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Imaging Diagnosis

There are no characteristic radiological findings in malaria. Ultrasonography or other scanning may demonstrate generalized lymphadenopathy. Splenic enlargement is common; the spleen may be slightly or grossly enlarged. It is homogeneous on ultrasonography or CT, unless there has been infarction or infection. When this occurs repeatedly and there is perisplenitis, there may be adhesions around the spleen, involving the omentum, diaphragm, and abdominal wall. The end result may be splenic encasement or fibrosis. This is particularly common in the 25 to 50 year age group with chronic malaria. Injury is common and rupture of the spleen can occur with minimal trauma. Ultrasonography will usually demonstrate splenic damage, but may have to be repeated when there is clinical suspicion but equivocal sonographic results. Removal of an enlarged malarial spleen in an endemic area must be followed by continuous antimalarial prophylaxis because the patient's immunity will be altered by the splenectomy. The patient has lost the great parasite trap. If there is severe splenic infarction and infection, the resulting splenic abscess may be demonstrated on an erect abdominal radiograph, appearing as a gas bubble and fluid level in the spleen, resembling the fundus of the stomach but situated more laterally (Fig. 46.4A); the abscess can also be demonstrated with ultrasonography (Fig. 46.4B).

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Fig. 46.4A,B. (A) Splenic infarction followed by splenic abscesses in an African from an area where malaria is endemic. The fluid level seen in this erect film lies within the spleen. (B) An ultrasound scan of a large splenic abscess. (Courtesy of WHO: Palmer PES (ed). Manual of Diagnostic Ultrasound, 1995).

Portal hypertension occurs in malaria; hepatomegaly is variable. When there is cerebral malaria the liver enlarges; in the patient with malarial anemia the liver is also enlarged, often due to an associated myocardial failure as well as the congestion caused by the parasitized erythrocytes.

In cerebral malaria in adults, CT scanning has not shown any really diagnostic abnormalities. There may be focal, asymmetrical cerebral edema (Fig. 46.5 and gross appearance in Fig. 46.6), sufficient in some cases to cause ventricular compression. Small areas of altered density have been reported; these do not always contrast enhance and cannot be correlated with the clinical neurological signs in every case. In one series of ten patients with cerebral malaria, five died, and two of those who died had normal CT scans. However, three of the five who died had pulmonary edema. There was no evidence of any vascular lesion (scan resolution 1 mm or larger). In another series of 14 unconscious African children, the CT findings were similar, including widespread low-density areas (thought to be suggestive of ischemia) in four children, all of whom had serious neurological sequelae. Cerebral perfusion was monitored in two of these children and was critically reduced, suggesting that the brain damage may be, in part, the result of the intracranial hypertension.

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Fig. 46.5 A-F. CT scanning in cerebral malaria. (A) Acute stage The brain is swollen and diffusely hypodense, except for the basal ganglia. (B) During recovery there is cerebral atrophy, with infarction in the right frontal and parietal regions. (C) The acute stage in another patient shows the same diffuse brain swelling, with superficial hypodensity. In this patient the basal ganglia are also hypodense. (D) In recovery a contrast scan shows enhancement of the zone between the left middle and the posterior cerebral artery areas. (E) In a third patient there are scattered areas of hypodensity throughout the diffusely swollen brain and basal ganglia. (F) In this patient there is cerebral atrophy, when clinically the malaria has been cured. (Courtesy of Dr. C. R. J. C. Newton et al. and Arch Dis Child).

Fig. 46.6. Gross sagittal section of brain with acute cerebral malaria. Note the edema of the cortex and the vascular congestion. AFIP 70-11566. (From Marty and Andersen 1995).

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