Complications of Dentoalveolar Surgery

This article explores how to prevent and manage complications of dentoalveolar surgery. Many complications are avoidable. Surgical skills and knowledge of anatomy play an important role in prevention of complications. Prevention starts with detailed history and physical examination of the patient. Key to perioperative management of patients is risk assessment. Without a proper history and physical examination, the clinician is unable to assess the risk of performing surgery and anesthesia for each patient. Some illnesses and medications increase the risk of complications. The following complications are discussed: alveolar osteitis, displacement, fracture, hemorrhage, infection, nonhealing wound, oroantral communication, swelling, and trismus.

Key points

  • The cause of dentoalveolar complications are discussed.

  • Strategies to prevent dentoalveolar complications are stressed.

  • Management of dentoalveolar complications can minimize morbidity and mortality.

Alveolar osteitis

Background

Alveolar osteitis (AO) ( Box 1 ) is commonly known as a “dry socket” because the socket is many times devoid of a blood clot with exposed bone. The disorder is defined as increased fibrinolytic activity within the early postextraction tooth socket probably secondary to a subclinical infection. It is reported to occur in approximately 2% (1%–3%) of routine extractions and 20% (0.5%–37.5%) of impacted mandibular third molar extractions. It usually occurs on the third or fourth day postextraction, although it can occur earlier. The classic triad of AO is: early onset clot lysis, fetor oris, and intense pain. Smoking, oral contraceptives, inexperienced surgeon, poor oral hygiene, increased age, female gender, partial impaction, and periodontal disease have all been reported to increase the risk of AO. ,

Box 1
Alveolar osteitis

Key features
  • Early onset clot lysis

  • Fetor oris

  • Intense pain

Prevention
  • Perioperative antibiotics

  • Preoperative and postoperative chlorhexidine rinse

  • Topical Acemannan hydrogel

  • Topical chlorhexidine gel

Management
  • Irrigation

  • Debridement

  • Sedative dressing place (eugenol, benzocaine, and balsam of Peru)

Prevention

The risk of AO has been reported to be reduced with the use of various agents. Agents that have been used include systemic antibiotics, topical antibiotics, steroids, nonsteroidal anti-inflammatory drugs, clot stabilizers (gelatin sponge, oxidized cellulose, bovine collagen), chlorhexidine mouth rinse, antifibrinolytic agents, antiseptics, and aloe vera. ,

Meta-analyses that investigated the efficacy of prophylactic systemic antibiotic use found a positive effect in reducing the incidence of AO. Tetracycline has been shown to be an effective antibiotic. However, broad- and narrow-spectrum antibiotics have been effective.

Multiple topical agents with and without antibiotics, especially tetracycline, have been used with varying degrees of success. Topical antibiotics can cause delayed healing, giant cell reaction, nerve injury, and myospherulosis from petroleum-based carrier. , Topical SaliCept (Carrington Laboratories, Inc, Irving, TX) reportedly only had a 1.1% incidence of AO compared with 8.0% in the clindamycin group. SaliCept Patch (Carrington Laboratories, Inc) contains Acemannan Hydrogel, a beta-(1,4)-acetylated mannan, obtained from Aloe Vera L.

Routine use of chlorhexidine rinse 1 week preoperatively and for 1 week postoperatively is recommended in the prevention of AO. This regimen resulted in an 8% incidence (38%–60% reduction) of AO following third molar removal. , ,

Management

Once a diagnosis is made the wound is irrigated with saline or mouthwash. Dry socket dressing is placed in the socket. Common ingredients include eugenol, benzocaine, and balsam of Peru. Placement of the ointment on a resorbable gelatin or collagen sponge can avoid dressing changes. Another suggested treatment is socket curettage. Treatment with low-level laser therapy reportedly resulted in a more rapid resolution of signs and symptoms when compared with SaliCept and dry socket dressing.

Displacement

Background

Displacement of teeth, implants, dental restorations, small dental instruments, or injection needles is uncommon but difficult to truly estimate ( Box 2 ). These objects are displaced into the airway, gastrointestinal tract, buccal space, infratemporal fossa, maxillary sinus, sublingual space, submandibular space, lateral pharyngeal space, and the inferior alveolar canal (IAC). The combination of unique anatomy, poor surgical technique, and failure to use safety precautions can result in displacement.

Box 2
Displacement of teeth, restorations, and instruments

Key features
  • Unique anatomy

  • Proximity to other structures

  • Poor surgical technique

  • Failure to use safety precautions

Prevention
  • Oropharyngeal screen

  • Proper flap design

  • Adequate exposure

  • Good surgical technique

Management
  • Three-dimensional imaging for localization

  • Surgical access

  • Navigation based on location

  • Bronchoscopy if aspirated

Prevention

Displacement of root fragments and teeth is sometimes preventable using proper surgical techniques. Proper imaging (plain film and computed tomography [CT] scans) is important in planning the surgical procedure. At the beginning of the procedure an oropharyngeal screen in a conscious patient or a throat pack with umbilical tape during general anesthesia should be used to protect the airway. An adequate flap for visualization and surgical access is an important first step. A broad retractor that rests on the bone, above the level of the tooth or root, can prevent displacement into the buccal or infratemporal space. Displacement of a root into the sinus or through a thin lingual cortex is prevented by proper placement of the dental elevator between the root and the bone socket and avoiding excessive force. Creating a small window above the level of the apex of the root can allow for excellent access and preserve crestal bone.

Management

The tooth can usually be palpated if it is displaced into the buccal or sublingual space. The clinician should attempt to trap the tooth between their finger and the bone. The tooth can then be pushed toward the occlusal edge of the flap and removed with a large hemostat. A tooth or implant that is displaced into the maxillary sinus is usually removed through a window placed in the canine fossa with a suction tip or aid of an endoscope ( Fig. 1 ). Teeth or implants that have been displaced into the submandibular space are approached through an osteotomy along the lingual aspect of the third molar tooth socket, leaving it attached to the lingual mucosa. The lingual aspect of the socket is then out-fractured, allowing more direct visual access to the fragment than the traditional sulcular approach. Removal of fragments that have been displaced into the IAC entails obtaining access through a buccal flap. The IAC is exposed with a small to medium size round bur or pieziotome.

Fig. 1
Displacement of dental implant into the maxillary sinus. ( A ) CT scan showing an oroantral communication during dental implant placement. ( B ) CT scan showing a dental implant in the maxillary sinus. ( C ) Intraoperative view showing a window created into the maxillary sinus. ( D ) Dental implant removed from the maxillary sinus through the sinus window. ( E ) Buccal fat pad flap to close the oroantral communication.

Three-dimensional imaging or films at right angles to each other are used for localization. When a tooth or broken needle is displaced into a deep fascial space, the surgeon should consider the use of navigation in the operating room to help in localization. A maxillofacial CT scan is obtained just before surgery. Depending on surgical approach, it may be beneficial to image the patient with a bite-block in place to accurately reflect the position of the mandible at the time of surgery. In cases where the tooth or root fragment has been displaced into the infratemporal fossa a coronal flap may be needed for access. Aspiration in an awake or moderately sedated patient usually results in violent coughing. If this fails to bring the tooth up, then transfer the patient to the hospital for retrieval via bronchoscopy. Chest and abdominal radiographs may be indicated to localize the tooth.

Fracture

Background

The reported incidence of iatrogenic mandibular fractures associated with the removal of teeth ranges from 0.0034% to 0.0075%. They can occur during the procedure or within the first 4 weeks ( Box 3 ). Iatrogenic mandibular fractures associated with third molar removal may increase with depth of impaction, type of tooth angulation, length of roots, patient age, inexperience of the surgeon, presence of a cyst or tumor around an impacted third molar, systemic disease or medications that may impair bone strength, preoperative infections in the third molar site, and inadequate preoperative examination. In a systematic review, men aged greater than 35 years, with teeth in positions II/III and B/C, complete bony impaction, and local bone alterations, were found to have a higher frequency of fracture.

Box 3
Fracture associated with dentoalveolar surgery

Key features
  • Mandibular third molar risk factors

    • Men >35 y of age

    • Depth of impaction

    • Amount of bone removal

    • Impaired bone healing

  • Maxillary third molar risk factors

    • Lone standing

    • Widely divergent roots

    • Hypereruption

Prevention
  • Tooth sectioning

  • Reduce the amount of bone removal

  • Decreased force applied during removal

Management
  • Usually treated closed

  • Atrophic fractures may require open repair

Fractures associated with implant placement in the atrophic mandible are most commonly reported in the symphysis region. The timing of implant-related mandibular fracture is extremely variable; most occurring either 3 to 6 weeks or 3 months after implant placement, before and after loading. ,

Maxillary tuberosity and alveolar segment fractures can occur during dental extractions and occasionally associated with significant hemorrhage.

Prevention

When removing deeply impacted third molars, it is advisable to perform adequate bone removal, and tooth sectioning, to reduce the amount of bone removal and lessen the force required to remove the tooth. A recent literature review reported 74% of fractures occurred postoperatively, and 26% of pathologic mandibular fractures were observed intraoperatively. A soft diet is recommended for 4 weeks postoperatively, especially in patients with full dentition who have risk factors for mandibular fracture. ,

In the severely atrophic mandible, the clinician should avoid wide diameter implants and penetration through the inferior border of the mandible, which can significantly weaken the jaw. Good oral hygiene, proper maintenance of implants, and proper biomechanics of the restoration can prevent late fractures. Nerve repositioning procedures and alveolar osteotomies can also result in fracture of the body of the mandible in atrophic cases ( Fig. 2 ). ,

Fig. 2
Mandibular fracture after posterior alveolar osteotomy to increase ridge height. ( A ) Preoperative radiograph showing an atrophic left posterior mandible. ( B ) Postoperative radiograph showing left mandibular fracture after a sandwich osteotomy. ( C ) Postoperative radiograph after repair and healing of the left mandibular fracture.

Management

Fractures of the mandible are treated via open or closed reduction. Principles of fracture management must be followed. Implants in the line of fracture are left in place when they are osseointegrated, not mobile, not infected, and are not near areas of osteomyelitis.

Hemorrhage

Background

The rich network of vessels in the head and neck can increase the risk of persistent hemorrhage in the perioperative period ( Box 4 ). The risk of hemorrhage associated with third molar removal is estimated at 0.2% to 1.4%. Causes of bleeding during surgery are caused by local and systemic factors. Local causes of bleeding include normal anatomic structures and pathologic lesions. , Systemic causes include hereditary and acquired coagulopathies and medications. ,

Box 4
Hemorrhage

Key features
  • Sources include

    • Normal anatomy

    • Pathologic lesions

    • Coagulopathies

    • Anticoagulant and antiplatelet medications

Prevention
  • Thorough patient evaluation

  • Avoidance of vessels

  • Identification of vascular lesions

  • Correction of coagulopathies

Management
  • Immediate measures

    • Pressure

    • Topical hemostatic agents

    • Cauterization and ligation

  • Additional measures as indicated

    • Correction of the coagulopathy

    • Transfusion

    • Intubation

    • Embolization

Life-threatening hemorrhage and airway compromise has been reported during dental implant placement in the mandible. , Vessels that may be encountered include the lingual, facial, inferior alveolar, sublingual, submental, mental, buccal, and greater palatine arteries (GPA) and veins.

Pathologic lesions that can bleed if encountered during dentoalveolar procedures include arteriovenous malformation (AVM), hemangioma, giant cell tumor (GCT), aneurysmal bone cyst (ABC). AVMs occur from a lack of differentiation of arteries, veins, and capillaries during development. This results in direct communication between arteries and veins. AVMs grow throughout life and are characterized according to the main vessel type and flow that comprise it. The character of the bleeding from an AVM is usually brisk because of the high pressure and high flow associated with these lesions. Hemangiomas are present at birth if not clinically apparent. They typically appear during the first 2 years of life. Classically a rapid proliferative phase occurs that outpaces body growth. Approximately 50% of hemangiomas involute by age 5 and about 70% by age 7. ABCs are reactive lesions and are associated with other bony lesions. The histologic examination reveals sinusoidal blood spaces devoid of endothelial lining. GCTs are characterized by a proliferation of fibroblast with various amounts of collagen with multinucleated giant cells dispersed throughout. A recent hypothesis is that these lesions be considered proliferative vascular in origin or angiogenesis-dependent ( Fig. 3 ). ,

Fig. 3
Giant cell tumor of the right maxilla. ( A ) Preoperative radiograph showing a radiolucent lesion in the right maxilla with root resorption. ( B ) Intraoperative view of right maxillary sinus lesion. ( C ) Intraoperative view after resection of right maxillary tumor. ( D ) Postoperative radiograph after removal of the right maxillary lesion. ( E ) Intraoperative view after staged bone graft. ( F ) Intraoperative view after reconstruction with implants and epithelial graft. ( G ) Postoperative radiograph after reconstruction of the right maxilla with bone graft and implants.

Systemic disorders associated with an increased risk of bleeding are termed coagulopathies. They are divided into hereditary and acquired causes. The more common hereditary clotting factor deficiencies include hemophilia A, hemophilia B, and von Willebrand disease (VWD). These are x-linked recessive diseases. Hemophilia A and hemophilia B are caused by missing or deficient normal factor VIII and IX, respectively. In the general population the incidence of these disorders is 1:5000 to 10,000 male births for hemophilia A, and 1:20,000 to 34,000 male births for hemophilia B. Mild disease is characterized by 5% to 35% factor level, moderate disease has 1% to 5% factor level, and severe disease has less than 1% factor level. VWD is caused by deficient or defective plasma von Willebrand factor (VWF). It mediates platelet hemostatic function and stabilizing blood coagulation factor VIII. It affects 0.16% to 1% of the population (approximately 1 in 10,000). It is classified into three subtypes. Type 1 VWD is a partial quantitative deficiency of essentially normal VWF. Type 2 VWD is characterized by a qualitative deficiency and defective VWF (further subdivided into types 2A, 2B, 2M, and 2N). Type 3 VWD is a virtually complete quantitative deficiency of VWF. Acquired VWD has been described from multiple causes.

Thrombocytopenia is defined as a platelet count lower than the 2.5th lower percentile of the normal platelet count distribution. However, the adoption of a cutoff value of 100 × 10 9 /L may be more appropriate to identify a pathologic condition. , The major mechanisms for a reduced platelet count are decreased production (eg, aplastic anemia, myelodysplastic syndromes, and chemotherapy-induced thrombocytopenia) and increased destruction of platelets (eg, disseminated intravascular coagulation and the thrombotic microangiopathies). Less common mechanisms are platelet sequestration (congestive splenomegaly) and hemodilution (massive blood transfusion). , Other platelet disorders include adhesion effects, aggregation defects, and granular defects. ,

Medications that prolong bleeding include antiplatelet drugs (cyclooxygenase [COX] inhibitors, GPIIb/IIIa inhibitors, P2Y12 inhibitors, and phosphodiesterase inhibitors) and anticoagulants (direct thrombin inhibitors, indirect thrombin inhibitors, direct Xa inhibitors, and vitamin K antagonist). Additionally, some herbal remedies can interfere with coagulation.

  • COX-1 inhibitors: inhibits COX-1 in such a way that only thromboxane A 2 production is inhibited and not prostaglandin I 2 . Aspirin antiplatelet affects are irreversible and last for the life of the platelet (7–10 days). Other COX-1 inhibitor effects are reversible.

  • GPIIb/IIIa inhibitors: various modes of action to inhibit GPIIb/IIIa.

  • P2Y12 inhibitor: irreversibly binds to the P2Y12 adenosine diphosphate receptors, reducing platelet aggregation and adhesion. The antiplatelet affects are irreversible and last for the life of the platelet (7–10 days).

  • Phosphodiesterase inhibitors: aid in degradation of cyclic adenosine monophosphate and cyclic guanosine monophosphate, two substances that play a pivotal role in platelet activation.

  • Indirect thrombin inhibitors: binds to antithrombin III and accelerates activity, inhibiting thrombin and factor Xa.

  • Direct thrombin inhibitors: directly and reversibly inhibits thrombin by interfering with the conversion of fibrinogen into fibrin.

  • Direct factor Xa inhibitors: bind to factor Xa.

  • Vitamin K antagonist: inhibits vitamin K–dependent coagulation factors and its effect is dose dependent.

Table 1 summarizes the antiplatelet and anticoagulation medications, their half-life, the recommended time for discontinuation of therapy for more invasive procedures, reversal agents, and the recommended management of uncontrolled bleeding. , ,

Table 1
Antiplatelet and anticoagulation medications
Drug Receptor Binding Half-Life Recommended Discontinuation Reversal Treatment
Cox inhibitor
Aspirin Irreversible 2–6 h 5–7 d None Platelet transfusion
Desmopressin
P2Y12 inhibitors
Cangrelor (Inj) Reversible 6 min 90 min None Platelet transfusion
Desmopressin
Clopidogrel Irreversible 6 h 5–7 d
Prasugrel Irreversible 7 h 5–9 d
Ticagrelor Reversible 7–9 h 4–5 d
GP IIb/IIIa inhibitors
Abciximab (Inj) Irreversibly binds 10–30 min 2–3 d None Platelet transfusion
Desmopressin
Cryoprecipitate
Eptifibatide (Inj) Reversibly binds 15 min–2.5 h 8–12 h
Tirofiban (Inj) Reversibly binds 2 h 8 h
Phosphodiesterase inhibitors
Cilostazol 11–13 h 2 d None Platelet transfusion
Desmopressin
Dipyridamole 10 h 2 d
Direct thrombin inhibitors
Argatroban (Inj) 39–51 min 5 h None None
Bivalirudin (Inj) 25–34 min 3 h
Dabigatran 12–17 h 3–4 d Idarucizumab Idarucizumab
Indirect thrombin inhibitors
Dalteparin (Inj) 3–5 h 12–24 h Protamine
Andexanet alpha
Protamine
PCC
Andexanet alpha
Enoxaparin (Inj) 4.5–7 h 12–24 h
Fondaparinux 17–21 h 4 d
Heparin 1.5 h 6–24 h Protamine Protamine
Direct Xa inhibitors
Apixaban 12 h 3 d Protamine
Andexanet alpha
Protamine
PCC
Andexanet alpha
Betrixaban 19–27 h 5 d
Edoxaban 10–14 h 3 d
Rivaroxaban 5–9 h 3 d
Vitamin K antagonist
Warfarin 36 h 5 d Vitamin K PCC
Fresh frozen plasma
Vitamin K

Antiplatelet and anticoagulation medications; half-life, recommended discontinuation time before surgery, reversal agents, and treatment of correct the antiplatelet or anticoagulant medication.
Abbreviation: Inj, Injectable; PCC, prothrombin complex concentrate.

Prevention

Damage to the GPA is avoided by placing full-thickness incisions in the midline or along the palatal gingival crevice. A subperiosteal dissection can proceed to and around the foramen with care. The greater palatine foramen was palatal to the second molar (35.7%), and, interproximal to the second and third molars (35.7%) in women, and palatal to the second molar in men (65%). When harvesting connective tissue grafts, partial-thickness incisions are generally placed in the premolar region and anteriorly to avoid the GPA. The GPA branches most frequently at the level of first premolar (38%) and at the first and second molar region (43%) in women. In men, branching was commonly observed at the level of first and second premolars region (56%), and at the level of second and third molars region (32%). The sublingual artery is avoided by performing a subperiosteal dissection along the lingual aspect of the mandible. Life-threatening hemorrhage can occur during implant placement secondary to lingual cortical perforation. , In the inferior neurovascular bundle, the vein was superior to the nerve and there are often multiple veins. The artery was solitary and lingual to the nerve, slightly above the horizontal position. This position seemed to be consistent in all cases. Thus, it is possible to have injury to the vessels without injury to the nerves.

Vascular lesions may seem to be a periapical granuloma or abscess on plain films. Many patients give a history of previous episodes of bleeding from the area. When performing a biopsy of a radiolucent lesion, it is recommended that needle aspiration be performed first. When the aspirate is blood under pressure the lesion is considered to be an AVM until proven otherwise. Bleeding from these lesions is life threatening, thus additional work-up is indicated, including a CT scan with contrast. If the aspirate is blood but low flow, then other lesions should be considered, such as an ABC or GCT.

The two main treatments for VWD are desmopressin (1-deamino-8-Darginine vasopressin) and clotting factor concentrates containing VWF and FVIII (VWF/FVIII concentrate). For surgical procedures where significant bleeding is anticipated the goal is to achieve a factor level between 60% and 100%, depending on the type of hemophilia. The use of epsilon aminocaproic acid can help with clot stabilization and reduce the need for additional factor after tooth extraction. Thrombocytopenia is managed by transfusion with platelets. Platelet counts less than 30,000 to 50,000 are usually transfused when performing procedures that are more invasive. , Patients with end-stage liver disease must be thoroughly evaluated to determine the risk of bleeding. International normalized ratio (INR) close to a normal range is recommended in these patients because of a significant risk of bleeding.

When discontinuing antiplatelet and anticoagulant therapies, it is important to consult the prescribing physician to determine whether bridging-therapy with enoxaparin or heparin is indicated. This is always indicated in high-risk patients, to shorten the time they are at risk for a thrombotic event. It is considered safe to proceed with minor dentoalveolar procedures, such as dental extractions, when the patient’s INR is between 2 and 4. Surgical extractions and dentoalveolar procedures with significant risk of bleeding require an INR of less than 2 or discontinuing other antiplatelet and anticoagulant therapy.

  • Low risk for thrombotic event

    • 1.

      When indicated, consult the prescribing physician regarding holding anticoagulant therapy.

    • 2.

      Hold anticoagulant and antiplatelet therapy based on recommendations (see Table 1 ).

  • High risk for thrombotic event

    • 1.

      When indicated, consult the prescribing physician regarding holding anticoagulant therapy.

    • 2.

      Hold anticoagulant and antiplatelet therapy based on recommendations (see Table 1 ).

    • 3.

      Begin bridging therapy with short-acting anticoagulant (eg, enoxaparin) the day after holding anticoagulant.

    • 4.

      Hold short-acting anticoagulant on the morning of surgery based on half-life.

    • 5.

      After surgery, restart short-acting anticoagulant based on current recommendations.

    • 6.

      Restart long-acting anticoagulant when considered safe, based on type of surgery.

Laboratory monitoring of the newer anticoagulants is not usually recommended. Ecarin clotting time is the most sensitive assay for monitoring dabigatran, but it is not readily available. Thrombin time has been reported to be inaccurate at high concentrations of dabigatran. Because rivaroxaban and apixaban inhibit factor Xa levels, ecarin clotting time or thrombin time are not affected. Activated partial thromboplastin time is the best test for monitoring dabigatran, but sensitivity is reduced at higher concentrations. Although activated partial thromboplastin time also may be prolonged by rivaroxaban, the activated partial thromboplastin time is less reliable than prothrombin time at high concentrations of rivaroxaban. , The chromogenic anti-FXa assay is used to quantitatively measure the anticoagulant activity of the FXa inhibitors.

Management

When acute hemorrhage is encountered from an extraction site, digital pressure is placed. The socket should be packed tightly with a hemostatic agent, such as a gelatin sponge or oxidized cellulose. The socket is sutured in a figure-of-eight fashion. Pressure with gauze is held for 20 to 30 minutes. With soft tissue bleeding or bone sources that are not as easily packed, other techniques must be used. Digital pressure is the first line of treatment. Electrocautery is used for small vessels, whereas larger vessels are usually ligated.

If the bleeding is not controlled with these maneuvers, then transport the patient to the hospital. Intravenous (IV) access must be established and fluid resuscitation started with lactated Ringer or normal saline. If the airway is compromised secondary to the amount of bleeding or airway swelling, then secure the airway with a laryngeal mask or endotracheal tube. In some cases, a surgical airway must be established. Once in the hospital, consider blood transfusion with O or type and crossmatched blood. The restrictive transfusion strategy is a threshold for transfusion of red blood cells for a hemoglobin level of 7 g/dL, with a target of 7 to 9 g/dL (70–90 g/L) in adults and most children. , , A more liberal transfusion strategy is recommended for preterm infants or children with cyanotic heart disease, severe hypoxemia, active blood loss, or hemodynamic instability with a threshold of 9.5 g/dL and a target of 11 to 12 g/dL. , , Laboratory test should include prothrombin time (INR), partial thromboplastin time, and complete blood count with platelets. CT scan with contrast is beneficial in evaluating pathology (neoplasm or hematoma).

When normal structures are the source of the bleeding or when a pathologic lesion is the source of hemorrhage, ligation or embolization is the treatment of choice. The choice is determined by the accessibility to the source of bleeding and potential complexity of surgery. Ligation close to the source of bleeding is more effective than external carotid ligation because of the rich anastomosis of vessels in the head and neck. Selective embolization is recommended for AVMs, bleeding sources that are difficult to access, and/or have failed previous surgery.

When a coagulopathy is suspected to be the cause of the bleeding, this must be corrected. Additional laboratory test that may be helpful include clotting factor assay. This takes valuable time and treatment cannot be delayed while waiting for results. Acute correction of a coagulopathy is performed with the use of fresh frozen plasma (FFP) or prothrombin complex concentrates (PCCs). Plasma transfusion is recommended in patients with active bleeding and an INR greater than 1.6 or before an invasive procedure or surgery if a patient has been anticoagulated. Platelet transfusion is indicated for the management of patients on antiplatelet therapy or patients with thrombocytopenia of less than 20,000 or between 20,000 and 30,000 when there is active bleeding.

PCCs are concentrated pooled plasma products that typically contain three (factors II, IX, and X) or four (factors II, VII, IX, and X) clotting factors. PCCs have been reported to have advantages over FFP. PCCs correct the INR more rapidly than does FFP in patients taking warfarin who develop nontraumatic intracranial hemorrhage. Preparation time for PCCs is shorter than for FFP, which must be thawed before use. PCCs contain a higher concentration of clotting factors than FFP, thus smaller infusion volumes are required. ,

Delayed bleeding after a surgical procedure is just as serious as immediate hemorrhage. When the patient calls or returns to the office with the concern of postoperative bleeding, the clinician must determine the amount and intensity of the bleeding. If the bleeding is slow, then pressure with gauze over the site may be helpful. When bleeding is moderate to severe or has occurred over a prolonged period, then the patient should return to the office or go to the emergency room of a hospital. Of particular concern is an expanding hematoma because of the potential for airway issues. Pressure over the suspected source, airway management, CT scan with contrast, and laboratory data should be part of the initial management. The definitive management may require embolization and/or surgery, and correction of any coagulopathy.

Infection

Background

As categorized by the American Society of Health-System Pharmacists, most of the dentoalveolar procedures are classified as clean-contaminated (procedures that violate the gastrointestinal or respiratory tract), and contaminated (procedures in acute inflammation situations). In a systematic review on lower third molar surgery, the incidence of infection in the control groups ranged from 0% to 14.8% , and from 0% to 6.5% in the antibiotic prophylaxis groups. , , The bacteria associated with surgical site infections (SSI) for dentoalveolar procedures are usually opportunistic, from the existing microflora of the oral cavity. The culturable bacterial microbiota of the saliva is dominated by the Streptococcus , Prevotella , and Veillonella genera, which comprise 70% of this microbiota. The most predominant bacteria in the oral cavity include Fusobacteria, Actinobacteria, Proteobacteria, Bacteroidetes, and Spirochaete ( Box 5 ). , When categorizing the microbiota by location in the oral cavity, most sites are dominated by the Streptococcus genus, followed by Hemophilus in the buccal mucosa, Actinomyces in the supragingival plaque, and Prevotella in the subgingival plaque. ,

Box 5
Infection

Key features
  • Risk of infection is low

  • Predominant bacteria in the oral cavity

    • Fusobacteria, Actinobacteria, Proteobacteria, Bacteroidetes, and Spirochaeta

Prevention
  • Perioperative antibiotics especially in the immunocompromised

Management
  • Irrigation

  • Debridement

  • Antibiotics of choice

    • Penicillins

    • Clindamycin

  • Antibiotics for resistant organisms

    • B-lactamase inhibitors

    • Flagyl

    • Cephalosporins

    • Fluoroquinolones

Prevention

Patient-related risk factors, such as poor nutritional status, smoking, diabetes, and impaired immune system, can increase the risk of SSI and must be taken into consideration. A systematic review of latest evidence on the use of prophylactic antibiotic in oral surgical procedures reported no justification for antibiotics when performing intra-alveolar dental extraction. For third molar surgery, there is good evidence to support the use of perioperative antibiotics, , but three meta-analyses concluded no support for routine prescription for healthy people undergoing third molar removal.

For dental implants, there is good evidence that perioperative antibiotic as a single-shot prophylaxis before placement can reduce dental implant failure but not SSI. A retrospective study with high risk of bias found antibiotics for 7 days effective in implant survival. However, other studies with low risk of bias reported no statistically significant differences in survival between single-shot prophylaxis and a prolonged postoperative course of antibiotics. , Thus, except in patients with an increased risk of infection, only perioperative antibiotics are recommended for routine dentoalveolar surgeries.

Management

An important aspect of treatment is reduction of the bacterial load by incision and drainage if an abscess has developed, wound debridement to remove necrotic tissue, and wound irrigation. Amoxicillin and clindamycin provide adequate coverage for the usual organisms that are encountered for odontogenic infections after dentoalveolar alveolar procedures. Estimates of penicillin and clindamycin resistance vary but some reports are as high as 20%. B-lactamase inhibitor, or Flagyl are often added to the regimen to expand coverage. Less resistance is seen with cephalosporins and fluoroquinolones and could be considered.

Although not the scope of this article, patients that are immunocompromised, or that develop deep space infections, airway compromise, sepsis, other complications of deep space infections or osteomyelitis, usually require admission to the hospital for more aggressive management.

Nonhealing wound

Background

Failure of a wound to heal can result from local and systemic disorders. Medications that suppress steps of wound healing, radiation therapy, and nutritional deficiencies can have devastating effect on the body’s ability to heal. These are initialed by dentoalveolar surgery but are associated with trauma or uncertain cause ( Box 6 ).

Oct 10, 2020 | Posted by in Oral and Maxillofacial Surgery | Comments Off on Complications of Dentoalveolar Surgery
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