria patients. Most studies
performing peripheral blood smear, various coagulation           demonstrate an alteration in the hemostasis toward the
profile, blood culture, stool culture and Widal test, we         hypercoagulable state in acute malaria, especially falci-
concluded that the only cause of splenic infarction in this      parum malaria.(5) In severe cases it proceeds to a disse-
patient was vivax malaria.                                       minated intravascular coagulation. Some studies demons-
  Radiologic studies used for diagnosis of splenic               trated that in malarial parasitaemia serum FDP and

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