Chapter 4

One major cause of morbidity and mortality affecting surgical patients in general and specifically in the ICU is thromboembolic disease. This topic is discussed in a separate chapter in the book.

Release of antidiuretc hormone (ADH) and aldosterone is a well-known response to surgical stress and fasting.1,2 These hormones result in sodium and water retention as well as decreasing urine output. The decrease in urine output may persist in spite of normovolemia. These changes, combined with unmeasurable third space loss secondary to surgical procedures and peritonitis make estimation of circulating volume status very difficult. Traditional estimate of volume requirements based on urine output³ is therefore likely to be very inaccurate and frequently leads to fluid overload and pulmonary edema related hypoxemia in the presence of “inadequate” urine output. In these circumstances, clinical indices other than urine output must be used to assess adequacy of fluid volume status, such as level of consciousness, capillary return, skin warmth, pulse rate, and character as well as blood pressure. In situations where these clinical indices also prove imprecise especially in the elderly surgical patient with poor cardiopulmonary reserve, central hemodynamic monitoring in the ICU environment is required. In addition, the syndrome of inappropriate ADH release (SIADH) is relatively common in the postoperative period resulting in water intoxication and severe hyponatremia⁴ even when water in modest volume is administered. In these circumstances treatment should be guided by frequent monitoring of electrolytes and central hemodynamics.

The early phase of negative nitrogen balance following surgical stress can be shortened or even aborted by appropriate nutritional support before and after surgery. Early institution of enteric feeding has been reported to decrease postoperative complications including septic sequelae after abdominal surgery.⁵ If daily caloric goals could not be achieved entirely by enteric feeds before day 8 of ICU stay then parenteral nutrition should be instituted to meet the estimated caloric needs and to prevent further loss of muscle mass.⁶ Loss of muscle mass affects the ability to maintain normal respiratory function and results in dependence on ventilatory support as well as prolongation of the time to weaning off the respirator. The increased metabolic rate after surgery is associated with an increase in oxygen requirement and utilization, and a fall in muscle protein synthesis.^7,8 While this increased oxygen demand is easily met without untoward sequelae in patients with normal cardiorespiratory reserve, nutritionally depleted patients and those with already compromised cardiorespiratory function may be unable to meet these increased oxygen demands leading to decompensation, muscle fatigue, and respiratory failure. Such patients may require intubation and mechanical ventilatory support until the acute insult has abated and the oxygen demand can be met.

Apart from loading oxygen onto the red cell for delivery to the tissues, the respiratory apparatus is responsible for providing the necessary ventilation for carbon dioxide elimination. Excessive caloric delivery particularly in the form of carbohydrates,8 can lead to production of Carbon dioxide (CO₂) in amounts that exceeds the ventilatory capacity of the lung to excrete the CO₂ thus leading to respiratory failure, the requirement for respirator support and prolongation of weaning.⁹ Thus, in providing nutritional support not only should one try to provide the necessary calories, but also prevent overburdening of the respiratory system. If the caloric requirements are such that they cannot be provided without overwhelming the respiratory capability then the choice is between limiting caloric delivery and adding mechanical ventilator support to the treatment regime.

Generally, since the magnitude and duration of the surgical procedure affect the intensity of the metabolic response, the aim should be to decrease the duration and extent as well as frequency of surgical procedures in critically ill patients particularly in those with poor nutritional or cardiopulmonary reserve. This aim, however, should be considered in the context of the patient’s underlying problem. The surgical procedure should not be minimized at the expense of incomplete eradication of a surgical lesion such as a source of sepsis since failure to eradicate the septic focus would result in further complications including respiratory failure. In the setting of the multiple injured patient requiring massive blood transfusion, who is hypocoagulable, hypothermic, and/or acidotic, abbreviated laparotomy (‘damage control laparotomy’) should be considered in which the patient’s bleeding is stopped by techniques such as packing, control of sources of contamination by such procedures as irrigating, suctioning, and stapling without resection or anastomosis and taking the patient to the ICU for monitoring, warming, blood replacement, correction of hypothermia, and metabolic derangements including acidosis with mechanical ventilatory support which is followed as soon as possible by return to the Operating Room (OR) for completion of definitive care as the patient’s condition in the ICU allows.¹⁰

Elaboration of Extravascular Lung Water in Surgical Patients

As aforementioned, the metabolic response to surgery and stress involves release of ADH, aldosterone, and catecholamines. We have discussed how water and sodium retention combined with low urine output in response to ADH and aldosterone release could lead the clinician who uses urine output as an endpoint of fluid resuscitation, to unintentionally fluid overload the surgical patient leading to increased capillary hydrostatic pressure particularly in the patient with poor cardiopulmonary reserve thus generating pulmonary edema and hypoxemia. The increase in afterload that accompanies the effect of catecholamine release on the systemic arteriolar bed can result in a decrease in left ventricular systolic stoke volume. This could result in a relative increase in end diastolic ventricular volume and thus ventricular end diastolic pressure which will be reflected in an increase in pulmonary capillary hydrostatic pressure predisposing to the elaboration of extra vascular lung water and hypoxemia particularly in the patient with diminished cardiorespiratory reserve. This may not only occur secondary to the response to stress and surgery, but has been implicated as one of the mechanisms in neurogenic pulmonary edema in the head injured patient although there is suggestion that some degree of increased capillary permeability may also play a role in the pathogenesis of neurogenic pulmonary edema.11 Because of these factors consideration should be given to central hemodynamic monitoring in the ICU using a pulmonary artery catheter in these patients during fluid administration.

Oncotic pressure

The nutritionally depleted surgical patient with an underlying hypoalbuminemia or the patient with decreased intravascular protein concentration from non-colloid fluid infusion could also be at risk for pulmonary edema because of this decrease in capillary oncotic pressure. However, attempts to attenuate this effect by protein infusion has not been uniformly successful.

Capillary permeability

Increased pulmonary capillary permeability occurs in many settings in the surgical patient with the systemic release of cytokines and other vasoactive agents12,13 but the most common cause is unrecognized sepsis which commonly arises in the abdomen as a result of complications of such inflammatory conditions as appendicitis, diverticulitis, perforated ulcer, or other perforations which could be secondary to abdominal trauma which is a frequent source of unrecognized sepsis and death. Increased capillary permeability is also implicated in reperfusion injury after restoration of perfusion after a period of ischemia in vascular occlusive disorders, or after shock resuscitation, after decompression of fascial compartments in compartment syndromes, early and late phases of multiple organ dysfunction syndrome etc. Intra-abdominal sepsis is frequently secondary to an undrained intraabdominal abscess requiring a surgical or percutaneous radiologic approach.

Although both increased microvascular hydrostatic pressure and capillary permeability are important in the generation of extravascular lung water, manipulation of the microvascular hydrostatic pressure (by the use of vasoactive agents and regulation of the state of hydration) is the most direct means of altering pulmonary edema in the surgical patient. A search for a septic focus is crucial when increased capillary permeability is suspected. Control of capillary permeability can then be achieved, though indirectly, by treating the septic focus which may require a surgical approach. The link between sepsis and permeability is thus broken and the capillary permeability lesion is allowed to resolve with time. The resolution of the increased capillary permeability is accompanied by improvement in perioperative respiratory failure. An undrained septic focus should be suspected in patients who continue to have worsening of respiratory function including failure to wean off the respirator and until that septic focus is eradicated, dependence on ventilatory support and inability to wean will continue. Aggressive investigation for a septic source followed by appropriate eradication of this source is of paramount importance in managing these patients. Until the permeability is corrected, though indirectly, reduction of pulmonary artery wedge pressure to the lowest level compatible with adequate peripheral perfusion should be the goal.

Differentiation between pulmonary edema due to increased pulmonary capillary hydrostatic pressure and that due to capillary permeability is very important because the treatment may need to be modified based on which one of these entities may be considered responsible for the pulmonary edema. Treatment based on hemodynamic and fluid volume endpoints such as the use of diuretics, inotropes, vasodilators guided by central hemodynamic monitoring are the main focus in treating the high hydrostatic pressure pulmonary edema whereas pulmonary edema secondary to capillary leak requires a focus on trying to identify and treat the cause of the capillary leak such as identification and eradication of a septic focus. Usually, identification of a high measured capillary hydrostatic pressure with a central catheter such as SwanGanz catheter in the presence of radiologic and clinical evidence of pulmonary edema is considered evidence of high hydrostatic pressure pulmonary edema. However, caution must be exercised because of the recognized lag phase between the normalization of central hemodynamics and the radiologic clearance of signs of pulmonary edema.14 In these settings, the presence of normal capillary hydrostatic pressure with radiologic signs of pulmonary edema could be falsely considered to be due to capillary leak edema not recognizing that the pulmonary edema occurred initially under high pulmonary capillary hydrostatic pressure conditions and with diuresis and other maneuvers the hydrostatic pressure is normalized, but the radiologic signs of pulmonary edema persists for a variable period.

Atelectasis and Hypoventilation

Ventilation and perfusion are not equally matched in the normal lung, because the shape of the thoracic cavity and the descent of the diaphragm result in greater expansion of the dependent areas of the lobes. Also blood flow is greater in dependent areas of the lung during spontaneous ventilation and changes with body position. The normal lung has an average ventilation perfusion ratio of approximately 0.8. In the surgical patient, many factors cause a reduction in these ratios to very low values, causing severe ventilation/perfusion mismatch and hypoxemia. Similar factors result in resorption of alveolar gas behind closed airways (compression atelectasis). This resorption atelectasis can occur as early as five minutes after induction of anesthesia.^15,16

In surgical patients, hypoventilation is characteristically caused by impairment of ventilation due to the restrictive effect of painful incisions or peritonitis. It may also result from Central Nervous System (CNS) depression secondary to poorly titrated narcotic analgesia, anesthesia, or CNS injury.

The respiratory system is protected from sepsis and atelectasis by a respiratory mechanism that responds to hypoxemia, hypercapnia, acidosis, and the presence of irritating or noxious stimuli in the airway. These defense mechanisms can be significantly depressed by excessive postoperative narcotic analgesia or anesthesia. Inhalational anesthetics are noted for their respiratory depressive effect resulting in hypoventilation and a reduced to carbon dioxide as well as blunted response to hypoxemia and acidosis. Whereas in optimal doses narcotic analgesics decrease abdominal pain and increase the ability to clear secretions and ambulate, in larger doses they may depress the respiratory center leading to hypoventilation, hypercapnia, and hypoxemia.

Related posts:

Thrombo-Embolism in the ICU patient Abdominal Trauma Multiorgan Dysfuntion Syndrome in the Surgical Patient Nutrition in the Surgical ICU Patient The Pediatric Surgical ICU Patient Thoracic Trauma

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