Postoperative bleeding is one of the most common complications after nasal surgery. Prevention of postoperative bleeding depends on identifying patients at risk, and those patients with a personal or family history of bleeding disorders should be investigated using specific tests. The use of anticoagulant drugs, aspirin, and NSAIDs should be interrupted at least 2 weeks before surgery in all patients.
Epistaxis is most frequently mild but may be severe. The most common causes of mild epistaxis are bleeding from the incision sites and traumatized mucosa. Fortunately, mild postoperative bleeding can generally be controlled with 60-degree head elevation, gentle nostril pressure for 15 minutes, and application of topical decongestant nasal sprays.
If bleeding persists, the septal splints should be removed, and the nasal passages should be gently suctioned to remove blood clots and crusts. Focal areas of bleeding may be cauterized with silver nitrate, or a light hemostatic packing made of methylcellulose may be placed over the bleeding surface. Newer topical hemostatic sealants containing thrombin may alleviate diffuse mucosal bleeding. Continued bleeding may require a formal nasal pack, either in the form of gauze or a commercially available nasal tampon. Bleeding that persists despite anterior packing may signify a posterior bleed from a branch of the sphenopalatine artery, and a posterior pack may be required. Patients should be observed for airway compromise while a posterior pack is in place. Antibiotics should be administered while packing is in place to reduce the risk of toxic shock syndrome.
Serious bleeding occurs in less than 1% of patients and warrants operative exploration when conservative measures fail. Persistent bleeding may require endoscopic ligation of the sphenopalatine artery, internal maxillary artery, or anterior and posterior ethmoidal arteries. Alternatively, bleeding that is refractory to all of these measures can be addressed with angiographic embolization.
A septal hematoma is a potentially serious complication of rhinoplasty. Patients may present with symptoms of nasal obstruction, pain, rhinorrhea, or fever. The typical finding on physical examination is an ecchymotic nasal septal mass. An untreated septal hematoma can have serious implications, as it may lead to cartilage necrosis with subsequent loss of dorsal support and a saddle-nose deformity. Proper management consists of early recognition with prompt evacuation of the hematoma, either via needle aspiration or incision and drainage. Antimicrobial therapy should be initiated if a secondary nasal septal abscess is suspected.
In spite of the fact that rhinoplasty is a “non-sterile operation”, infections happen in less than 1% of all interventions. Postoperative infections following rhinoplasty can range in severity from mild cellulitis of the soft tissue envelope to life-threatening systemic illness resulting from cavernous sinus thrombosis or toxic shock syndrome. The rhinoplasty surgeon should be diligent in examining his or her patient for signs of infection and initiating treatment early.
Local wound infections, such as cellulitis, can be treated with systemic antibiotics and close observation; however, any suspected abscess requires prompt surgical drainage in addition to antibiotic therapy. Common sites of abscess formation following rhinoplasty include the nasal dorsum, nasal tip, and septum.
A septal abscess usually arises in the setting of an infected septal hematoma that has gone unrecognized or inadequately treated. Treatment of a septal abscess begins with incision and drainage. Packing the abscess site with gauze may aid in local wound debridement and a means of egress for residual infection. Generally, patients should be administered intravenous antibiotics until the infection is under control. Cavernous sinus thrombosis, meningitis, or a brain abscess may result without adequate treatment.
Toxic shock syndrome, an acute, multisystem disease, has been described after nasal surgery with the use of both nasal packing and intranasal splints. Toxic shock syndrome is usually caused by the release of an exotoxin, toxic shock syndrome toxin-1, created by Staphylococcus aureus. The exotoxin acts as a superantigen that causes leukocytes to release massive amounts of proinflammatory cytokines. Symptoms occur early and can include nausea or vomiting, rash, fever, tachycardia, and hypotension. Treatment requires the immediate removal of the offending object, intensive care unit admission, intravenous antibiotics, and supportive care.
When harvesting septal cartilage, most authors recommend preserving a 1-cm-wide septal L-strut that should remain attached to the perpendicular plate of the ethmoid and the nasal spine– maxillary crest area. When L-strut fractures occur, they should be repaired immediately to prevent significant deformity because the cartilaginous septal segment tends to rock posteriorly, resulting in a loss of dorsal support and a saddle-nose deformity.
For fractures of the midportion of the dorsal septal L-strut, the fracture can be stabilized with suture techniques and spreader grafts. When the fracture occurs cephalad to the nasal bone edges, the fractured L-strut can be rigidly fixated using percutaneous Kirschner wires that are placed through the