Common Postoperative Complications: Oliguria, Dyspnea, Fever, and Hypotension
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Mrs. Jones is a 70-year-old woman without previous known medical history who had not seen a physician in many years. She presented to the emergency department of your hospital complaining of 3 days of nausea, vomiting, and abdominal pain. Although her vital signs were stable on admission, she required fluid resuscitation in the emergency department for low urine output. At surgery, strangulation obstruction of the small bowel was found and a resection of some necrotic bowel and primary anastomosis was performed. Mrs. Jones remained stable throughout surgery and was admitted to the surgical intermediate care unit postoperatively.
Why was Mrs. Jones admitted to an intermediate care unit after surgery?
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.
Six hours postoperatively the nurse calls you because Mrs. Jones’ urine output has been 15 mL per hour for 2 hours and she has produced no urine output for the last hour. Vital signs are stable but she is slightly tachycardic at a rate of 110 beats per minute. Mrs. Jones’s problem must be evaluated.
What is normal urine output?
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).
TABLE 31.1. Common Etiologies of Oliguria in the Surgical Patient Listed by Physiologic Category
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.
While you are considering the etiology of oliguria in the postoperative setting, the nurse asks you what you want to do.
How do you proceed?
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.
When should pulmonary artery catheterization be considered and how does it work?
Failure to obtain urine output with therapy directed by CVP may be an indication for placement of a flow-directed pulmonary artery catheter (3,4). The pulmonary artery catheter has a balloon at its tip. Inflation of this balloon causes the catheter to float across the tricuspid valve, into the right ventricle, and across the pulmonic valve. The catheter and tip rest in the proximal pulmonary artery of either the right or the left lung.
When the balloon is inflated, the catheter wedges in the pulmonary artery. The pressure sensor at the tip of the catheter reads the pressure downstream, called the pulmonary capillary wedge pressure (PCWP). Because there are no valves between the left atrium and the pulmonary arteries, the PCWP closely approximates left atrial pressure and is an excellent barometer of left ventricular preload. A low PCWP indicates hypovolemia and prompts further fluid loading. If the PCWP is normal (10 to 14 mmHg), intravascular volume is adequate and a search for other causes of oliguria is necessary. Persistent oliguria in the face of a high PCWP raises the possibility of renal failure or postrenal obstruction.
When reviewing Mrs. Jones’s flowsheet you note that she received only 2 L of fluid during her surgery. Although her recorded operative fluid loss was minimal, you are aware that she probably had the small-bowel obstruction for several days and had come to surgery with a considerable pre-existing deficit. Vital signs are normal. Examination shows clear lungs and dry mucus membranes. Urine specific gravity is 1.025. Hematocrit is elevated at 46% and blood urea nitrogen (BUN) elevated at 21 mg/dL. You are confident that Mrs. Jones is hypovolemic and order two 500-mL fluid boluses of normal saline (NS). An hour later, the urine output has not picked up. A central venous line is inserted and the CVP is 4 mmHg. Another liter of NS is given, raising the CVP to 7 mm Hg. The urine output improves significantly.
Mrs. Jones remains well with normal vitals signs until the middle of postoperative day 1. She has previously been resting comfortably but now the nurse calls to inform you she is complaining of dyspnea or shortness of breath. You are told that her respiratory rate is 34 breaths per minute and she is tachycardic to 105 breaths per minute. Her oxygen saturation is 94% on 2-L nasal cannula. Her blood pressure is normal.
Mrs. Jones’s arterial saturations are adequate; should you be concerned?
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 you arrive in the intermediate care unit, you note that Mrs. Jones is slightly tachypneic as claimed. Her heart rate is 90 beats per minute. She is not breathing with accessory muscles, is pink, and is easily able to talk. Intubation does not seem necessary at this time. On examination, Mrs. Jones has decreased breath sounds at the bases and is taking shallow breaths at a slightly increased rate of 30 breaths per minute. Her incentive spirometry is only 4 mL per kg (greater than 10 mL per kg acceptable), and she volunteers that deep breathing is painful.
A chest radiograph obtained by the nurse shows only decreased lung volumes and increased density at the bases. Oxygen saturation improves to 98% on 4 L. Your presumptive diagnosis is atelectasis and you order increased analgesia and aggressive physiotherapy and encourage spirometry. On a follow-up visit later that evening, Mrs. Jones is much improved and appreciative of your help.
Why did you choose this course of action?
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).
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