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Up-to-date in severe malaria with pulmonary complication: world english medical literature review

By the case report of severe malaria with pulmonary form and other complications in Vietnam. We would like to share with colleagues o­n pulmonary complication in pernicious-severe malaria via medical literature review.

1. Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation (Charoenpan P et al., 1990)

This study was performed to extend the knowledge of the pathogenesis of PE in severe falciparum malaria. Sequential hemodynamic studies were conducted in 13 patients with severe falciparum malaria. Seven patients developed PE, while the other six patients had NPE. Two patients died, o­ne in each group. Hemodynamic changes were found in both groups, including an initial reduction in SVR and PVR, along with an increased CI and variable values (normal and increased) of PCWP. All abnormalities persisted for at least two days; changes in PVR lasted especially longer (throughout five days). The initial hemodynamic changes cannot predict the development of PE; however, heavy parasitemia of more than 60 percent and severe hypoalbuminemia were found to be more common in PE than NPE. Of three patients with PE who had normal PCWP, o­ne died, with postmortem findings of increased pulmonary capillary permeability. The increased PCWP which was found in the other four cases of PE was proven to be volume overload without evidence of CHF. It was concluded that the pathophysiologic changes in severe falciparum malaria were systemic and pulmonary vasodilation. The abnormal pulmonary vascular change was found to be the cause of PE. Volume overload and hypoalbuminemia could aggravate further pulmonary capillary leakage in these cases.

2. Pulmonary manifestations of malaria (Rauber K, 1987)

We report o­n the two different types of pulmonary manifestations in acute plasmodium falciparum malaria. The more severe variant shows long standing interstitial pulmonary infiltrates, whereas in the more benign courses o­nly short-term pulmonary edemas are visible.

3. Pulmonary damage associated with falciparum malaria: a report of ten cases (James MF et al., 1985)

Ten cases of pulmonary involvement associated with falciparum malaria are described. Measurements of pulmonary capillary wedge pressure were made in five of the ten cases, and no evidence of raised hydrostatic pressure in the pulmonary microcirculation was found which could account for the pulmonary oedema observed. All cases were treated with oxygen and positive end expiratory pressure (PEEP), and there were six survivors. The evidence to support the presence of an Adult Respiratory Distress Syndrome (ARDS)-type lesion in malaria is discussed.

4. Acute respiratory distress syndrome (ARDS) in cerebral malaria (Blanloeil Y, 1980)

Non hemodynamic pulmonary edemas included by some authors in the acute respiratory distress syndrome (ARDS) had been reported in cerebral malaria. We describe a new case. Clinical data, hemodynamic studies with PWP measurement, and anatomic findings are coherent with the diagnosis of ARDS. Although the underlying causal mechanisms--the marked parasitemia and its consequence o­n permeability of the pulmonary capillary remain speculative, they seem credible. The pulmonary lesions are provoked by these main factors and worsened by hypoprotidemia and surinfection. Prevention of all these factors can stop the evolution towards refractory hypoxemia but the precocity of quinine treatment remains the most important point.

5. Cytoadherence in human falciparum malaria as a cause of respiratory distress (Corbett CE et al, 1989).

The ultrastructure of three cases of fatal human falciparum malaria was studied in order to identify the cytoadherence of the endothelial cells in relation to parasitized red blood cells and septal interstitial changes which could be related to respiratory distress. Two cases showed marked endothelial oedema narrowing the capillary lumen with areas of adherence preferentially related to knobs, accompanied by septal interstitial oedema. o­ne case showed no endothelial cells oedema, no knobs in parasitized red blood cells with no cytoadherence, no septal interstitial oedema and no respiratory distress. Cytoadherence seems to be the mechanism responsible for the septal pulmonary changes in severe falciparum malaria.

6. Cytoadherence of knobless Plasmodium falciparum-infected erythrocytes and its inhibition by a human monoclonal antibody (Udomsangpetch R, 1989).

Red blood cells infected with mature stages of the malaria parasite Plasmodium falciparum bind to the endothelial lining of capillaries and venules. This sequestration is important for the survival of the parasite but may have severe consequences for the host. For example, it is involved in the causation of cerebral malaria which carries 25% mortality. Knob-like protrusions present o­n the surface of infected erythrocytes have been considered necessary but not sufficient for this cytoadherence. Here we describe the adhesion to endothelial cells of infected erythrocytes which do not have knobs. A human monoclonal antibody (33G2) which was specific for an epitope containing regularly spaced dimers of glutamic acid present in the repeated amino-acid sequences of some defined P. falciparum antigens was found to inhibit cyto-adherence and may therefore be an important reagent for elucidating the molecular basis of parasite sequestration.

7. Plasmodium falciparum: analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332 (Iqbal J, 1993)

The capacity of a human monoclonal antibody (MAb 33G2) to interfere in vitro both with Plasmodium falciparum merozoite invasion and cytoadherence of infected erythrocytes to melanoma cells has been reported. MAb 33G2 cross-reacts with several P. falciparum antigens but shows highest reactivity with repeated sequences in the asexual blood stage antigen Pf332. This study was conducted in order to further analyze the cytoadherence inhibition mediated by MAb 33G2 and to evaluate the relative contribution of antibodies to Pf332 in the inhibitory activity of immunoglobulins from P. falciparum immune donors. We show here that MAb 33G2 inhibits cytoadherence of infected erythrocytes (PRBCs) with similar efficiency independently of the strain of parasite, while the inhibitory capacity of immunoglobulin fractions from Liberian immune donors was restricted to some strains o­nly. There appears to be no correlation between the reactivity with Pf332 of immunoglobulin preparations from different donors and their capacity to inhibit cytoadherence of PRBCs to melanoma cells. In contrast to MAb 33G2, polyclonal antibodies affinity purified o­n the Pf332 peptide containing the epitope seen by the MAb showed little or no inhibition of cytoadherence of infected erythrocytes.

8. Pulmonary edema in cerebral malaria patients in Thailand (Aursudkij B,1998)

Pulmonary edema is a serious complication of falciparum malaria that usually occurs in association with cerebral malaria, acute renal failure, high parasitemias, or delayed antimalarial treatment. From 1993 to 1996, 120 adult patients admitted to the intensive care unit of the Bangkok Hospital for Tropical Diseases were enrolled in a prospective study to assess the combination of artesunate and mefloquine for the treatment of cerebral malaria. Twenty-five patients (21%) presented with pulmonary edema and a majority developed complications in other organs as well, especially acute renal failure. In most patients (19 of 25), pulmonary edema was noted o­n the first day of admission and was associated with higher parasitemias and levels of acidemia, than in patients without pulmonary edema.

Ten of the 25 patients diagnosed with pulmonary edema developed signs consistent with adult respiratory distress syndrome (ARDS). The mean central venous pressure when pulmonary edema was diagnosed was markedly lower in ARDS than in non-ARDS patients, supporting the argument that fluid imbalance is not essential for malaria-induced lung injury. Seven of 10 patients with ARDS died, 5 within 24 hours of admission, but there were no deaths in the 15 pulmonary edema patients without ARDS. Early diagnosis and prompt treatment remain important principles to reduce the morbidity and mortality associated with complicated falciparum malaria. This report emphasizes that ARDS, when concurrently occurs, is a poor prognostic clinical indicator in cerebral malaria.

Treat Respir Med. 2006;5(6):419-28.

Pulmonary manifestations of malaria : recognition and management.

Taylor WR1, Caon V, White NJ.

Lung involvement in malaria has been recognized for more than 200 hundred years, yet our knowledge of its pathogenesis and management is limited. Pulmonary edema is the most severe form of lung involvement. Increased alveolar capillary permeability leading to intravascular fluid loss into the lungs is the main pathophysiologic mechanism. This defines malaria as another cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).Pulmonary edema has been described most often in non-immune individuals with Plasmodium falciparum infections as part of a severe systemic illness or as the main feature of acute malaria. P.vivax and P.ovale have also rarely caused pulmonary edema.Clinically, patients usually present with acute breathlessness that can rapidly progress to respiratory failure either at disease presentation or, interestingly, after treatment when clinical improvement is taking place and the parasitemia is falling. Pregnant women are particularly prone to developing pulmonary edema. Optimal management of malaria-induced ALI/ARDS includes early recognition and diagnosis. Malaria must always be suspected in a returning traveler or a visitor from a malaria-endemic country with an acute febrile illness. Slide microscopy and/or the use of rapid antigen tests are standard diagnostic tools. Malaria must be treated with effective drugs, but current choices are few: e.g. parenteral artemisinins, intravenous quinine or quinidine (in the US o­nly). A recent trial in adults has shown that intravenous artesunate reduces severe malaria mortality by a third compared with adults treated with intravenous quinine. Respiratory compromise should be managed o­n its merits and may require mechanical ventilation.Patients should be managed in an intensive care unit and particular attention should be paid to the energetic management of other severe malaria complications, notably coma and acute renal failure. ALI/ARDS may also be related to a coincidental bacterial sepsis that may not be clinically obvious. Clinicians should employ a low threshold for starting broad spectrum antibacterials in such patients, after taking pertinent microbiologic specimens. Despite optimal management, the prognosis of severe malaria with ARDS is poor.ALI/ARDS in pediatric malaria appears to be rare. However, falciparum malaria with severe metabolic acidosis or acute pulmonary edema may present with a clinical picture of pneumonia, i.e. with tachypnea, intercostal recession, wheeze or inspiratory crepitations. This results in diagnostic confusion and suboptimal treatment. Whilst this is increasingly being recognized in malaria-endemic countries, clinicians in temperate zones should be aware that malaria may be a possible cause of 'pneumonia' in a visiting or returning child.

Braz J Infect Dis. 2005 Oct;9(5):425-30. Epub 2006 Jan 6.

Acute respiratory distress syndrome due to vivax malaria: case report and literature review.

Lomar AV1, Vidal JE, Lomar FP, Barbas CV, de Matos GJ, Boulos M.

Severe pulmonary involvement in malaria has been frequently reported in cases of Plasmodium falciparum infection, but rarely in vivax malaria. Among the 11 previous cases of vivax-related severe respiratory involvement described in the literature, all except o­ne developed it after the beginning of anti-malarial treatment; these appear to correspond to an exacerbation of the inflammatory response. We report the case of a 43-year-old Brazilian woman living in a malaria-endemic area, who presented acute respiratory distress syndrome (ARDS) caused by P. vivax before starting anti-malarial treatment. The diagnosis was made based o­n microscopic methods. A negative rapid immunochromatographic assay, based o­n the detection of Histidine Rich Protein-2 (HRP-2) of P. falciparum, indicated that falciparum malaria was unlikely. After specific anti-plasmodial therapy and intensive supportive care, the patient was discharged from the hospital. We conclude that vivax malaria-associated ARDS can develop before anti-malarial therapy.

Trop Doct. 2013 Apr;43(2):83-5. doi: 10.1177/0049475513485733. Epub 2013 May 24.

Plasmodium vivax malaria presenting as acute respiratory distress syndrome: a case report.

Rahman AK1, Sulaiman FN.

Severe pulmonary involvement in malaria has been frequently reported in cases of Plasmodium falciparum infection but rarely in vivax malaria. We look at a case of a 38-year-old man living in a malaria endemic area who presented with acute respiratory distress syndrome (ARDS) caused by P. vivax. DNA polymerase chain reaction (PCR) confirmed that it was not a mixed infection. After specific antimalarial therapy and intensive supportive care, the patient was discharged from the hospital. This case illustrates that P. vivax-induced ARDS is not uncommon and should be readily recognized by the treating physicians. A confirmatory test with PCR is required in order to exclude P. falciparum co-infection.

J Infect Dev Ctries. 2015 Aug 29;9(8):910-3. doi: 10.3855/jidc.6813.

Plasmodium vivax infection causes acute respiratory distress syndrome: a case report.

Gupta H1, Afsal MP, Shetty SM, Satyamoorthy K, Umakanth S.

Plasmodium falciparum (Pf) is associated with numerous complications and high mortality, whereas Plasmodium vivax (Pv) infection is generally considered to be benign. However, severe complications, such as acute respiratory distress syndrome (ARDS) in Pv infection, are emerging. This case report highlights the complication of ARDS during the course of Pv infection in a 60-year-old woman. The diagnosis of the patient was made using microscopy, immunochromatography, and polymerase chain reaction assays for Pf and Pv species. The data indicated the presence of mono-Pv infection in the patient's blood, and Pf infection was specifically ruled out. The patient was discharged after intensive supportive care and antimalarial treatment. Pv infection is associated with ARDS and other complications such as sepsis and multi-organ dysfunction syndrome; this enhanced severity of Pv infection, if unrecognized, can lead to more deaths in malaria-endemic areas.

ARDS (Srinivas, 2015)

Acute pulmonary edema is a grave and usually fatal complication of severe falciparum malaria with more than 50% mortality. Acute lung injury is defined as the acute o­nset of bilateral pulmonary infiltrates with an arterial oxygen tension/fractional inspired oxygen ratio of 300 mmHg or less, a pulmonary artery wedge pressure of 18 mmHg or less, and no evidence of left atrial hypertension. ARDS is defined as acute lung injury and an arterial oxygen tension/fractional inspired oxygen ratio of 200 mmHg or less. Volume overload and hypoalbuminemia may aggravate pulmonary capillary leakage. Chest radiograph abnormalities range from confluent nodules to basilar and/or diffuse bilateral pulmonary infiltrates. Noncardiogenic pulmonary edema rarely occurs with P. vivax and P. ovale malaria.

In addition to severe falciparum parasitemia and sequestration, secondary infections, severe anemia, hyperpyrexia, dehydration/fluid overload, metabolic acidosis, hypoxia and disseminated intravascular coagulation can also contribute to the cardiovascular problems in malaria. Although myocardial function is generally well preserved in severe falciparum malaria, malaria can complicate pre-existing cardiac decompensation and may even prove fatal for patients with compromised heart. Cardiac arrhythmias are uncommon.

Pathology of Acute Pulmonary Oedema: In a few patients it could be due to fluid overload as a result of enthusiastic fluid therapy. In others it develops even with normal or negative fluid balance. Pulmonary oedema develops later compared to other complications and it may even appear several days after treatment for malaria, when the patient is otherwise improving with a reduction in peripheral parasitemia.

The mechanism of pulmonary oedema is not clearly understood. It has a close resemblance to adult respiratory distress syndrome. While over-hydration may be the cause in some cases of pulmonary oedema, it can also develop in patients with normal capillary wedge pressures. Such cases may be due to increased permeability of pulmonary capillaries. Sequestration of red cells and clogging of pulmonary microcirculation and disseminated intravascular coagulation may also play their role. Pulmonary oedema is more common in patients with hyperparasitemia, renal failure and pregnancy and it is commonly associated with hypoglycemia and metabolic acidosis. It may develop suddenly after delivery, due to fluid overload. Pulmonary oedema may be the terminal event in many cases of fatal falciparum infection.

The first sign of impending pulmonary oedema is an increase in the respiratory rate. Tachypnoea may also be the first indicator of aspiration bronchopneumonia and metabolic acidosis and a chest X-ray will help in differentiating these conditions. Then patient develops signs of pulmonary oedema like basal crackles, cyanosis, tachycardia etc. The breathlessness worsens rapidly and the patient may die within a few hours. Hypoxia can cause convulsions and deterioration in the level of sensorium.


Management:

Pulmonary oedema is the most fatal of the complications of falciparum malaria and therefore calls for careful and energetic management.

Fluid overload should be avoided at all costs, especially in pregnant women. The central venous pressure should be maintained between 0-5 cm of H2O by regulating fluid intake and nursing the patient propped up at 450. All intravenous fluids should be stopped immediately and diuretics may have to be administered.

Initial management of pulmonary oedema includes treatment with oxygen, back-rest and diuretics if there is evidence of fluid overload. Inj. Furoscemide 40 mg should be given intravenously and if there is no desired response, the dose can be progressively increased up to 200 mg. Fluid volume can be further reduced by venesection and letting of 250 ml of blood initially. This blood or its packed cells can be re-transfused o­nce the problem settles down. The procedure can be repeated carefully if needed.

If the patient deteriorates with conservative treatment, mechanical ventilation is indicated. Positive end expiratory pressure ventilation may also be needed. Drugs like corticosteroids are not of any proven benefit in the management of these cases.

Overall, pulmonary oedema carries a poor prognosis.



17. Enhancing blockade of Plasmodium falciparum erythrocyte invasion: assessing combinations of antibodies against PfRH5 and other merozoite antigens.

Williams AR, Douglas AD, Miura K, Illingworth JJ, Choudhary P, Murungi LM, Furze JM, Diouf A, Miotto O, Crosnier C, Wright GJ, Kwiatkowski DP, Fairhurst RM, Long CA, Draper SJ.

PLoS Pathog. 2012;8(11):e1002991. doi: 10.1371/journal.ppat.1002991. Epub 2012 Nov 8.

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Khattab A, Bonow I, Schreiber N, Petter M, Schmetz C, Klinkert MQ.

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Singh AP, Puri SK, Chitnis CE.

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Am J Trop Med Hyg. 2005 Jul;73(1):222-8.

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63. Invasion of red blood cells by malaria parasites-what are the components that determine specificity?

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64. Antibodies and DNA probes used to analyze variant populations of the Indochina-1 strain of Plasmodium falciparum.

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Ti li?u tham kh?o

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2.Charoenpan P1, Indraprasit S, Kiatboonsri S, Suvachittanont O, Tanomsup S. (1987). Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation. Rofo. 1987 May;146(5):507-10.

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8.Iqbal J, Perlmann P, Berzins K (1993). Plasmodium falciparum: Analysis of the cytoadherence inhibition of the human monoclonal antibody 33G2 and of antibodies reactive with antigen Pf332. Exp Parasitol. 1993 Aug;77(1):79-87.

9.Aursudkij B, Wilairatana P, Vannaphan S, Walsh DS, Gordeux VR, Looareesuwan S (1998). Pulmonary edema in cerebral malaria patients in Thailand. Southeast Asian J Trop Med Public Health. 1998 Sep;29(3):541-5.

10.Taylor WR, Caon V, White NJ (20060. Pulmonary manifestations of malaria: Recognition and management. Treat Respir Med. 2006;5(6):419-28.

11.Lomar AV, Vidal JE, Lomar FP, Barbas CV, de Matos GJ, Boulos M (2005). Acute respiratory distress syndrome due to vivax malaria: case report and literature review. Braz J Infect Dis. 2005 Oct;9(5):425-30. Epub 2006 Jan 6.

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14.  Srinivas | February 27, 2015 | Complications. ARDS

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11/02/2018
Dr. Huynh Hong Quang
Institute of Malariology, Parasitology, and Entomology Quy Nhon
 

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