Pulmonary edema (PE) can occur after subarachnoid hemorrhage and can jeopardize arterial oxygenation, which is essential for a suffering brain. In some cases PE is evident in the emergency room, being the direct consequence of intracranial bleeding, which causes an immediate and overwhelming catecholamine discharge. In the following days, PE can occur because of cardiac failure, often related to initial cardiac damage, concurrent therapies with fluid overload and vasopressors, infections, or pre-existing co-morbidities. The causes of PE need to be identified for appropriate treatment

Stocchetti, Nino

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Nino Stocchetti

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Wet lungs, broken hearts and difficult therapies after subarachnoid hemorrhage

Pulmonary edema (PE) can occur after subarachnoid hemorrhage and can jeopardize arterial oxygenation, which is essential for a suffering brain. In some cases PE is evident in the emergency room, being the direct consequence of intracranial bleeding, which causes an immediate and overwhelming catecholamine discharge. In the following days, PE can occur because of cardiac failure, often related to initial cardiac damage, concurrent therapies with fluid overload and vasopressors, infections, or pre-existing co-morbidities. The causes of PE need to be identified for appropriate treatmen

N. Stocchetti

AIR Universita degli studi di Milano

An acute catecholamine discharge immediately following intracranial bleeding can have devastating extracranial eﬀ ects: the heart, lungs, ﬂ uids and electrolytes can be severely aﬀ ected. Hoﬀ  and colleagues report on pulmonary edema (PE) following subarachnoid hemor-rhage (SAH) [1]. Th ey found a high incidence of PE, usually several days after the initial bleeding, and an asso-ciation of PE with lower intra vascular volumes (compared with cases without PE). PE is not uncommon after SAH, both as an early compli cation and as a late complication.Neurogenic PE is an acute event directly linked with an intracranial disaster; as such, it is often diagnosed on admission in cases with severe SAH [2]. PE in the days following SAH has been reported in association with triple-H therapy, which includes hypervolemia and induced arterial hypertension [3]. In diﬀ erent series, the PE incidence varied from 14 to 23% [4,5]. Increasing evidence is accumulating on the myocardial dysfunction that follows SAH, as well as other acute intracranial disasters. Takot subo syndrome – with typical left ventricular abnor malities (bulging out of the apex of the heart with preserved function of the base, which earned the syndrome its name – a kind of a pot used as octopus trap in Japan), ECG abnormalities and biomarker changes – is a typical example of how much an injured brain can break the heart [6]. Neurogenic in origin, left ventricular failure causes congestion in the pulmonary vasculature and PE in Takotsubo syndrome.What is concerning in the report of Hoﬀ  and colleagues is that PE, often labeled in the text as neurogenic PE, has been diagnosed days after the initial bleeding, without concurrent reduction of the cardiac index and in the absence of volume expansion [1]. Th e clinical implica-tions of these ﬁ ndings, as pointed out by the authors, would be that PE more than 4 days after SAH is not cardiogenic and would not be suitable for treatment with diuretics. It is therefore hard to reconcile the ﬁ ndings of this paper with current knowledge.Perhaps the methodology and terminology used in Hoﬀ  and colleagues’ paper require further attention. PE has been identiﬁ ed by clinical signs and bilateral pulmonary inﬁ ltrates on the chest X-ray scan, without quantitative measures concerning the cardiac and respiratory func-tion at the time of PE diagnosis. It is surprising that no data on oxygenation, such as a simple blood gas analysis, are reported. Th e hemodynamic status seems better docu mented, since the cardiac index and the circulating blood volume were estimated. Th ere are two weaknesses in these data, however, the ﬁ rst of which is the reliance on a single technique without conﬁ rmation by independent measures. Th e second, and more relevant, weakness concerns the data used in this speciﬁ c analysis: the data do not represent the actual circulating blood volume and cardiac index at the time of PE. In fact, mean values calculated from day 1 to the day when PE developed have been entered in the analysis. It becomes almost impossible, therefore, to use these mean data for correctly understanding what caused PE. Interestingly, diuretics were used in 65% of patients with PE in the days before the PE diagnosis. Were they used for correcting an AbstractPulmonary edema (PE) can occur after subarachnoid hemorrhage and can jeopardize arterial oxygenation, which is essential for a suff ering brain. In some cases PE is evident in the emergency room, being the direct consequence of intracranial bleeding, which causes an immediate and overwhelming catecholamine discharge. In the following days, PE can occur because of cardiac failure, often related to initial cardiac damage, concurrent therapies with fl uid overload and vasopressors, infections, or pre-existing co-morbidities. The causes of PE need to be identifi ed for appropriate treatment.© 2010 BioMed Central LtdWet lungs, broken hearts and diffi  cult therapies after subarachnoid hemorrhageNino StocchettiSee related research by Hoff  et al., http://ccforum.com/content/14/2/R43COMMENTARY*Correspondence: stocchet@policlinico.mi.itMilan University, Terapia Intensiva Neuroscienze, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milano ItalyStocchetti Critical Care 2010, 14:140 http://ccforum.com/content/14/2/140© 2010 BioMed Central Ltdexcessive volume expansion, as seems likely? If that was the case, PE could have been cardiogenic, and/or some-how related to ﬂ uid manage ment, without necessarily depending on a neurogenic cause.Managing patients after severe SAH is challenging: on one hand, their brain requires normal (or even high, in the case of vasospasm) arterial pressure to warrant cerebral perfusion and prevent delayed ischemic deﬁ cits; on the other hand, their heart may be damaged by an early sympathetic discharge, causing ischemic damage, and does not tolerate an increased workload. PE is a deleterious complication that may worsen systemic and cerebral oxygenation, and as such needs to be quickly recognized and treated [7]. Th e enthusiasm for triple-H therapy, which carries the risk of ﬂ uid overload and an indiscriminate use of vasopressors, must therefore be tempered.Perhaps the most important lesson to be drawn from this paper [1] is the need for accurate monitoring, both cardiovascular and respiratory, in all SAH cases. Some patients may simply require good clinical surveillance and careful ﬂ uid balance. Th e more severe cases, on the contrary, should be cared for by a team capable of detect-ing early signs of heart failure, identifying the causes of PE and treating them, still preserving cerebral perfusion.AbbreviationsPE, pulmonary edema; SAH, subarachnoid hemorrhage.Competing interestsThe author declares that they have no competing interests.Published: 16 April 2010References1. Hoff  RG, Rinkel GJ, Verweij BH, Algra A, Kalkman CJ: Pulmonary edema and blood volume after aneurysmal subarachnoid hemorrhage: a prospective observational study. Crit Care 2010, 14:R43.2. Macmillan CS, Grant IS, Andrews PJ: Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management? Intensive Care Med 2002, 28:1012-1023.3. Muench E, Horn P, Bauhuf C, Roth H, Philipps M, Hermann P, Quintel M, Schmiedek P, Vajkoczy P: Eff ects of hypervolemia and hypertension on regional cerebral blood fl ow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage. Crit Care Med 2007, 35:1844-1851.4. Solenski NJ, Haley EC Jr, Kassell NF, Kongable G, Germanson T, Truskowski L, Torner JC: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Crit Care Med 1995, 23:1007-1017.5. Wartenberg KE, Schmidt JM, Claassen J, Temes RE, Frontera JA, Ostapkovich N, Parra A, Connolly ES, Mayer SA: Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 2006, 34:617-624.6. Pilgrim TM, Wyss TR: Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review. Int J Cardiol 2008, 124:283-292.7. Ware LB, Matthay MA: Clinical practice. Acute pulmonary edema. N Engl J Med 2005, 353:2788-2796.doi:10.1186/cc8936Cite this article as: Stocchetti N: Wet lungs, broken hearts and diffi  cult therapies after subarachnoid hemorrhage. Critical Care 2010, 14:140.Stocchetti Critical Care 2010, 14:140 http://ccforum.com/content/14/2/140Page 2 of 2

CJ: Pulmonary edema and blood volume after aneurysmal subarachnoid hemorrhage: a prospective observational study. Crit Care

Clinical practice. Acute pulmonary edema.

Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management? Intensive Care Med

SA: Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med

Torner JC: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Crit Care Med

Vajkoczy P: Eff ects of hypervolemia and hypertension on regional cerebral blood fl ow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage. Crit Care Med

Wyss TR: Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review.

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Wet lungs, broken hearts and difficult therapies after subarachnoid hemorrhage

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