Article, Neurology

Neurogenic pulmonary edema after severe head injury: a transpulmonary thermodilution study

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Neurogenic pulmonary edema after severe “>Case Report

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American Journal of Emergency Medicine

journal homepage: www. elsevier. com/ locate/ajem

American Journal of Emergency Medicine 33 (2015) 858.e1-858.e3

Neurogenic pulmonary edema after severe head injury: a transpulmonary thermodilution study?

Abstract

Neurogenic pulmonary edema (NPE) is a possible complication of severe central nervous system insult. Its physiopathology is still debat- ed. We report a fatal case of a 55-year-old man who was admitted be- cause of severe head injury. The diagnosis of NPE was considered according to clinical and radiologic findings. Transpulmonary thermodilution study showed decreased stroke volume index and car- diac function index. Indexed extravascular lung water was increased as well as pulmonary vascular permeability index. The impairment of the left ventricular function was confirmed by the echocardiographic study. Our case suggests that NPE imply both cardiac dysfunction and lung injury. Thus, transpulmonary thermodilution can be helpful in managing fluid balance and the choice of vasopressors in patients with life-threatening NPE.

Neurogenic pulmonary edema (NPE) has been described as a possi- ble complication of severe central nervous system insult, such as sei- zure, spontaneous subarachnoid hemorrhage, and head trauma [1-4]. The pathophysiology of this condition is still debated with conflicting clinical and hemodynamic monitoring findings: several experimental reports suggest that the increase in microvascular permeability is the main leading mechanism of NPE onset [5,6], whereas other reports highlighted the importance of the pulmonary vasoconstriction and left ventricular dysfunction [1,7]. Transpulmonary thermodilution (TPT) is a technique that offers the possibility to quantify the amount of extra- vascular lung water (EVLW) and to appreciate the microvascular per- meability. We herein report the case of a critically ill head injured patient who had an acute NPE. Our patient was monitored by both echo- cardiography and TPT. The underlying Pathophysiologic mechanisms leading to this condition are discussed.

A 55-year-old man was admitted to our emergency department after being hit in the left parietal region by a bar of iron. He was con- scious and had no motor deficit. Systolic blood pressure was 100 mm Hg, and diastolic blood pressure was 60 mm Hg. Heart rate was 80 beats/min and respiratory rate was 22 breaths/min. SatO2 measured by pulse oximetry was 96%. Four hours later, the neurologic status progres- sively worsened and Glasgow Coma Scale decreased to 10. The patient was transferred to our intensive care unit where he was sedated and mechanically ventilated. Pink frothy sputum was suctioned through the endotracheal tube. Pulmonary auscultation revealed bilateral diffuse crackles. The arterial blood gas sampled under FiO2 = 1 and positive end expiratory pressure = 8 cm H2O showed the following results: pH =

? Conflict of interest: None.

7.27, PaCO2 = 44 mm Hg, Pa O2 = 189 mm Hg, bicarbonates = 20 mmol/L, and SatO2 = 99%. Troponin levels were not increased, and the electrocardiogram did not show any abnormality, except a sinusal tachycardia. The plain chest x-ray performed on admission to our inten- sive care unit (ICU) showed bilateral alveolar infiltrate without cardiomegaly (Fig. 1). Our patient underwent a cranial computed to- mography (CT), showing an extradural hematoma in the left parietal oc- cipital region (36 mm) with 4 mm of Midline shift (Fig. 2). He also underwent a thoracic CT showing bilateral alveolar infiltrates (Fig. 3). The evacuation of the hematoma was performed on the fifth hour after the trauma. The intervention lasted 3 hours, and during the oper- ative period, our patient received 1000 mL of NaCl 0.9%. During the in- tervention, the hemodynamic status also worsened and mean blood pressure was kept at 70 mm Hg under dobutamine and norepinephrine perfused through a central venous catheter inserted in the superior vena cava territory. Upon his return from the operative room, our pa- tient was equipped with an arterial catheter (Pulsion Medical System AG, Munchen, Germany) placed in the femoral site and connected to a PiCCO device. Transpulmonary thermodilution measures were then performed while the patient was still receiving the same doses of vaso- pressors. All the measures were indexed to the ideal body weight. The results of these measures are shown in (Table). Concomitantly, an echo- cardiographic study was performed showing a decreased ventricular ejection fraction (52%). The end-diastolic left ventricular diameter was

Fig. 1. Plain chest x-ray performed on admission showing bilateral alveolar infiltrate without cardiomegaly.

0735-6757/(C) 2014

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Table

Evolution of TPT parameters during the ICU stay period

Day 1

Day 3

Day 5

Day 7

Norepinephrine (mg/h)

3

5

5

4

Dobutamine (ug kg-1 min-1)

20

20

Epinephrine (mg/h)

7.5

3

Fluid balance (mL)

+2200

-1500

-1400

-1700

SBP (mm Hg)

105

122

138

112

DBP (mm Hg)

65

75

94

88

Heart rate (/min)

101

95

131

122

MBP (mm Hg)

78

91

109

97

IC (L min-1 m-2)

3.3

2.9

3.7

2.6

SVI (mL/m2)

33

30

28

22

GEDVI (mL/m2)

696

726

891

873

SVRI (dyne . s cm-5 m-2)

1711

1850

2220

2479

CFI (/min)

4.6

3.9

2.6

3.7

EVLW (mL/m2)

18

18

25

20

PVPI

3.9

3.8

3.7

4.4

CFI, cardiac function index; DBP, diastolic blood pressure; EVLW, extravascular lung water; GEDVI, global end diastolic volume index; MBP = mean blood pressure; PPV, Pulse pressure variation; SBP, systolic blood pressure; SVI, systolic volume index.

Fig. 2. cranial CT performed on admission showing an extradural hematoma in the left parietal and occipital region (36 mm) with 4 mm of midline shift.

48 mm, whereas the end-systolic left ventricular diameter was 35 mm. The mitral flow velocities study with pulse wave Doppler showed E = 81 cm/s, A = 60.7 cm/s, and E/A = 1.3. Tissue Doppler imaging showed that Ea wave velocity was 18 cm/s, and E/Ea ratio was equal to 4.5. The systolic pulmonary artery pressure was 36 mm Hg. Despite a restrictive fluid management strategy and a daily negative fluid balance, the extra- vascular lung water remained increased with a permeability index higher than 3 during all the ICU stay period (Table). A cranial CT per- formed 24 hours after the intervention showed that the evacuation of the extradural hematoma was successful. However, the evolution was unfavorable with the onset of a multiorgan failure leading to death after 10 days of resuscitation.

Neurogenic pulmonary edema is a serious complication induced by severe insults of the central nervous system [4]. The pathophysiology of this syndrome is still debated. Although several authors highlighted the importance of cardiac dysfunction and the magnitude of pulmonary venoconstriction after the autonomic storm [1,7], others support the “blast theory” that implies a damage of the capillary-alveolar membrane after an overwhelming release of catecholamine [4]. The repeated TPT

Fig. 3. Chest CT performed on admission showing bilateral and diffuse alveolar infiltrate.

measures in our case showed that the extravascular lung water index was increased during all the ICU stay. Our results suggest that both mechanisms of (NPE) may coexist. In fact, the stroke volume index and the contractility function index were both decreased during the ICU stay despite high doses of dobutamine and norepinephrine which is in favor of a deep impairment of cardiac function [8]. These findings were corroborated by the echocardiographic study showing a decreased LVEF. However, the increase of the pulmonary vascular permeability index (PVPI) suggests an acute injury of the lungs [9]. Beside its diagnos- tic value, TPT is also helpful for guiding therapeutic management and for the assessment of the prognosis. In fact, Jozwiak et al [9] reported that in patient with acute respiratory distress syndrome, a maximum indexed extravascular lung water higher than 21 mL/kg predicted day 28 mor- tality with a sensitivity of 54% and a specificity of 73%, whereas a maxi- mum PVPI higher than 3.8 predicted day 25 mortality with a sensitivity of 68% and a specificity of 65%.

Conclusion

The TPT measures in our patient show that NPE may imply both car- diac dysfunction and lung injury. Thus, this technique is helpful for managing fluid balance and guiding the choice of vasopressors. Further studies are needed to confirm its prognosis value in NPE.

Anis Chaari, MD? Kamilia Chtara, MD

Department of Intensive Care, Faculty of Medicine, Sfax, Tunisia

?Corresponding author. Tel.: +216 26349334; fax: +216 74891335

E-mail address: [email protected]

Nozha Toumi

Department of radiology, Faculty of Medicine, Sfax, Tunisia

Mabrouk Bahloul, MD Mounir Bouaziz, MD

Department of Intensive Care, Faculty of Medicine, Sfax, Tunisia

http://dx.doi.org/10.1016/j.ajem.2014.12.009

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