Letter to the Editor: Volume management after subarachnoid hemorrhage

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TO THE EDITOR: We read with interest the article by Obata and colleagues5 (Obata Y, Takeda J, Sato Y, et al: A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage. J Neurosurg 125:254–263, August 2016), describing hemodynamic changes after ruptured aneurysm treatment by using a PiCCO-plus device (Pulsion Medical Systems) in a prospective multicenter cohort study. The authors found an incidence of pulmonary edema of 25.5% in patients with subarachnoid hemorrhage (SAH). Patients who developed pulmonary edema presented with a higher World Federation of Neurosurgical Societies (WFNS) grade and were older. Moreover, the authors found a decrease in cardiac index in the pulmonary edema group, and, at the time of PiCCO catheter insertion, the mean serum brain natriuretic peptide levels were higher than those in the non–pulmonary edema group in the early phase. The authors concluded that pulmonary edema occurring in the early phases after SAH is caused by cardiac failure, whereas pulmonary edema occurring in the delayed phases after SAH is caused by inflammatory (i.e., noncardiogenic) conditions.

This article is important, being one of the few to report the use of hemodynamic PiCCO-plus monitoring for early identification of pulmonary edema in patients with SAH. Nevertheless, we have some questions regarding the validity of the conclusions, as insufficient information is presented on the methods used and because the incidence of pulmonary edema is extraordinarily high.

What surprised us is the study population: having 204 patients in a time frame of 43 months reflects an accrual rate of fewer than 5 patients per month from 9 different institutions, which amounts to 1 patient per 2 months per center. We wonder whether this low accrual rate provides enough of a routine to recommend such complex monitoring in these critically ill patients. Furthermore, the number of enrolled patients implies that a significant selection bias has taken place, but no information is provided on the volume of SAH patients treated per center and which patients were not included. This impression of selection bias is further strengthened by the observation that the authors found a staggeringly high percentage of patients who developed pulmonary edema (25.5%) compared with that reported in the literature (8%–23%).1,4,7–9 Moreover, it would be very interesting to be informed about the standard protocol(s) used in the participating centers for SAH patients, especially regarding fluid volume management. What would have strengthened this article is a discussion regarding influences that led to this high percentage.

It is remarkable that more patients were treated with triple-H therapy (hypertension, hypervolemia, and hemodilution) than there were patients with delayed cerebral ischemia, suggesting a kind of “prophylactic” triple-H therapy, although triple-H therapy has been shown not to be superior to normovolemic fluid therapy in the prevention of delayed cerebral ischemia. The high percentage (22%) of patients who developed pulmonary edema with a WFNS Grade I seems to support this assumption, as pulmonary edema is a known complication of hypervolemia.2,3

No information was presented about patients' outcomes after 30 days in Results, although this parameter was mentioned in Methods. The definition of morbidity used (“any result other than satisfactory recovery”) also seems a very subjective measure, easily prone to bias. Moreover, the mortality rates of 7.7% and 5.8% in the pulmonary edema group and non–pulmonary edema group, respectively, were quite low compared with percentages reported in the literature.4,6

In conclusion, the additional use of hemodynamic PiCCO- plus monitoring might well be a useful tool to reduce the risk of developing (secondary) pulmonary edema in selected patients after SAH, but without further information we think that this is a premature conclusion.

References

  • 1

    Bruder NRabinstein A: Cardiovascular and pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurocrit Care 15:2572692011

  • 2

    Egge AWaterloo KSjøholm HSolberg TIngebrigtsen TRomner B: Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study. Neurosurgery 49:5936062001

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3

    Medlock MDDulebohn SCElwood PW: Prophylactic hypervolemia without calcium channel blockers in early aneurysm surgery. Neurosurgery 30:12161992

  • 4

    Muroi CKeller MPangalu AFortunati MYonekawa YKeller E: Neurogenic pulmonary edema in patients with subarachnoid hemorrhage. J Neurosurg Anesthesiol 20:1881922008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Obata YTakeda JSato YIshikura HMatsui TIsotani E: A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage. J Neurosurg 125:2542632016

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Saracen AKotwica ZWoźniak-Kosek AKasprzak P: Neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage. Adv Exp Med Biol 952:35392016

  • 7

    Solenski NJHaley EC JrKassell NFKongable GGermanson TTruskowski L: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med 23:100710171995

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8

    Vespa PMBleck TP: Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage. Neurocrit Care 1:1571702004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    Wartenberg KESchmidt JMClaassen JTemes REFrontera JAOstapkovich N: Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 34:6176242006

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation

Disclosures

The authors report no conflict of interest.

Keywords:

Response

We thank Dr. Post and colleagues for their interest in our study and for their comments on our paper.

We reported that 25.5% of patients with SAH developed pulmonary edema. This incidence of pulmonary edema was slightly high, as was pointed out. Here, we discuss possible causes for this outcome. First, patients with severe SAH grades were brought to emergency and critical care centers and underwent surgery. Of these patients, those for whom hemodynamic monitoring would be useful in the management of their postoperative condition were enrolled in our study by attending physicians from each participating institution. In addition, the neurosurgical specialists themselves treated the patients, even after surgery for SAH. Thus, there was no standard protocol, even for fluid volume management, for patients with SAH. Second, the patients who were enrolled in our study underwent hemodynamic monitoring for 10 consecutive days after surgery. Hence, there may have been unintentional selection bias.

In such patients with SAH, we investigated the incidence and cause of pulmonary edema by using hemodynamic monitoring with PiCCO-plus pulse contour analysis and other clinical data. Therefore, we concluded that pulmonary edema occurring in the early and delayed phases after SAH was caused by cardiac failure and inflammatory conditions.

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Article Information

Contributor Notes

INCLUDE WHEN CITING Published online January 27, 2017; DOI: 10.3171/2016.9.JNS162321.
Headings
References
  • 1

    Bruder NRabinstein A: Cardiovascular and pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurocrit Care 15:2572692011

  • 2

    Egge AWaterloo KSjøholm HSolberg TIngebrigtsen TRomner B: Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study. Neurosurgery 49:5936062001

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3

    Medlock MDDulebohn SCElwood PW: Prophylactic hypervolemia without calcium channel blockers in early aneurysm surgery. Neurosurgery 30:12161992

  • 4

    Muroi CKeller MPangalu AFortunati MYonekawa YKeller E: Neurogenic pulmonary edema in patients with subarachnoid hemorrhage. J Neurosurg Anesthesiol 20:1881922008

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Obata YTakeda JSato YIshikura HMatsui TIsotani E: A multicenter prospective cohort study of volume management after subarachnoid hemorrhage: circulatory characteristics of pulmonary edema after subarachnoid hemorrhage. J Neurosurg 125:2542632016

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6

    Saracen AKotwica ZWoźniak-Kosek AKasprzak P: Neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage. Adv Exp Med Biol 952:35392016

  • 7

    Solenski NJHaley EC JrKassell NFKongable GGermanson TTruskowski L: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med 23:100710171995

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8

    Vespa PMBleck TP: Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage. Neurocrit Care 1:1571702004

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    Wartenberg KESchmidt JMClaassen JTemes REFrontera JAOstapkovich N: Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 34:6176242006

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
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