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vivax ARDS autopsy did not show sequestration of parasitized RBCs in
the pulmonary vasculature ( Valecha et al., 2009 ). As in ALI in other disease
settings, ARDS in vivax malaria probably results from soluble mediators,
diffuse alveolar-endothelial capillary damage, exacerbated by shock, with
increases in alveolar permeability and altered alveolar fluid clearance ( Tan
et al., 2008 ; Valecha et al., 2009 ; Suratt and Parsons, 2006 ).
The majority of cases of vivax-associated ARDS develop after the start
of antimalarial chemotherapy (see Taylor et al., 2012 ; Anstey et al., 2009 for
reviews) and gas transfer studies show progressive deterioration in alveo-
lar-capillary function following treatment ( Anstey et al., 2007 ). This may
reflect exacerbation of an inflammatory response associated with parasite-
killing and/or monocyte/pigment accumulation ( Tan et al., 2008 ; Anstey
et al., 2007 ), though vivax-associated ARDS can occur prior to the start
of antimalarial chemotherapy ( Valecha et al., 2009 ; Lomar et al., 2005 ). As
chloroquine-resistance spreads, and other treatment regimens without the
anti-inflammatory effects of chloroquine become necessary ( Douglas et al.,
2010 ), it is possible that the incidence of ARDS post-treatment may rise
( Anstey et al., 2007 ).
The majority of respiratory distress, in both falciparum and vivax malaria,
occurs in young children ( Tjitra et al., 2008 ; Genton et al., 2008 ; Marsh et al.,
1995 ). ALI is reportedly rare in young children, but is described in recent
paediatric severe vivax malaria series ( Lanca et al., 2012 ). An increase in
mortality in children with severe falciparum malaria receiving fluid boluses
( Maitland et al., 2011 ) suggests that pulmonary oedema in children with
severe malaria may be more prevalent than previously realized. Nevertheless,
while ALI appears to be a major cause of vivax-associated respiratory dis-
tress in adults, other causes are likely to be important in causing respiratory
distress in children. As in falciparum malaria, these may include metabolic
acidosis, reported in paediatric vivax-associated respiratory distress ( Kochar
et al., 2010 ), as well as severe anaemia ( Tjitra et al., 2008 ), pneumonia and/
or sepsis. Concomitant pneumonia was seen in 8% of children with severe
vivax malaria in a recent series ( Kaushik et al., 2012 ).
11.2.3. Acute kidney injury
Mechanisms underlying AKI in vivax malaria are not clear. With its frequent
association with shock and multiorgan dysfunction, a sepsis-like syndrome
either from P. vivax itself (see below) or concomitant bacterial sepsis may be
a significant contributor to AKI. The extent to which acute tubular necrosis
underlies AKI in the setting of multiorgan dysfunction, as seen frequently
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