Mrs. Jones is at risk for developing significant complications, even though her surgery went uneventfully. Although some complications may result from intraoperative events, others are related to pre-existing medical conditions, the clinical situation, and the urgency of operation. Mrs. Jones has no known medical history; however, occult cardiovascular disease is certainly possible. She was dehydrated at presentation with evidence of organ malperfusion and is at significant risk for infectious complications from her necrotic bowel.

Normal urine output is usually thought to be greater than 0.5 mL per kg per hour. It is an important estimate of the adequacy of end-organ (in this case, the kidney) perfusion, and it is important to focus on organ perfusion rather than the strict number of milliliters of urine. When urine output is low, it is useful to consider prerenal, renal, and postrenal causes (Table 31.1) (1).

Prerenal oliguria is caused by inadequate glomerular perfusion or renal ischemia; hypovolemia is a classic example and is the most common cause of oliguria in the postoperative patient. Low cardiac output syndromes and congestive heart failure can also cause prerenal azotemia.

Renal causes of oliguria include injury to the renal tubules from toxins, antibiotics, intravenous (IV) contrast, and other direct insults. They may progress to acute renal failure.

Postrenal causes of oliguria are those factors distal to the renal tubules that obstruct the drainage of urine. Eventually, this back-pressure leads to renal injury. The most common and easily correctable example of a postrenal process is obstruction of the urinary catheter by clot or debris. Obstruction of the ureter by hematoma can occur as a complication of certain abdominal procedures, but bilateral obstruction would be required to impair urine output.

First, confirm the patency of the indwelling bladder catheter. This is particularly crucial when it is reported that urine output has suddenly dropped to zero. Once this is done, assess the patient for signs and symptoms of hypovolemia or hypervolemia. The fluid balance since surgery and the dilutional state of the urine may provide further useful information. A urine specific gravity equal to or greater than 1.020 is concentrated and supports the assessment of hypovolemia. An increased hematocrit, sodium, or urea-to-creatinine ratio further strengthens this impression. A chest radiograph may complete the assessment of the patient’s volume status if it remains otherwise unclear.

Patients who are hypovolemic receive one or two fluid boluses of crystalloid or colloid solution; 500 mL of lactated Ringer’s solution or one unit of albumin constitute reasonable fluid boluses. Those patients who appear hypervolemic may receive a trial dose of an IV loop diuretic such as furosemide.

If there is no response to these diagnostic challenges or if the picture remains unclear, consider assessing the intravascular volume status with central venous pressure (CVP) monitoring. CVP roughly correlates with intravascular volume (2), although the normal CVP may range between 0 and 8 mm Hg. A low or equivocal CVP may justify further fluid resuscitation and monitoring of urine output. An elevated CVP indicates a need for more aggressive diuresis. It is particularly useful to follow the trends in CVP as therapeutic interventions are made.

Yes. When assessing patients with respiratory complaints, it is necessary to differentiate those with subjective dyspnea who are well compensated, those with true but mild insufficiency, and those with impending respiratory failure (5,6). Patients in acute respiratory distress requiring intubation will need ventilatory support before determination of the exact cause of the problem. Arterial oxygen desaturation on pulse oximetry may provide a clue, but arterial desaturation is a late event, particularly if supplemental oxygen is being provided. A rapid, shallow respiratory pattern (rate greater than 40 breaths per minute), the use of accessory muscles of respiration, or paradoxical motion of the diaphragm may indicate respiratory muscle fatigue and impending mechanical ventilatory failure. Confusion, anxiety, or cyanosis are signs of inadequate oxygen delivery and should prompt inhalation of ventilatory support.

When respiratory failure is not impending, increasing supplemental oxygen may improve arterial blood saturation and improve symptoms but may not address the primary problem. Assessment of events surrounding the patient’s symptoms may be helpful. For example, sudden onset of dyspnea may occur due to mucus plugging in a sedentary patient. Pulmonary embolism may present suddenly in a patient recently mobile. Gradual worsening of breathing may be more indicative of atelectasis or a developing pneumonia (7). Sudden shortness of breath while eating may indicate aspiration.

The physical examination is particularly important and can suggest a diagnosis, as in patients with bronchospasm, congestive heart failure, or a pneumothorax. A chest radiograph should routinely be obtained and can make the diagnosis. Arterial blood gases are helpful to define worsening oxygenation and hypercapnia.

Finally, cardiovascular complications such as acute myocardial infarction can manifest with respiratory distress. The diagnostic features and major treatments for the most common causes of postoperative respiratory insufficiency are outlined in Table 31.2 (8, 9, 10).