Neurogenic pulmonary edema in a fatal case of subarachnoid hemorrhage

Neurogenic pulmonary edema in a fatal case of subarachnoid hemorrhage

Journal of Clinical Anesthesia (2008) 20, 129–132 Case report Neurogenic pulmonary edema in a fatal case of subarachnoid hemorrhage Jörg Ahrens MD (...

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Journal of Clinical Anesthesia (2008) 20, 129–132

Case report

Neurogenic pulmonary edema in a fatal case of subarachnoid hemorrhage Jörg Ahrens MD (Resident)a,⁎, Hans-Holger Capelle MD (Consultant)b , Michael Przemeck MD (Head)c a

Department of Anesthesiology, Hannover Medical School, D-30625 Hannover, Germany Department of Neurosurgery, Hannover Medical School, D-30625 Hannover, Germany c Annastift Hospital, D-30625 Hannover, Germany b

Received 3 October 2006; revised 15 June 2007; accepted 20 June 2007

Keywords: Neurogenic pulmonary edema; Respiratory dysfunction; Subarachnoid hemorrhage

Abstract Neurogenic pulmonary edema (NPE) is caused by a variety of central nervous system lesions and may appear as a subclinical complication. The fulminant form of NPE is always life-threatening. Many pathophysiologic mechanisms have been implicated in the development of NPE, but the exact interaction remains unknown. We report a case of a fulminant NPE with fatal consequences associated with a subarachnoid hemorrhage. Treatment focuses on ventilatory support and measures to reduce intracranial pressure. © 2008 Elsevier Inc. All rights reserved.

1. Introduction The fulminant form of the neurogenic pulmonary edema (NPE) is a rare, life-threatening complication in patients with central nervous system (CNS) lesions. It is mostly observed in young patients and is associated with brain or spinal cord hemorrhage, trauma, tumors, epilepsy, or infections [1-3]. All of the different etiologies have one characteristic feature: an acute incident that causes increased intracranial pressure (ICP). Fulminant pulmonary edema may develop within minutes of the CNS lesion and may initially be the predominating feature at emergency department presentation. Neurogenic pulmonary edema also may be delayed in ⁎ Corresponding author. Dept. of Anesthesiology, OE 8050, Hannover Medical School, D-30625 Hannover, Germany. Tel.: +49 511 532 2489; fax: +49 511 532 5649. E-mail addresses: [email protected] (J. Ahrens), [email protected] (H.-H. Capelle), [email protected] (M. Przemeck). 0952-8180/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2007.06.021

onset or even remain subclinical [4]. Increased permeability of the pulmonary vascular bed as well as a stunned myocardium contribute to this clinical condition. The presence of NPE as a consequence of the CNS lesions influences management and may affect outcome [5]. Knowledge of NPE is essentially based on case reports or postmortem examinations. We report a case of a fulminant NPE with fatal consequences that were associated with a subarachnoid hemorrhage.

2. Case report A previously healthy, 19-year-old man was found comatose in the bathroom. On arrival at the emergency medical service, examination of the patient showed the following clinical findings: blood pressure (BP) 160/90 mmHg, heart rate 108 beats per minute (bpm), and oxygen saturation (SpO2) 83%. Glasgow Coma Scale was 4; the


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pupils were fixed in a wide position without reaction to light. As a consequence of severe respiratory dysfunction (gasping), he was sedated with 0.5 mg of fentanyl and 20 mg of etomidate, and his trachea was intubated by the emergency medical service. During the intubation, the patient showed a cough and a swallowing reflex. During transport, the patient received 0.5 mg of fentanyl and 15 mg of midazolam. When he arrived at the emergency department, his Glasgow Coma Scale was 3 and his vital signs were BP 150/80 mmHg, heart rate 124 bpm, and SpO2 89%. Respiratory parameters included a tidal volume (VT) of 750 mL, respiratory rate (RR) of 12 (breaths/min), inspired oxygen concentration (FIO2) of 100%, and positive endexpiratory pressure (PEEP) of 5 cm H2O. In the emergency department, the patient received arterial and central venous catheters. Chest radiography showed diffuse bilateral infiltrates (Fig. 1). A severe CNS event in combination with a secondary aspiration of gastric contents was assumed. Creatine kinase level was 1,058 U/L (normal b170 U/L). Computed tomography (CT) showed global cerebral edema, massive subarachnoid hemorrhage, and blood in all ventricles corresponding to a Fisher's grade 4 [6,7]. Computed tomographic angiography showed an aneurysm of the right internal carotid artery. Clinically, the patient presented with Hunt and Hess grade 5. Based on the morphological findings in the imaging studies and the clinical presentation, neurosurgical treatment of the aneurysm was deferred. For treatment and monitoring of the ICP, two external ventricular drainages were inserted in the lateral ventricles. The CT scan is shown in Fig. 2. Bronchoscopy was ordered to confirm the assumed aspiration of gastric contents and to clean the respiratory tract. During the bronchoscopy, no gastric contents were found in the patient's respiratory tract. Therefore, pulmonary edema was diagnosed, presumably due to NPE. Respiratory parameters included VT 680 mL, RR 15 (breaths/min), FIO2 1.0, and PEEP 8 cm H2O. Arterial blood gas analysis yielded a pH value of 7.23; partial carbon dioxide pressure (pCO2), 51 mmHg; partial oxygen pressure (pO2), 137 mmHg; base

Fig. 2 Computed tomographic scan showing a massive subarachnoid hemorrhage and blood in all ventricles caused by a rupture of an aneurym of the right internal carotid artery.

excess of −5.6; HCO3 concentration, 22.5 mmol/L; and SpO2, 94%. The patient was admitted to the intensive care unit and received pharmacologic therapy including intravenous fluid support, sodium bicarbonate, mannitol, three units of fresh frozen plasma, and norepinephrine to increase BP so as to ensure brain perfusion. The ICP continuously increased over the next 12 hours up to levels of 36 mmHg, and even high doses of norepinephrine could not maintain cerebral perfusion pressure greater than 50 mmHg. Although attempts were made to correct it, the patient's severe electrolyte disturbance was not reversible with sodium 154 mmol/L, potassium 2.7 mmol/L, chloride 131 mmol/L, or calcium 1.32 mmol/L. During his second hospital day, the patient's oxygenation deteriorated, with pH 7.15, pCO2 72 mmHg, pO2 pressure 96 mmHg, base excess −4.6, HCO3 concentration 24 mmol/L, and SpO2 93%. The ventilator settings at the time of arterial blood gas analysis were VT 700 mL, RR 18 (breaths/min), FIO2 0.85, and PEEP 9 cm H2O. In spite of hyperventilation, repeated administration of mannitol, and barbiturate-induced coma, the patient's condition continued to deteriorate. Brain death and concomitant multiple organ failure were diagnosed 36 hours after hospital admission.

3. Discussion

Fig. 1

Chest radiograph showing diffuse bilateral infiltrates.

Neurogenic pulmonary edema may be associated with many forms of cerebral lesions and probably remains unrecognized due to a lack of clinical signs. When clinically apparent, there are two distinct forms of the syndrome: an early form that develops within minutes to hours after the CNS lesion and a delayed form that may take days to occur [8]. Mortality of the fulminant form of NPE is between 60% and 100%. Thirty-one percent of the patients who died of

Neurogenic pulmonary edema by subarachnoid hemorrhage cerebral hemorrhage had a clinical diagnosis of pulmonary edema before death [2]. In a postmortem review of 686 deaths from head injury or spontaneous CNS hemorrhage, an incidence of pulmonary edema in approximately 75% of patients with nontraumatic intracranial hemorrhage has been reported. The report also considered the dynamics of NPE development: Of 73 patients dying within one hour of injury or spontaneous bleeding, approximately 60% had pulmonary edema at autopsy [9]. Several mechanisms have been implicated in the pathogenesis of NPE, but the exact interactions remain unknown. The edema and alveoli of patients who have developed NPE have a protein concentration similar to that of plasma. Thus, it seems that an increase in microvascular permeability may play an important role in the development of NPE [9,10]. Another mediator for the formation of NPE is the widely recognized phenomenon of a massive sympathetic discharge [10,11]. Catecholamine release causes systemic arterial hypertension, peripheral vasoconstriction, increased pulmonary artery pressure, pulmonary microvascular vasoconstriction, and neurogenic stunned myocardium [12-14]. Rapid development of an intense, generalized vasoconstriction is thought to occur. This phenomenon leads to a shift of intravascular volume from high-resistance systemic circulation to low-resistance pulmonary circulation. The formation of pulmonary edema in this setting is thought to occur secondary to direct hydrostatic forces as well as to increased permeability from endothelial injury [15]. The clinical syndrome of severe acute stunned myocardium is characterized by metabolic acidosis, cardiogenic shock, pulmonary edema, T-wave inversions with a prolonged QT interval, and left ventricular wall motion abnormalities as seen on echocardiography [5]. Neurogenic pulmonary edema often presents in the emergency department, and the symptoms could be mistaken for aspiration pneumonia [11]. Unconscious patients are at risk of aspiration of gastric contents. In the case reported above, chest radiography showed diffuse bilateral pulmonary infiltrates with normal heart size, which resembles the radiographic findings in pulmonary edema or sometimes in aspiration pneumonia. Thus, the patient was found comatose, a secondary aspiration of gastric contents was assumed. Therefore, a diagnosis of NPE was delayed, and NPE was not considered until bronchoscopy ruled out aspiration. The treatment of NPE is primarily supportive. Thus, the therapeutic approach needs to be focused on decreasing ICP as a primary goal. The patient in our case received external ventricular drainage implantation and pharmacologic therapy with mannitol to reduce the increased ICP. Mannitol is effective and is recommended by both the Brain Trauma Foundation and the European Brain Injury Consortium as the osmotic drug of choice [16]. The severity of the cerebral injury as measured by the Hunt and Hess scale correlates with the occurrence of neurogenic stunned myocardium [17]. Because the patient had a grade 5 subarachnoid hemorrhage, it is likely that neurogenic stunned

131 myocardium contributed to the pulmonary edema. Further diagnostics such as echocardiography or troponin and atrial natriuretic peptide (ANP) level determination were not performed. Attempts should be made to improve myocardial contractility and to decrease preload and afterload. Ventilatory support is important in the treatment of patients with cerebral lesions and NPE. The goals of mechanical ventilation are to assure adequate oxygenation and ventilation. To avoid excessively high inflation pressures, VTs between 5 and 8 mL/kg are used. With the use of low inflation volumes, PEEP is added to prevent compression atelectasis. Recent studies have shown that a mechanical ventilation strategy using low VTs reduces mortality in patients with acute lung injury [18]. As in this case, ventilatory PEEP is commonly used and is effective in the treatment of hypoxia secondary to alveolar capillary leak, increasing intrathoracic pressure, and improving arterial oxygenation. However, the effect of PEEP on ICP is controversial, with some investigators reporting no correlation between PEEP and ICP [19-21], whereas others reported significant elevations in ICP as PEEP increases [22]. Therefore, close monitoring of systemic BP, arterial oxygenation, ICP, and cerebral perfusion pressure is required when PEEP is used in patients with increased ICP. This case report highlights the fact that NPE may be a common complication of a variety of CNS lesions. Many cases of NPE probably remain unrecognized because of nonspecific clinical signs. Thus, physicians should be encouraged to consider this clinical entity when caring for patients with acute respiratory failure after neurologic emergencies.

References [1] Rogers FB, Shackford SR, Trevisani GT, Davis JW, Mackersie RC, Hoyt DB. Neurogenic pulmonary edema in fatal and nonfatal head injuries. J Trauma 1995;39:860-6. [2] Weir BK. Pulmonary edema following fatal aneurysm rupture. J Neurosurg 1978;49:502-7. [3] Fredberg U, Botker HE, Romer FK. Acute neurogenic pulmonary oedema following generalized tonic clonic seizure. A case report and a review of the literature. Eur Heart J 1988;9:933-6. [4] Colice GL. Neurogenic pulmonary edema. Clin Chest Med 1985;6: 473-89. [5] Wartenberg KE, Mayer SA. Medical complications after subarachnoid hemorrhage: new strategies for prevention and management. Curr Opin Crit Care 2006;12:78-84. [6] Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980;6:1-9. [7] Frontera JA, Claassen J, Schmidt JM, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified fisher scale. Neurosurgery 2006;59:21-7. [8] Colice GL, Matthay MA, Bass E, Matthay RA. Neurogenic pulmonary edema. Am Rev Respir Dis 1984;130:941-8. [9] Malik AB. Mechanisms of neurogenic pulmonary edema. Circ Res 1985;57:1-18. [10] Rassler B. The role of catecholamines in formation and resolution of pulmonary oedema. Cardiovasc Hematol Disord Drug Targets 2007;7: 27-35.

132 [11] Baumann A, Audibert G, McDonnell J, Mertes PM. Neurogenic pulmonary edema. Acta Anaesthesiol Scand 2007;51:447-55. [12] Luisada AA. Mechanism of neurogenic pulmonary edema. Am J Cardiol 1967;20:66-8. [13] Maron MB, Dawson CA. Pulmonary venoconstriction caused by elevated cerebrospinal fluid pressure in the dog. J Appl Physiol 1980; 49:73-8. [14] Lambert G, Naredi S, Edén E, Rydenhag B, Friberg P. Monoamine metabolism and sympathetic nervous activation following subarachnoid haemorrhage: influence of gender and hydrocephalus. Brain Res Bull 2002;58:77-82. [15] Theodore J, Robin ED. Pathogenesis of neurogenic pulmonary oedema. Lancet 1975;2(7938):749-51. [16] Maas AI, Dearden M, Teasdale GM, et al. EBIC—guidelines for management of severe head injury in adults. European Brain Injury Consortium. Acta Neurochir (Wien) 1997;139:286-94.

J. Ahrens et al. [17] Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke 2004;35:548-51. [18] Brower RG, Rubenfeld GD. Lung-protective ventilation strategies in acute lung injury. Crit Care Med 2003;31(4 Suppl):S312-6. [19] Frost EA. Effects of positive end-expiratory pressure on intracranial pressure and compliance in brain-injured patients. J Neurosurg 1977; 47:195-200. [20] Huynh T, Messer M, Sing RF, Miles W, Jacobs DG, Thomason MH. Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury. J Trauma 2002;53:488-92. [21] Muench E, Bauhuf C, Roth H, et al. Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Crit Care Med 2005;33:2367-72. [22] Apuzzo JL, Wiess MH, Petersons V, Small RB, Kurze T, Heiden JS. Effect of positive end expiratory pressure ventilation on intracranial pressure in man. J Neurosurg 1977;46:227-32.