Selected Postoperative Complications

I. Pleural Effusion

A small amount of fluid is present in the pleural cavity. The reabsorption of this pleural fluid is mainly through the venous system and to some degree through the lymphatic system. Any increase in capillary hydrostatic pressure as a result of disrupted systemic venous hemodynamics (e.g., Fontan surgery, right ventricular failure) may result in accumulation of transudates in the pleural cavity. Trauma to the lymphatic system as is caused by cutting large tributaries of the thoracic duct causes buildup of chyle in the pleural space. Both conditions create a management problem.

Duration of persistent pleural effusion , as a result of increased systemic venous pressure that is common after Fontan operation, may be shortened by intraoperative creation of baffle fenestration. Symptoms may include fever, tachycardia, tachypnea, increased work of breathing, and, in severe cases, respiratory failure. Diagnosis is usually made by chest radiography (frontal, lateral, and decubitus films). Thoracentesis (with ultrasonographic guidance) may be necessary for determination of etiology and/or for treatment. Transudates can be differentiated by amount of protein (<3▒g/100▒mL) and lactate dehydrogenase (LDH) (<200 IU/L) from exudates (protein >3▒g/100▒mL and LDH >200 IU/L), which are caused by increased capillary permeability and may be a sign of infection. In addition, transudates have fewer leukocytes (<10,000/mm3), have more glucose (60▒mg/dL), and have a serous appearance compared with exudates, which are cloudy and have significantly more leukocytes (>50,000/mm ³ ). Furthermore, fluid-to-serum ratios of LDH (>0.6) and protein (>0.5) are further clues to the exudative nature of the fluid.

A small amount of pleural effusion can be tolerated well. It usually responds to medical management with diuresis, afterload reduction, and inotropic support. However, significant and recurrent amounts of pleural effusion will cause cardiorespiratory compromise and will require more aggressive management strategies, including chest tube drainage, now rarely implemented pleurodesis with a sclerosing agent (e.g., talc), and/or Fontan revision. When the drainage is large, appropriate replacement of fluid, electrolytes, and protein is essential.

Chylothorax , an accumulation of chyle in the pleural cavity, may be caused by trauma to peritracheal lymphatics or transmission of increased systemic venous pressure to the thoracic duct, or a combination of both. It may be seen after surgery (up to about 6% of cases) such as COA repair, B-T shunt, or cavopulmonary anastomosis (e.g., Glenn or Fontan operation), or rarely, after ligation of PDA. Occasionally, chylothorax occurs in combination with chylopericardium.

Chyle may or may not have a creamy appearance, depending on the nutritional status of the patient (consumption of fat results in creamy appearance), but a triglyceride level above 110▒mg/dL is highly probable for the diagnosis, whereas a triglyceride concentration of less than 50▒mg/dL makes the diagnosis of chylothorax extremely unlikely. The fluid is usually sterile and is abundant of lymphocytes (2,000 to 20,000/mm ³ ). Presence of chylomicrons (triglyceride-rich lipoprotein particles containing some phospholipids and cholesterol) confirms a diagnosis of chylothorax.

Treatment, apart from medical management (i.e., diuresis, improvement of cardiac output) described previously, is directed at drainage of chylothorax (chest tube placement) and reducing the flow of lymph (by limiting physical activity to reduce lymph flow from the extremities).

• 1.

  In most cases, chest tube drainage is all that is necessary. If chylothorax develops after chest tube removal, needle aspiration every 3 to 4 days usually constitutes adequate treatment. The drainage slows or stops within 7 days in most cases.

• 2.

  Careful attention to the nutrition of the patient is important. Either parenteral hyperalimentation or a diet with medium-chain triglycerides (MCTs) as the fat source is called for. As MCT oil does not contribute in chylomicron formation, it is absorbed by the portal system and not by the lymphatic system. Serum albumin should be followed closely and replaced if necessary.

• 3.

  In persistent cases, continuous intravenous (IV) octreotide (0.5 to 10 μg/kg/hr), a somatostatin analog, has been used effectively.

• 4.

  If the drainage persists, making the patient’s status non per os (NPO) and starting total parenteral nutrition therapy and/or surgical intervention may be considered because continuous loss of chyle results in lymphocyte depletion and subsequent immunocompromise. Indications for the intervention may include (a) average daily loss above 1000▒mL, or, in children, chest tube output more than 2▒mL/kg/day), (b) the chyle flow not slowing after 2 weeks, or (c) imminent nutritional complications.

• 5.

  Thoracic duct ligation with or without chemical pleurodesis has been used successfully. During pleurodesis, the introduced chemicals cause inflammation between the parietal and visceral pleura. This reaction causes adhesions between the layers and prevents further fluid accumulation. The procedure may be painful and cause fever and nausea so that this procedure has become out of favor at most centers.

II. Paralysis of the Diaphragm

Paralysis or paresis of a hemidiaphragm occurs in about 0.5% to 2% of patients after thoracic surgery, though the incidence may be as high as 10% in young children. It is the result of damage to the phrenic nerve. It may occur after COA repair, PDA ligation, B-T shunt, or open heart surgery and may be due to nerve transection, blunt trauma, stretching during retraction, electrocautery, or hypothermic injury. Infants are more vulnerable to respiratory distress owing to their greater dependence on the diaphragm for respiration.

The diagnosis should be suspected if there is persistent unexplained tachypnea, respiratory distress, hypoxia and/or hypercapnia, atelectasis, inability to wean from the ventilator, or persistent elevation of a hemidiaphragm on serial chest radiographs. Fluoroscopy or sonogram that reveals paradoxical motion of the hemidiaphragms is diagnostic if it is done during spontaneous breathing. When paralysis is not caused by transection, return of function usually occurs in 2 weeks to 6 months. In 20% of the cases the paralysis is permanent.

Management ranges from conservative to surgical intervention.

• 1.

  Some investigators recommend ventilator support only for the initial 2 to 6 weeks.

• 2.

  Continuous positive airway pressure (CPAP) may be useful in management as well as in identifying patients who may benefit from plication.

• 3.

  If respiratory insufficiency persists, surgical plication should be considered. Plication of the diaphragm usually is not necessary as long as the patient can be extubated without developing respiratory insufficiency.