Page 993 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

724 PART 5: Infectious Disorders

TABLE 78-1 Manifestations and Complication of Severe Falciparum Malaria
Manifestation or
Complication Pathophysiology Treatment
Coma (Glasgow Sequestration of parasitized Hypoglycemia and other causes
Coma Score <11; red blood cells in the cerebral of meningo/encephalitis should
Blantyre Coma microcirculation and other be excluded. Good general
Score <3) and factors intensive nursing care, including
convulsions close observation of breathing,
eye care, nasogastric tube, Foley
catheter. If feasible: intubation to
protect airway. Frequent moni-
toring of blood glucose. Treat
convulsions (eg, lorazepam).
Prophylactic anticonvulsive treat-
ment is not recommended
Anemia (Hct Loss of parasitized red blood cells, General recommendation:
<20%, in presence increased splenic clearance of unin- transfusion if in distress, or Hct
of parasitemia fected red blood cells (decreased <20% (adults), or Hb <5 g/dL
>100,000/μL) red cell deformability, immuno- in children
logical factors?), dyserythropoiesis FIGURE 78-3. Postmortem brain smear from an adult with cerebral malaria showing
Hyperparasitemia Host immunological factors Promptly start parenteral anti- intense sequestration of parasitized erythrocytes in brain capillaries. (Used with permission
(>10% infected and parasite virulence factors malarial drugs in effective doses of Dr. Kamolrat Silamut.)
red blood cells) ( multiplication rate, red cell (artemisinins; if quinine: give load-
selectivity) ing dose). Exchange transfusion (?)
Hypoglycemia Increased use, decreased Glucose 10%, 4 mg/kg body- although these complications are more likely to develop in those with
(blood glucose production, quinine related weight chronic underlying morbidities such as renal impairment or diabetes.
<40 mg/dL) hyperinsulinism The degree to which P vivax also exhibits cytoadherence is not well stud-
ied, with some reports suggesting that P vivax can cytoadhere and form
Acute kidney injury Acute tubular necrosis Record fluid balance (Foley rosettes in ex vivo models. 22,23 Unlike for many P falciparum infections,
catheter) however, circulating parasites often include later stages of development
Prerenal component Check biochemistry (BUN, suggesting that the numbers of adherent mature stages of P vivax are fewer.
(dehydration) electrolytes), early start of renal P knowlesi is now an established cause of severe and fatal disease, and
replacement therapy (hemofil- infections can be associated with very high peripheral parasitemias that
tration or hemodialysis preferred are comparable in density to those seen in some P falciparum infections.
over peritoneal dialysis) The shorter (24 hours) life cycle may also explain, at least in part, why
Severe jaundice Mainly in adults; multifactorial No specific treatment, monitor later stages of development can also be seen on the peripheral blood
( bilirubin >3.0 mg/ blood glucose film. In a single fatal case studied at postmortem, there was accumula-
dL, with parasitemia tion of parasitized erythrocytes in organ capillaries and venules, giving
>100,000/μL) appearances similar to those of fatal cases of cerebral malaria caused by
Fluid, electrolyte Dehydration, SIADH (?), only Careful fluid resuscitation. P falciparum, although coma was not a prominent clinical feature ante
4,8
imbalances, meta- minor increase in capillary per- Dialysis as treatment for severe mortem. There is also some evidence that P knowlesi can cytoadhere
bolic acidosis (venous meability, compromised micro- acidosis has been advocated to host ligands in ex vivo studies, providing further mechanistic insights
plasma bicarbonate circulation by sequestration and into its pathophysiology.
<15 mmol/L or other factors causing anaerobic P ovale and P malariae are also infections that have been identified in
lactate >4 mmol/L) glycolysis nonhuman primates, although they are not zoonoses, unlike P knowlesi.
Their parasitemias are not usually very high, and these infections can
Respiratory distress Acidosis-related deep breathing. See also “acidosis”; ARDS: persist for long periods of time. P malariae, for example, can persist for
and pulmonary Pulmonary edema (ARDS) mainly restricted fluid management, decades, and a chronic infection can cause an immune complex glomer-
edema in adults and pregnant women. positive-pressure mechanical ulonephritis and nephrotic syndrome. They otherwise very rarely cause
Etiology unknown; cytokines ventilation with PEEP etc. Do not severe or fatal infections, unless they predispose to splenic rupture,
mediated (?) allow “permissive hypercapnia” which can take place with all species of malaria.
(cerebral edema)
Distinguish from pneumonia ■ CYTOADHERENCE, CYTOKINES, AND SEVERE DISEASE
Blackwater fever Related to severe malaria, Transfusion if needed; bicarbon- Cytoadherence of parasitized cells to blood vessels in different organs,
quinine use and G6PD deficiency ate administration (?) and the release of host cytokines and other mediators when infected
Shock Rare in malaria (NO binding by Fluids, inotropic drugs (don’t use red cells rupture are important causes of disease and death due to
free hemoglobin?), consider norepinephrine because of induc- malaria. Pigment produced by maturing parasites may contribute
concurrent bacteremia tion of lactic acidosis), antibiotics to both pathophysiological pathways by stimulating production of
host cytokines as well as reducing red cell deformability and enhanc-
Abnormal bleeding Disseminated intravascular No specific treatment, packed ing properties that favor cytoadherence. The relative contributions
coagulation: consider concomi- red cell transfusion if indicated of cytoaherence and cytokines or other host responses to infection
tant bacterial infection
may vary with the genetic and immune status of the individual, as
Isolated thrombocytopenia (very well as the species or strain of parasite. In one comparative study,
common) P knowlesi patients had lower markers of macrophage activation such
Controversial aspects are marked with “?.” as MIP-1β and MCP-1 compared with P falciparum infections, while

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