Department of Emergency Medicine, Yale School of Medicine, New Haven, CT.
London School of Hygiene and Tropical Medicine, London, United Kingdom.
Pediatr Crit Care Med. 2018 Mar;19(3):179-185. doi: 10.1097/PCC.0000000000001411.
Perturbed hemodynamic function complicates severe malaria. The Fluid Expansion as Supportive Therapy trial demonstrated that fluid resuscitation, involving children with severe malaria, was associated with increased mortality, primarily due to cardiovascular collapse, suggesting that myocardial dysfunction may have a role. The aim of this study was to characterize cardiac function in children with severe malaria.
A prospective observational study with clinical, laboratory, and echocardiographic data collected at presentation (T0) and 24 hours (T1) in children with severe malaria. Cardiac index and ejection fraction were calculated at T0 and T1. Cardiac troponin I and brain natriuretic peptide were measured at T0. We compared clinical and echocardiographic variables in children with and without severe malarial anemia (hemoglobin < 5 mg/dL) at T0 and T1.
Mbale Regional Referral Hospital.
Children 3 months to 12 years old with severe falciparum malaria.
Usual care.
We enrolled 104 children, median age 23.3 months, including 61 children with severe malarial anemia. Cardiac troponin I levels were elevated (> 0.1 ng/mL) in n equals to 50, (48%), and median brain natriuretic peptide was within normal range (69.1 pg/mL; interquartile range, 48.4-90.8). At T0, median Cardiac index was significantly higher in the severe malarial anemia versus nonsevere malarial anemia group (6.89 vs 5.28 L/min/m) (p = 0.001), which normalized in both groups at T1 (5.60 vs 5.13 L/min/m) (p = 0.452). Cardiac index negatively correlated with hemoglobin, r equals to -0.380 (p < 0.001). Four patients (3.8%) had evidence of depressed cardiac systolic function (ejection fraction < 45%). Overall, six children died, none developed pulmonary edema, biventricular failure, or required diuretic treatment.
Elevation of cardiac index, due to increased stroke volume, in severe malaria is a physiologic response to circulatory compromise and correlates with anemia. Following whole blood transfusion and antimalarial therapy, cardiac index in severe malarial anemia returns to normal. The majority (> 96%) of children with severe malaria have preserved myocardial systolic function. Although there is evidence for myocardial injury (elevated cardiac troponin I), this does not correlate with cardiac dysfunction.
严重疟疾可导致血流动力学紊乱。在 Fluid Expansion as Supportive Therapy 试验中,我们发现对伴有严重疟疾的儿童进行液体复苏会增加死亡率,主要原因是心血管衰竭,这表明心肌功能障碍可能起作用。本研究旨在描述严重疟疾患儿的心脏功能。
这是一项前瞻性观察研究,对伴有严重疟疾的患儿在就诊时(T0)和 24 小时(T1)采集临床、实验室和超声心动图数据。在 T0 和 T1 计算心输出量指数和射血分数。在 T0 测量心脏肌钙蛋白 I 和脑钠肽。我们比较了 T0 和 T1 时伴有和不伴有严重疟疾性贫血(血红蛋白 < 5 mg/dL)患儿的临床和超声心动图变量。
姆巴莱地区转诊医院。
3 个月至 12 岁患有严重恶性疟原虫疟疾的儿童。
常规治疗。
我们纳入了 104 名儿童,中位年龄为 23.3 个月,其中 61 名儿童伴有严重疟疾性贫血。50 名(48%)患儿的心脏肌钙蛋白 I 水平升高(> 0.1ng/mL),中位脑钠肽在正常范围内(69.1pg/mL;四分位间距为 48.4-90.8)。在 T0,严重疟疾性贫血组的中位心输出量指数明显高于非严重疟疾性贫血组(6.89 比 5.28 L/min/m)(p = 0.001),两组在 T1 时均恢复正常(5.60 比 5.13 L/min/m)(p = 0.452)。心输出量指数与血红蛋白呈负相关,r = -0.380(p < 0.001)。4 名患儿(3.8%)存在收缩功能降低的证据(射血分数 < 45%)。总体而言,有 6 名儿童死亡,无一例出现肺水肿、全心衰竭或需要利尿剂治疗。
严重疟疾中由于心搏量增加而导致的心输出量指数升高是循环受损的生理反应,与贫血有关。在全血输注和抗疟治疗后,严重疟疾性贫血的心输出量指数恢复正常。大多数(>96%)严重疟疾患儿的心肌收缩功能正常。尽管有心肌损伤(心脏肌钙蛋白 I 升高)的证据,但这与心功能障碍无关。