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KEY POINTS
The systemic response to surgery and trauma results in fluid, electrolyte, and hormonal changes that impact ICU management of the surgical patient.
In planning nutritional support, the effect of surgical stress on nitrogen balance and on insulin and blood glucose levels is important.
Surgical stress promotes a hypercoagulable state that warrants consideration of prophylaxis against thromboembolism.
Prompt identification with control of bleeding and sepsis is crucial for management of these patients.
Surgery increases cardiorespiratory demand and the likelihood that mechanical ventilatory assistance will be needed.
Pulmonary edema and atelectasis characterize perioperative respiratory failure; hypoventilation and aspiration also contribute.
Where possible, a reduction of pulmonary capillary hydrostatic pressure in the perioperative period improves gas exchange by decreasing lung water.
The concept of closing volume and its relationship to functional residual capacity (FRC) is important in understanding perioperative atelectasis.
Risk factors for perioperative atelectasis include obesity, smoking, advanced age, anesthesia, recumbency, and incisional pain.
Diaphragmatic dysfunction is a major component of perioperative respiratory failure.
Preoperative assessment of respiratory function makes it possible to predict operative risk and to correct abnormalities before operation, particularly in the patient undergoing lung resection.
Early ambulation, physiotherapy, treatment of sepsis and shock, adequate analgesia, and early operative stabilization of fractures are key elements in the treatment and prevention of perioperative respiratory failure.
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There are many factors unique to surgical patients that warrant special consideration if management is to be appropriately directed in the ICU environment.
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Surgical stress or injury stimulates an orchestrated biologic response1–4 including the increased release of adrenocortical hormones, catecholamines, and glucagon; a decrease in insulin release resulting in hyperglycemia; the secretion of antidiuretic hormone (ADH) and aldosterone; and the release of cytokines and the initiation of a hypercoagulable state. These responses affect the critically ill surgical patient in many ways:
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Acute fluid and electrolyte shifts may occur.
The renal response to volume infusion may be altered.
The resulting catabolic response results in a phase of negative nitrogen balance.
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All these responses vary in intensity, depending on the magnitude and duration of the injury, the adequacy of resuscitation, and the presence of complications such as hemorrhage and sepsis. The increase in metabolic rate increases oxygen requirement. The management implications of these responses to surgical stress are outlined in the following sections.
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The Endocrine Response
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The increase in glucagon release and blunted insulin release in response to injury can lead to major changes in glucose metabolism. Hyperglycemia may occur in a patient who has previously demonstrated no evidence of abnormality in glucose metabolism. A latent diabetic state or a prediabetic state may be unmasked. The management of already established stable diabetes mellitus may become more complicated in the critically ill surgical patient because of changes in glucagon and insulin activity secondary to the critical illness or surgical ...