Fluid Management During Lung Resection

Introduction

Managing fluid administration during lung resection by the anesthesiologist is very similar to a tightrope walker trying to balance the risk of acute lung injury (ALI) and that of acute kidney injury (AKI); there is a narrow margin of safety between fluid overload and hypovolemia, two conditions that may impair lung and renal function, respectively.

Maintaining fluid and electrolyte homeostasis represents a crucial challenge because of the profound impact on perioperative morbidity and mortality. The evolution in surgical techniques lead to reduction of in-hospital mortality rates to less than 2% for lobectomies and less than 6% for pneumonectomies. ^, The length of hospital stay is also shorter, and with cumulative experience, procedural complications are less frequent. The main causes of mortality are not from surgical or cardiac complications, but rather being replaced by pulmonary pathology, such as pneumonia, empyema, and ALI.

Pulmonary complications are caused by a combination of multiple factors acting together and among them, the volume of intravenous fluids administered intraoperatively plays an important role.

The aim of this chapter is to provide a guide for fluid management during lung resection, answering some question, yet raising some others.

From Postpneumonectomy Pulmonary Edema to Acute Lung Injury

Postpneumonectomy pulmonary edema (PPPE) was first reported by Zeldin, who described the correlation between the amount of perioperative fluid, over 37 mL/kg intraoperatively and for the first 24 hours after surgery, and pulmonary complications.

This article laid the foundations for establishing an association between fluid overload and development of lung injury but has some issues to consider. First, the edema affected only 10 patients, which makes the sample size low for current standards. Most of the PPPE occurred in patients who had right pneumonectomies, which has a larger parenchymal tissue. These pulmonary complications can be present not only in pneumonectomies, but also after less extensive resections or even after thoracotomies without resections.

However, after Zeldin, several investigators attempted to explore the correlation between fluid administration and lung outcome.

Licker et al. in a multivariate analysis, described two independent risk factors for ALI: the extent of lung resection (pneumonectomy was associated to the highest risk) and fluid overload (meaning 9.1 mL/kg/h intraoperatively and 1 mL/kg/h for the first 24 hours). This study however, did not provide for protective lung ventilation (PLV): a latter comparison with a group of patients with adoption of PLV showed a pronounced decrease in the incidence of ALI/acute respiratory distress syndrome (ARDS), despite no change in fluid administration. This finding suggests the importance of ventilation strategy in lung outcomes. However, some studies report the presence of lung injury even when applying a “very restrictive ventilatory strategy.”

Postoperative lung injury usually occurs 1 to 4 days after surgery, and presents with a low pulmonary capillary wedge pressure, which raises questions if the fluid overload is the sole accountable factor. Certainly, this measure confirms that this type of edema has not its origin from heart failure, but—au contraire—it challenges the hypothesis of hypervolemia. In addition, the edema fluid has high concentrations of proteins. This type of pulmonary edema seems to be the result of an increase in pulmonary capillary permeability, associated with a rise in plasma protein content; it suggests that this lung injury could occur despite normovolemia, and most likely is being just exacerbated by fluid overload.

The clinical pattern formerly known as PPPE shares many clinical and histologic features with ARDS. It is unclear which studies are referring to ALI or postoperative lung injury rather than PPPE.

Definitions and Epidemiology

Postthoracotomy Acute Lung Injury

The definition of ALI and ARDS, according to the American-European Consensus Conference on ARDS, consists of a syndrome of inflammation and increased permeability with:

Acute onset
Bilateral infiltrates on chest radiograph
Hypoxemia (partial pressure of arterial oxygen [PaO2] ≤300 mm Hg for ALI and PaO2 ≤200 for ARDS), despite positive end-expiratory pressure
No evidence of left atrial hypertension or pulmonary capillary occlusion pressure below 18 mm Hg

This definition can be applied to postthoracotomy ALI, even if there is a broad spectrum of clinical pictures described in patients with postthoracotomy lung injury.

Lung injury following lung resection occurs in 2.5% of all lung resections, with increased incidence of 7.9% after pneumonectomy.

Acute Kidney Insufficiency

Historically, the incidence of kidney damage in thoracic surgery was reported to be quite low. The Society of Thoracic Surgeons database cited an overall incidence of 1.4%. These data pertained only to patients who required renal suppurative replacement therapy, and a subsequent assessment using standardized criteria reported a much higher incidence.

In 2002, the Acute Dialysis Quality Initiative Group presented a classification system for AKI named RIFLE (risk, injury, failure, loss, and end-stage renal disease), based on increased serum creatinine (SCr) associated with a decrease in glomerular filtration rate (GFR) and urinary output. A more recent system was reported, called AKIN (Acute Kidney Injury Network) criteria: this system is considering an absolute increase in SCr of 0.3 mg/dL as a diagnostic criteria in identifying stage 1 disease. These criteria attracted much criticism by clinicians, questioning the clinical relevance of a minimal increase in SCr. However, Basile et al. showed worse outcomes in patients with postoperative AKI, even with slight increases of SCr and with complete restoration of kidney function; postthoracotomy AKI, specifically, was associated with a hazard ratio of 1.6 in terms of long-term survival.

Studies using the AKIN criteria report a higher incidence of kidney injury. Ishikawa et al. reported an incidence of renal impairment in 5.9% of thoracic surgical patients, and Hobson reached 33% of incidence in a high-risk group.

The classification systems are summarized in Tables 21.1 and 21.2 .

Table21.1

Risk, Injury, Failure, Loss, End-Stage Renal Disease Criteria of Acute Kidney Injury

Stage	Glomerular Filtration Rate	Urinary Output
Risk	↑SCr × 1.5 or ↓GFR >25%	<0.5 mL/kg/h for 6 hours
Injury	↑SCr × 2 or ↓GFR >50%	<0.5 mL/kg/h for 12 hours
Failure	↑SCr × 3 or ↓GFR >75% or SCr 4 mg/dL with acute rise of 0.5	<0.3 mL/kg/h for 24 hours or anuria >12 hours
Loss	Complete loss of kidney function for > 4 weeks
End-stage	End-stage kidney disease >3 months

GFR , Glomerular filtration rate; SCr , serum creatinine.

Table21.2

Acute Kidney Injury Network Criteria of Acute Kidney Injury

Stage	Creatinine	Urinary Output
I	↑SCr × 1.5–2 or ↑SCr 0.3 mg/dL	<0.5 mL/kg/h for 6 hours
II	↑SCr × 2–3	<0.5 mL/kg/h for 12 hours
III	↑SCr × 3 or ↓GFR >75% or SCr 4 mg/dL with acute rise of 0.5 or any dialysis	<0.3 mL/kg/h for 24 hours or anuria >12 hours

GFR , Glomerular filtration rate; SCr , serum creatinine.

Ventilator-Induced Lung Injury

Ventilation can cause a broad spectrum of local and systemic pathophysiologic changes, in particular in patients requiring lung surgery and one-lung ventilation (OLV), defined as ventilator-induced lung injury (VILI). The causes of these adverse effects are barotrauma (direct consequence of high pressure on the lung), volutrauma (effect of excessive distension of the lung), atelectotrauma (cyclic opening and closing of alveoli) and biotrauma (inflammatory cascades triggered by cytokines release). ^,

Transfusion-Related to Acute Lung Injury

Transfusion-related to acute lung injury (TRALI) diagnosis was classically based upon development of a new ALI within 6 hours of transfusion, not ascribable to another ALI risk factor.

Recently, an updated TRALI definition/classification scheme has been published with several modifications. Among them is the distinction between two types of TRALI that should be noted TRALI type I applies to patients without an ARDS risk factor, TRALI type II to cases with an ARDS risk factor or even with mild preexisting ARDS. At first glance, one should immediately notice that this second type is in contrast with the old definition.

This new diagnostic criteria for TRALI is listed in Box 21.1 .

• Box 21.1

New Consensus Transfusion-Related to Acute Lung Injury Definition

TRALI type I: Patients who have no risk factors for ARDS and meet the following criteria

Clinical features:
- Acute onset
- Hypoxemia (PaO2/FiO2 <300 or SpO2 <90% on room air)
- Clear evidence of bilateral pulmonary edema on imaging
- No evidence of LAH or, if LAH is present, it is not main contributor to hypoxemia
Onset during or within 6 hours of transfusion
No temporal relationship to an alternative risk factor for ARDS

TRALI type II: Patients who have risk factors for ARDS (but who have not been diagnosed with ARDS) or who have preexisting mild ARDS (PaO2/FiO2 of 200–300), but whose respiratory status deteriorates and is judged to be caused by transfusion based.
Findings as described in categories a and b of TRALI type I, and
Stable respiratory status in the 12 h before transfusion

ARDS , Acute respiratory distress syndrome; FiO2 , fraction of inspired oxygen; LAH , left atrial hypertension; PaO2 , partial pressure of arterial oxygen; TRALI , transfusion related acute lung injury.

Physiopathology

Acute Lung Injury

Understanding the two main mechanisms that play a crucial role in the development of pulmonary edema following thoracic surgery, which are an increase in pulmonary capillary hydrostatic pressure and/or an increase in capillary permeability, is essential to improve patient outcomes.

Starling Forces

In 1896, Ernest Starling working on an animal model, stated that the mechanism of fluid exchange (a combination of filtration and reabsorption between capillaries and interstitial space) was found in differences between hydrostatic and osmotic pressures, as well as in the capillary wall structure.

This observation led to the formulation of Starling equation as follows:

J _v /A = L _p [(P _c – P _i ) - σ (π _c – π _i )]

Likewise J _v / A is the rate of fluid exchange per unit area of the vessel, Lp is the permeability of the vessel wall, (P _c – P _i ) and (π _c – π _i ) with a difference between capillary and interstitial fluid in terms of hydrostatic and osmotic pressure, and σ is the reflection coefficient of the vessel wall to plasma proteins.

This equation depicts fluid exchange as a balance between opposing forces with capillary hydrostatic pressure representing the filtration force and the capillary osmotic pressure representing the reabsorption force; the larger is the difference, the greater is the exchange ( Fig. 21.1 ).

• Fig. 21.1, Starling forces across the capillary wall.

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