Pediatrics

 Compartment syndrome (CS) is one of the true orthopedic emergencies. Identifying the high-risk patient, making a prompt diagnosis, and initiating effective treatment are the crucial steps in avoiding a poor outcome. A physician’s inability to communicate with young children can interfere with diagnosing CS in a timely fashion. Many young patients in hospitals are admitted to pediatric floors where routine orthopedic care is not the norm and staff are unfamiliar with the signs and symptoms of evolving CS. As orthopedic surgeons are often involved in caring for these patients, they should be aware of the aspects of CS that are unique to children and should be able to identify patients who are at risk and would benefit from close monitoring. In addition, given the consequences of late diagnosis, early diagnosis is important from a medicolegal standpoint. Only 44% of cases of adult and pediatric CS are decided in favor of treating physicians, compared with 75% of cases in other orthopedic malpractice claims.1,2

Risk Factors for Posttraumatic Compartment Syndrome

Supracondylar Humeral Fracture

CS is a well-described complication of this injury. CS develops in 0.1% to 0.3% of children who present with supracondylar humeral fracture.^3,4 Casted elbow flexion beyond 90° and concomitant vascular injury put these children at increased risk for CS. Mubarak and Carroll⁵ reported 9 cases of CS in the volar compartment of the forearm after an extension-type supracondylar humeral fracture and attributed 8 of them to elbow flexion beyond 90° after closed reduction. In 29 children with supracondylar humeral fracture,Battaglia and colleagues³ found the highest compartment pressure in the deep volar compartment, especially near the fracture site, as well as a significant increase in pressure with the elbow flexed beyond 90°.

In a study of children with supracondylar humeral fracture, Choi and colleagues⁶ found 2 cases of CS among 9 patients who presented with a pulseless, poorly perfused hand and no cases of CS among 24 patients who presented with a pulseless but well-perfused hand.

Studies have found that a treatment delay of 8 to 12 hours did not increase the rate of CS in Gartland type 2 and type 3 fractures.^7-10 The investigators in these studies did not recommend delaying treatment of patients with neurologic deficit and absent radial pulse. Ramachandran and colleagues4 reported 11 cases of CS in patients with low-energy supracondylar humeral fracture and intact radial pulse at presentation. The patients who developed CS presented with severe swelling, and their mean treatment delay was 22 hours (range, 6-64 hours). Given the data, we do not recommend delayed treatment for children with supracondylar humeral fracture and neurologic deficit or absent pulse. We do recommend close inpatient preoperative monitoring of patients with severe swelling.

CS after supracondylar humeral fracture is mostly seen in the volar compartment of the forearm, but it has also been reported in the mobile wad, the anterior arm compartment, and the posterior arm compartment.^11,12

Floating Elbow

CS has been reported in children with ipsilateral humeral and forearm fractures. Blakemore and colleagues¹³ reported a 33% rate of CS in children with displaced distal humeral and forearm fractures. A retrospective review of 16 cases of floating elbow treated at Boston Children’s Hospital found CS in 2 patients and incipient CS in 4 of 10 patients with forearm fractures treated with closed reduction and plaster casting. There were no signs of CS in 6 patients with distal humeral and forearm fractures stabilized with Kirschner wires.¹⁴ Given the data, we do not recommend circumferential casting for forearm fractures in children with floating elbow.

Forearm Fracture

Haasbeek and Cole¹⁵ reported CS in 5 (11%) of 46 children with open forearm fracture. Yuan and colleagues¹⁶ reported CS in 3 (6%) of 50 open forearm fractures and 3 of 30 closed fractures treated with closed reduction and intramedullary nailing. They found increased risk for CS in patients with longer operative time, indicating prolonged closed manipulation of these fractures as a risk factor for CS. They did not find any cases of CS among 205 forearm fractures treated with closed reduction and casting.

Flynn and colleagues17 reported CS in 2 of 30 patients treated with intramedullary nailing within 24 hours of injury and in 0 of 73 patients treated after 24 hours.

Blackman and colleagues¹⁸ reported CS in 3 (7.7%) of 39 open forearm fractures and 0 of 74 closed fractures treated operatively. In their series, a small incision was made to facilitate reduction in 38 (51.4%) of 74 closed fractures to decrease closed manipulation and operative time. The rate of CS after intramedullary nailing of closed forearm fractures was lower in this series than in similar reports in the literature.

Reported data indicate increased risk for CS in children with open forearm fractures and fractures treated with closed reduction and intramedullary nailing, especially performed within 24 hours of injury, and prolonged closed manipulation performed during surgery. We recommend close monitoring of all children with operatively treated forearm fractures and, in particular, children with the risk factors mentioned.

Femoral Fracture

Although CS after femoral shaft fractures is not common, CS has been reported after 90/90 spica casting of femoral shaft fractures in children. Mubarak and colleagues19 reported on 9 children who developed calf CS after treatment of femoral shaft fracture in 90/90 spica casts. The technique used in 7 of the 9 reported cases involved initial application of a short leg cast and then traction applied to the leg—believed to cause impinging of the cast on the posterior compartment of the leg. The authors recommended an alternative method of applying spica casts, which is beyond the scope of this review.

Tibial Fracture

Children with tibial fracture, especially a fracture sustained in a motor vehicle accident, are at risk for CS. Hope and Cole²⁰ found CS in 4 (4%) of 92 children with open tibial fracture.

Children with tibial tubercle fracture are at increased risk for CS because of concomitant vascular injury. Pandya and colleagues²¹ reported CS or vascular compromise in 4 of 40 patients with tibial tubercle fracture. We recommend close monitoring for signs of impending CS in children who present with high-energy tibial shaft fracture and tibial tubercle fracture.

Flynn and colleagues²² reported outcomes of 43 cases of acute CS of the leg in children treated at 2 pediatric trauma centers. Mean time from injury to fasciotomy was 20.5 hours (range, 3.9-118 hours). Functional outcome was excellent at time of follow-up; 41 of 43 cases had no sequelae, and the 2 patients who lost function underwent fasciotomy more than 80 hours after injury. Despite the long interval between injury and surgery, excellent results were achieved with fasciotomy, suggesting an increased potential for recovery in the pediatric population.

Mubarak²³ reported on 6 cases of distal tibial physis fracture in patients who presented with severe pain and swelling of the ankle, hyposthesia of the first web space, weakness of the extensor hallucis longus and extensor digitorum communis, and pain on passive flexion of the toes. In all these patients, intramuscular pressure was more than 40 mm Hg beneath the extensor retinaculum and less than 20 mm Hg in the anterior compartment. All patients experienced prompt relief of pain and improved sensation and strength within 24 hours after release of the superior extensor retinaculum and fracture stabilization.

Miscellaneous and Nontraumatic Causes of Compartment Syndrome

Neonatal CS is very rare, and diagnosis is often missed. Neonatal CS is thought to be caused by a combination of low neonatal blood pressure and birth trauma.²⁴ Ragland and colleagues²⁵ reported on 24 cases of neonatal CS; in only 1 case was the diagnosis made within 24 hours.They described a “sentinel skin lesion” on the forearm of each patient as the sign of neonatal CS. Late diagnosis results in contracture and growth arrest of the involved extremity. In their series, only 1 patient underwent fasciotomy within 24 hours, and it resulted in a good functional outcome. High clinical suspicion is the key to early diagnosis and treatment of this rare pathology.

Medical problems that cause intracompartmental bleeding (hepatic failure, renal failure, leukemia, hemophilia) have been cited as causing CS.^26-28 CS may be the first symptom of occult hemophilia²⁹ Correction of the coagulation defect may take priority over surgical treatment in these cases, though the decision should be made on a case-by-case basis.²⁶

CS in children can also be caused by snakebites. Shaw and Hosalkar³⁰ reported on successful use of antivenin in preventing the need for surgical treatment in 16 of 19 patients with rattlesnake bites. Two patients had limited surgical débridement, and 1 underwent fasciotomy for CS. The authors recommended using antivenin to prevent CS in children with snakebites.³⁰

Prasarn and colleagues² reported on 12 cases of upper extremity CS in children in the absence of fractures. Of the 12 patients, 10 were managed in an intensive care unit and had an obtunded sensorium. Etiology in 7 (58%) of the 12 cases was iatrogenic (intravenous infiltration, retained phlebotomy tourniquet). In this series, 4 amputations were performed on affected extremities.

Diagnosis

Identification of evolving CS in a child is difficult because of the child’s limited ability to communicate and anxiety about being examined by a stranger. Orthopedists are trained to look for the 5 Ps (pain, paresthesia, paralysis, pallor, pulselessness) associated with CS. Examining an anxious, frightened young child is difficult, and documenting the degree of pain is not practical in a child who may not be able or willing to communicate effectively.

In a series of 33 children with CS, Bae and colleagues³¹ found that the 5 Ps were relatively unreliable in making a timely diagnosis. The authors also found that increased analgesic use was documented a mean of 7.3 hours before a change in vascular status and that it was a more sensitive indicator of CS in children. The resulting recommendation is that children at risk for CS be closely monitored for the 3 As (increasing analgesic requirement, anxiety, agitation).³²

Regional anesthesia is used to control postoperative pain in adults and children.^33,34 Injudicious use may mask the primary symptom (pain) of CS.^32,35-38 Use of regional anesthesia in patients at high risk for CS is highly discouraged.

Although CS is a clinical diagnosis, compartment pressure measurements can be useful in making decisions in certain clinical scenarios. In an obtunded child or in a child with severe mental and communication disability, such a measurement can help confirm or rule out the diagnosis.

Normal compartment pressures are higher in children than in adults. Staudt and colleagues³⁹ compared pressures in 4 lower leg compartments of 20 healthy children and 20 healthy adults. Mean pressure varied from 13.3 mm Hg to 16.6 mm Hg in children and from 5.2 mm Hg to 9.7 mm Hg in adults—indicating higher normal pressure in lower leg compartments in children.

Compartment pressures were reported highest within 5 cm of the fracture site.⁴⁰ When clinically indicated, they should be measured in that area in an injured extremity. The pressure threshold that requires fasciotomy is debatable. Intracompartmental pressures of 30 to 45 mm Hg, or measurements less than 30 mm Hg of diastolic blood pressure (pressure change = diastolic blood pressure – compartment pressure), have been recommended as cutoffs by some authors.^41-44 As resting normal compartment pressures are higher in children, these cutoffs cannot be used as reliably in children as in adults. Direct measurement of intracompartmental pressure is invasive and can be difficult in an agitated, awake child. The potential utility of near-infrared spectroscopy in the diagnosis of increased compartment pressure has been reported.^45,46 This method uses differential light absorption properties of oxygenated hemoglobin to measure tissue ischemia—similar to the method used in pulse oximetry. Compared with pulse oximetry, near-infrared spectroscopy can sample deeper tissue (3 cm below skin level). Shuler and colleagues⁴⁵ reported near-infrared spectroscopy findings for 14 adults with acute CS. Lower tissue oxygenation levels correlated with increased intracompartmental pressures, but the authors could not define a cutoff for which near-infrared spectroscopy measurements would indicate significant tissue ischemia. Use of this method in diagnosing CS in children was described in a case report.⁴⁶

CS remains a clinical diagnosis. Informing family and staff about the signs and symptoms of this syndrome and closely monitoring analgesic use in these patients are crucial. Compartment pressure measurements can be used when the diagnosis is unclear, particularly in noncommunicative patients, but these values should be interpreted with caution.

Treatment

Once CS is diagnosed, emergent fasciotomy and decompression are indicated. Surgeons planning fasciotomy should be aware of the definitive treatment of the CS etiology. Treatment of clotting deficiency in cases caused by excessive bleeding, fracture fixation, and vascular repair may be indicated during fasciotomy and decompression.

Summary

Increased need for analgesics is often the first sign of CS in children and should be considered the sentinel alarm for ongoing tissue necrosis. CS remains a clinical diagnosis, and compartment pressure should be measured only as a confirmatory test in noncommunicative patients or when the diagnosis is unclear. Children with supracondylar humeral fractures, forearm fractures, tibial fractures, and medical risk factors for coagulopathy are at increased risk and should be monitored closely. When the diagnosis is made promptly and the condition is treated with fasciotomy, good long-term clinical results can be expected.

 Compartment syndrome (CS) is one of the true orthopedic emergencies. Identifying the high-risk patient, making a prompt diagnosis, and initiating effective treatment are the crucial steps in avoiding a poor outcome. A physician’s inability to communicate with young children can interfere with diagnosing CS in a timely fashion. Many young patients in hospitals are admitted to pediatric floors where routine orthopedic care is not the norm and staff are unfamiliar with the signs and symptoms of evolving CS. As orthopedic surgeons are often involved in caring for these patients, they should be aware of the aspects of CS that are unique to children and should be able to identify patients who are at risk and would benefit from close monitoring. In addition, given the consequences of late diagnosis, early diagnosis is important from a medicolegal standpoint. Only 44% of cases of adult and pediatric CS are decided in favor of treating physicians, compared with 75% of cases in other orthopedic malpractice claims.1,2

Risk Factors for Posttraumatic Compartment Syndrome

Supracondylar Humeral Fracture

CS is a well-described complication of this injury. CS develops in 0.1% to 0.3% of children who present with supracondylar humeral fracture.^3,4 Casted elbow flexion beyond 90° and concomitant vascular injury put these children at increased risk for CS. Mubarak and Carroll⁵ reported 9 cases of CS in the volar compartment of the forearm after an extension-type supracondylar humeral fracture and attributed 8 of them to elbow flexion beyond 90° after closed reduction. In 29 children with supracondylar humeral fracture,Battaglia and colleagues³ found the highest compartment pressure in the deep volar compartment, especially near the fracture site, as well as a significant increase in pressure with the elbow flexed beyond 90°.

In a study of children with supracondylar humeral fracture, Choi and colleagues⁶ found 2 cases of CS among 9 patients who presented with a pulseless, poorly perfused hand and no cases of CS among 24 patients who presented with a pulseless but well-perfused hand.

Studies have found that a treatment delay of 8 to 12 hours did not increase the rate of CS in Gartland type 2 and type 3 fractures.^7-10 The investigators in these studies did not recommend delaying treatment of patients with neurologic deficit and absent radial pulse. Ramachandran and colleagues4 reported 11 cases of CS in patients with low-energy supracondylar humeral fracture and intact radial pulse at presentation. The patients who developed CS presented with severe swelling, and their mean treatment delay was 22 hours (range, 6-64 hours). Given the data, we do not recommend delayed treatment for children with supracondylar humeral fracture and neurologic deficit or absent pulse. We do recommend close inpatient preoperative monitoring of patients with severe swelling.

CS after supracondylar humeral fracture is mostly seen in the volar compartment of the forearm, but it has also been reported in the mobile wad, the anterior arm compartment, and the posterior arm compartment.^11,12

Floating Elbow

CS has been reported in children with ipsilateral humeral and forearm fractures. Blakemore and colleagues¹³ reported a 33% rate of CS in children with displaced distal humeral and forearm fractures. A retrospective review of 16 cases of floating elbow treated at Boston Children’s Hospital found CS in 2 patients and incipient CS in 4 of 10 patients with forearm fractures treated with closed reduction and plaster casting. There were no signs of CS in 6 patients with distal humeral and forearm fractures stabilized with Kirschner wires.¹⁴ Given the data, we do not recommend circumferential casting for forearm fractures in children with floating elbow.

Forearm Fracture

Haasbeek and Cole¹⁵ reported CS in 5 (11%) of 46 children with open forearm fracture. Yuan and colleagues¹⁶ reported CS in 3 (6%) of 50 open forearm fractures and 3 of 30 closed fractures treated with closed reduction and intramedullary nailing. They found increased risk for CS in patients with longer operative time, indicating prolonged closed manipulation of these fractures as a risk factor for CS. They did not find any cases of CS among 205 forearm fractures treated with closed reduction and casting.

Flynn and colleagues17 reported CS in 2 of 30 patients treated with intramedullary nailing within 24 hours of injury and in 0 of 73 patients treated after 24 hours.

Blackman and colleagues¹⁸ reported CS in 3 (7.7%) of 39 open forearm fractures and 0 of 74 closed fractures treated operatively. In their series, a small incision was made to facilitate reduction in 38 (51.4%) of 74 closed fractures to decrease closed manipulation and operative time. The rate of CS after intramedullary nailing of closed forearm fractures was lower in this series than in similar reports in the literature.

Reported data indicate increased risk for CS in children with open forearm fractures and fractures treated with closed reduction and intramedullary nailing, especially performed within 24 hours of injury, and prolonged closed manipulation performed during surgery. We recommend close monitoring of all children with operatively treated forearm fractures and, in particular, children with the risk factors mentioned.

Femoral Fracture

Although CS after femoral shaft fractures is not common, CS has been reported after 90/90 spica casting of femoral shaft fractures in children. Mubarak and colleagues19 reported on 9 children who developed calf CS after treatment of femoral shaft fracture in 90/90 spica casts. The technique used in 7 of the 9 reported cases involved initial application of a short leg cast and then traction applied to the leg—believed to cause impinging of the cast on the posterior compartment of the leg. The authors recommended an alternative method of applying spica casts, which is beyond the scope of this review.

Tibial Fracture

Children with tibial fracture, especially a fracture sustained in a motor vehicle accident, are at risk for CS. Hope and Cole²⁰ found CS in 4 (4%) of 92 children with open tibial fracture.

Children with tibial tubercle fracture are at increased risk for CS because of concomitant vascular injury. Pandya and colleagues²¹ reported CS or vascular compromise in 4 of 40 patients with tibial tubercle fracture. We recommend close monitoring for signs of impending CS in children who present with high-energy tibial shaft fracture and tibial tubercle fracture.

Flynn and colleagues²² reported outcomes of 43 cases of acute CS of the leg in children treated at 2 pediatric trauma centers. Mean time from injury to fasciotomy was 20.5 hours (range, 3.9-118 hours). Functional outcome was excellent at time of follow-up; 41 of 43 cases had no sequelae, and the 2 patients who lost function underwent fasciotomy more than 80 hours after injury. Despite the long interval between injury and surgery, excellent results were achieved with fasciotomy, suggesting an increased potential for recovery in the pediatric population.

Mubarak²³ reported on 6 cases of distal tibial physis fracture in patients who presented with severe pain and swelling of the ankle, hyposthesia of the first web space, weakness of the extensor hallucis longus and extensor digitorum communis, and pain on passive flexion of the toes. In all these patients, intramuscular pressure was more than 40 mm Hg beneath the extensor retinaculum and less than 20 mm Hg in the anterior compartment. All patients experienced prompt relief of pain and improved sensation and strength within 24 hours after release of the superior extensor retinaculum and fracture stabilization.

Miscellaneous and Nontraumatic Causes of Compartment Syndrome

Neonatal CS is very rare, and diagnosis is often missed. Neonatal CS is thought to be caused by a combination of low neonatal blood pressure and birth trauma.²⁴ Ragland and colleagues²⁵ reported on 24 cases of neonatal CS; in only 1 case was the diagnosis made within 24 hours.They described a “sentinel skin lesion” on the forearm of each patient as the sign of neonatal CS. Late diagnosis results in contracture and growth arrest of the involved extremity. In their series, only 1 patient underwent fasciotomy within 24 hours, and it resulted in a good functional outcome. High clinical suspicion is the key to early diagnosis and treatment of this rare pathology.

Medical problems that cause intracompartmental bleeding (hepatic failure, renal failure, leukemia, hemophilia) have been cited as causing CS.^26-28 CS may be the first symptom of occult hemophilia²⁹ Correction of the coagulation defect may take priority over surgical treatment in these cases, though the decision should be made on a case-by-case basis.²⁶

CS in children can also be caused by snakebites. Shaw and Hosalkar³⁰ reported on successful use of antivenin in preventing the need for surgical treatment in 16 of 19 patients with rattlesnake bites. Two patients had limited surgical débridement, and 1 underwent fasciotomy for CS. The authors recommended using antivenin to prevent CS in children with snakebites.³⁰

Prasarn and colleagues² reported on 12 cases of upper extremity CS in children in the absence of fractures. Of the 12 patients, 10 were managed in an intensive care unit and had an obtunded sensorium. Etiology in 7 (58%) of the 12 cases was iatrogenic (intravenous infiltration, retained phlebotomy tourniquet). In this series, 4 amputations were performed on affected extremities.

Diagnosis

Identification of evolving CS in a child is difficult because of the child’s limited ability to communicate and anxiety about being examined by a stranger. Orthopedists are trained to look for the 5 Ps (pain, paresthesia, paralysis, pallor, pulselessness) associated with CS. Examining an anxious, frightened young child is difficult, and documenting the degree of pain is not practical in a child who may not be able or willing to communicate effectively.

In a series of 33 children with CS, Bae and colleagues³¹ found that the 5 Ps were relatively unreliable in making a timely diagnosis. The authors also found that increased analgesic use was documented a mean of 7.3 hours before a change in vascular status and that it was a more sensitive indicator of CS in children. The resulting recommendation is that children at risk for CS be closely monitored for the 3 As (increasing analgesic requirement, anxiety, agitation).³²

Regional anesthesia is used to control postoperative pain in adults and children.^33,34 Injudicious use may mask the primary symptom (pain) of CS.^32,35-38 Use of regional anesthesia in patients at high risk for CS is highly discouraged.

Although CS is a clinical diagnosis, compartment pressure measurements can be useful in making decisions in certain clinical scenarios. In an obtunded child or in a child with severe mental and communication disability, such a measurement can help confirm or rule out the diagnosis.

Normal compartment pressures are higher in children than in adults. Staudt and colleagues³⁹ compared pressures in 4 lower leg compartments of 20 healthy children and 20 healthy adults. Mean pressure varied from 13.3 mm Hg to 16.6 mm Hg in children and from 5.2 mm Hg to 9.7 mm Hg in adults—indicating higher normal pressure in lower leg compartments in children.

Compartment pressures were reported highest within 5 cm of the fracture site.⁴⁰ When clinically indicated, they should be measured in that area in an injured extremity. The pressure threshold that requires fasciotomy is debatable. Intracompartmental pressures of 30 to 45 mm Hg, or measurements less than 30 mm Hg of diastolic blood pressure (pressure change = diastolic blood pressure – compartment pressure), have been recommended as cutoffs by some authors.^41-44 As resting normal compartment pressures are higher in children, these cutoffs cannot be used as reliably in children as in adults. Direct measurement of intracompartmental pressure is invasive and can be difficult in an agitated, awake child. The potential utility of near-infrared spectroscopy in the diagnosis of increased compartment pressure has been reported.^45,46 This method uses differential light absorption properties of oxygenated hemoglobin to measure tissue ischemia—similar to the method used in pulse oximetry. Compared with pulse oximetry, near-infrared spectroscopy can sample deeper tissue (3 cm below skin level). Shuler and colleagues⁴⁵ reported near-infrared spectroscopy findings for 14 adults with acute CS. Lower tissue oxygenation levels correlated with increased intracompartmental pressures, but the authors could not define a cutoff for which near-infrared spectroscopy measurements would indicate significant tissue ischemia. Use of this method in diagnosing CS in children was described in a case report.⁴⁶

CS remains a clinical diagnosis. Informing family and staff about the signs and symptoms of this syndrome and closely monitoring analgesic use in these patients are crucial. Compartment pressure measurements can be used when the diagnosis is unclear, particularly in noncommunicative patients, but these values should be interpreted with caution.

Treatment

Once CS is diagnosed, emergent fasciotomy and decompression are indicated. Surgeons planning fasciotomy should be aware of the definitive treatment of the CS etiology. Treatment of clotting deficiency in cases caused by excessive bleeding, fracture fixation, and vascular repair may be indicated during fasciotomy and decompression.

Summary

Increased need for analgesics is often the first sign of CS in children and should be considered the sentinel alarm for ongoing tissue necrosis. CS remains a clinical diagnosis, and compartment pressure should be measured only as a confirmatory test in noncommunicative patients or when the diagnosis is unclear. Children with supracondylar humeral fractures, forearm fractures, tibial fractures, and medical risk factors for coagulopathy are at increased risk and should be monitored closely. When the diagnosis is made promptly and the condition is treated with fasciotomy, good long-term clinical results can be expected.

 Compartment syndrome (CS) is one of the true orthopedic emergencies. Identifying the high-risk patient, making a prompt diagnosis, and initiating effective treatment are the crucial steps in avoiding a poor outcome. A physician’s inability to communicate with young children can interfere with diagnosing CS in a timely fashion. Many young patients in hospitals are admitted to pediatric floors where routine orthopedic care is not the norm and staff are unfamiliar with the signs and symptoms of evolving CS. As orthopedic surgeons are often involved in caring for these patients, they should be aware of the aspects of CS that are unique to children and should be able to identify patients who are at risk and would benefit from close monitoring. In addition, given the consequences of late diagnosis, early diagnosis is important from a medicolegal standpoint. Only 44% of cases of adult and pediatric CS are decided in favor of treating physicians, compared with 75% of cases in other orthopedic malpractice claims.1,2

Risk Factors for Posttraumatic Compartment Syndrome

Supracondylar Humeral Fracture

CS is a well-described complication of this injury. CS develops in 0.1% to 0.3% of children who present with supracondylar humeral fracture.^3,4 Casted elbow flexion beyond 90° and concomitant vascular injury put these children at increased risk for CS. Mubarak and Carroll⁵ reported 9 cases of CS in the volar compartment of the forearm after an extension-type supracondylar humeral fracture and attributed 8 of them to elbow flexion beyond 90° after closed reduction. In 29 children with supracondylar humeral fracture,Battaglia and colleagues³ found the highest compartment pressure in the deep volar compartment, especially near the fracture site, as well as a significant increase in pressure with the elbow flexed beyond 90°.

In a study of children with supracondylar humeral fracture, Choi and colleagues⁶ found 2 cases of CS among 9 patients who presented with a pulseless, poorly perfused hand and no cases of CS among 24 patients who presented with a pulseless but well-perfused hand.

Studies have found that a treatment delay of 8 to 12 hours did not increase the rate of CS in Gartland type 2 and type 3 fractures.^7-10 The investigators in these studies did not recommend delaying treatment of patients with neurologic deficit and absent radial pulse. Ramachandran and colleagues4 reported 11 cases of CS in patients with low-energy supracondylar humeral fracture and intact radial pulse at presentation. The patients who developed CS presented with severe swelling, and their mean treatment delay was 22 hours (range, 6-64 hours). Given the data, we do not recommend delayed treatment for children with supracondylar humeral fracture and neurologic deficit or absent pulse. We do recommend close inpatient preoperative monitoring of patients with severe swelling.

CS after supracondylar humeral fracture is mostly seen in the volar compartment of the forearm, but it has also been reported in the mobile wad, the anterior arm compartment, and the posterior arm compartment.^11,12

Floating Elbow

CS has been reported in children with ipsilateral humeral and forearm fractures. Blakemore and colleagues¹³ reported a 33% rate of CS in children with displaced distal humeral and forearm fractures. A retrospective review of 16 cases of floating elbow treated at Boston Children’s Hospital found CS in 2 patients and incipient CS in 4 of 10 patients with forearm fractures treated with closed reduction and plaster casting. There were no signs of CS in 6 patients with distal humeral and forearm fractures stabilized with Kirschner wires.¹⁴ Given the data, we do not recommend circumferential casting for forearm fractures in children with floating elbow.

Forearm Fracture

Haasbeek and Cole¹⁵ reported CS in 5 (11%) of 46 children with open forearm fracture. Yuan and colleagues¹⁶ reported CS in 3 (6%) of 50 open forearm fractures and 3 of 30 closed fractures treated with closed reduction and intramedullary nailing. They found increased risk for CS in patients with longer operative time, indicating prolonged closed manipulation of these fractures as a risk factor for CS. They did not find any cases of CS among 205 forearm fractures treated with closed reduction and casting.

Flynn and colleagues17 reported CS in 2 of 30 patients treated with intramedullary nailing within 24 hours of injury and in 0 of 73 patients treated after 24 hours.

Blackman and colleagues¹⁸ reported CS in 3 (7.7%) of 39 open forearm fractures and 0 of 74 closed fractures treated operatively. In their series, a small incision was made to facilitate reduction in 38 (51.4%) of 74 closed fractures to decrease closed manipulation and operative time. The rate of CS after intramedullary nailing of closed forearm fractures was lower in this series than in similar reports in the literature.

Reported data indicate increased risk for CS in children with open forearm fractures and fractures treated with closed reduction and intramedullary nailing, especially performed within 24 hours of injury, and prolonged closed manipulation performed during surgery. We recommend close monitoring of all children with operatively treated forearm fractures and, in particular, children with the risk factors mentioned.

Femoral Fracture

Although CS after femoral shaft fractures is not common, CS has been reported after 90/90 spica casting of femoral shaft fractures in children. Mubarak and colleagues19 reported on 9 children who developed calf CS after treatment of femoral shaft fracture in 90/90 spica casts. The technique used in 7 of the 9 reported cases involved initial application of a short leg cast and then traction applied to the leg—believed to cause impinging of the cast on the posterior compartment of the leg. The authors recommended an alternative method of applying spica casts, which is beyond the scope of this review.

Tibial Fracture

Children with tibial fracture, especially a fracture sustained in a motor vehicle accident, are at risk for CS. Hope and Cole²⁰ found CS in 4 (4%) of 92 children with open tibial fracture.

Children with tibial tubercle fracture are at increased risk for CS because of concomitant vascular injury. Pandya and colleagues²¹ reported CS or vascular compromise in 4 of 40 patients with tibial tubercle fracture. We recommend close monitoring for signs of impending CS in children who present with high-energy tibial shaft fracture and tibial tubercle fracture.

Flynn and colleagues²² reported outcomes of 43 cases of acute CS of the leg in children treated at 2 pediatric trauma centers. Mean time from injury to fasciotomy was 20.5 hours (range, 3.9-118 hours). Functional outcome was excellent at time of follow-up; 41 of 43 cases had no sequelae, and the 2 patients who lost function underwent fasciotomy more than 80 hours after injury. Despite the long interval between injury and surgery, excellent results were achieved with fasciotomy, suggesting an increased potential for recovery in the pediatric population.

Mubarak²³ reported on 6 cases of distal tibial physis fracture in patients who presented with severe pain and swelling of the ankle, hyposthesia of the first web space, weakness of the extensor hallucis longus and extensor digitorum communis, and pain on passive flexion of the toes. In all these patients, intramuscular pressure was more than 40 mm Hg beneath the extensor retinaculum and less than 20 mm Hg in the anterior compartment. All patients experienced prompt relief of pain and improved sensation and strength within 24 hours after release of the superior extensor retinaculum and fracture stabilization.

Miscellaneous and Nontraumatic Causes of Compartment Syndrome

Neonatal CS is very rare, and diagnosis is often missed. Neonatal CS is thought to be caused by a combination of low neonatal blood pressure and birth trauma.²⁴ Ragland and colleagues²⁵ reported on 24 cases of neonatal CS; in only 1 case was the diagnosis made within 24 hours.They described a “sentinel skin lesion” on the forearm of each patient as the sign of neonatal CS. Late diagnosis results in contracture and growth arrest of the involved extremity. In their series, only 1 patient underwent fasciotomy within 24 hours, and it resulted in a good functional outcome. High clinical suspicion is the key to early diagnosis and treatment of this rare pathology.

Medical problems that cause intracompartmental bleeding (hepatic failure, renal failure, leukemia, hemophilia) have been cited as causing CS.^26-28 CS may be the first symptom of occult hemophilia²⁹ Correction of the coagulation defect may take priority over surgical treatment in these cases, though the decision should be made on a case-by-case basis.²⁶

CS in children can also be caused by snakebites. Shaw and Hosalkar³⁰ reported on successful use of antivenin in preventing the need for surgical treatment in 16 of 19 patients with rattlesnake bites. Two patients had limited surgical débridement, and 1 underwent fasciotomy for CS. The authors recommended using antivenin to prevent CS in children with snakebites.³⁰

Prasarn and colleagues² reported on 12 cases of upper extremity CS in children in the absence of fractures. Of the 12 patients, 10 were managed in an intensive care unit and had an obtunded sensorium. Etiology in 7 (58%) of the 12 cases was iatrogenic (intravenous infiltration, retained phlebotomy tourniquet). In this series, 4 amputations were performed on affected extremities.

Diagnosis

Identification of evolving CS in a child is difficult because of the child’s limited ability to communicate and anxiety about being examined by a stranger. Orthopedists are trained to look for the 5 Ps (pain, paresthesia, paralysis, pallor, pulselessness) associated with CS. Examining an anxious, frightened young child is difficult, and documenting the degree of pain is not practical in a child who may not be able or willing to communicate effectively.

In a series of 33 children with CS, Bae and colleagues³¹ found that the 5 Ps were relatively unreliable in making a timely diagnosis. The authors also found that increased analgesic use was documented a mean of 7.3 hours before a change in vascular status and that it was a more sensitive indicator of CS in children. The resulting recommendation is that children at risk for CS be closely monitored for the 3 As (increasing analgesic requirement, anxiety, agitation).³²

Regional anesthesia is used to control postoperative pain in adults and children.^33,34 Injudicious use may mask the primary symptom (pain) of CS.^32,35-38 Use of regional anesthesia in patients at high risk for CS is highly discouraged.

Although CS is a clinical diagnosis, compartment pressure measurements can be useful in making decisions in certain clinical scenarios. In an obtunded child or in a child with severe mental and communication disability, such a measurement can help confirm or rule out the diagnosis.

Normal compartment pressures are higher in children than in adults. Staudt and colleagues³⁹ compared pressures in 4 lower leg compartments of 20 healthy children and 20 healthy adults. Mean pressure varied from 13.3 mm Hg to 16.6 mm Hg in children and from 5.2 mm Hg to 9.7 mm Hg in adults—indicating higher normal pressure in lower leg compartments in children.

Compartment pressures were reported highest within 5 cm of the fracture site.⁴⁰ When clinically indicated, they should be measured in that area in an injured extremity. The pressure threshold that requires fasciotomy is debatable. Intracompartmental pressures of 30 to 45 mm Hg, or measurements less than 30 mm Hg of diastolic blood pressure (pressure change = diastolic blood pressure – compartment pressure), have been recommended as cutoffs by some authors.^41-44 As resting normal compartment pressures are higher in children, these cutoffs cannot be used as reliably in children as in adults. Direct measurement of intracompartmental pressure is invasive and can be difficult in an agitated, awake child. The potential utility of near-infrared spectroscopy in the diagnosis of increased compartment pressure has been reported.^45,46 This method uses differential light absorption properties of oxygenated hemoglobin to measure tissue ischemia—similar to the method used in pulse oximetry. Compared with pulse oximetry, near-infrared spectroscopy can sample deeper tissue (3 cm below skin level). Shuler and colleagues⁴⁵ reported near-infrared spectroscopy findings for 14 adults with acute CS. Lower tissue oxygenation levels correlated with increased intracompartmental pressures, but the authors could not define a cutoff for which near-infrared spectroscopy measurements would indicate significant tissue ischemia. Use of this method in diagnosing CS in children was described in a case report.⁴⁶

CS remains a clinical diagnosis. Informing family and staff about the signs and symptoms of this syndrome and closely monitoring analgesic use in these patients are crucial. Compartment pressure measurements can be used when the diagnosis is unclear, particularly in noncommunicative patients, but these values should be interpreted with caution.

Treatment

Once CS is diagnosed, emergent fasciotomy and decompression are indicated. Surgeons planning fasciotomy should be aware of the definitive treatment of the CS etiology. Treatment of clotting deficiency in cases caused by excessive bleeding, fracture fixation, and vascular repair may be indicated during fasciotomy and decompression.

Summary

Increased need for analgesics is often the first sign of CS in children and should be considered the sentinel alarm for ongoing tissue necrosis. CS remains a clinical diagnosis, and compartment pressure should be measured only as a confirmatory test in noncommunicative patients or when the diagnosis is unclear. Children with supracondylar humeral fractures, forearm fractures, tibial fractures, and medical risk factors for coagulopathy are at increased risk and should be monitored closely. When the diagnosis is made promptly and the condition is treated with fasciotomy, good long-term clinical results can be expected.

I try to avoid revisiting a subject I have pontificated on in the recent past, but when I encounter a situation in which scientists are behaving unscientifically it is hard to remain silent. In 2002, a Pittsburgh neuropathologist named Bennet Omalu performed an autopsy on Mike Webster, a former National Football League (NFL) lineman who had died in his 50s. Webster had been exhibiting bizarre behaviors and was developing dementia. What Dr. Omalu found in Webster’s brain was a collection of changes that have become known as chronic traumatic encephalopathy (CTE).

In the decade following the publication of Dr. Omalu’s findings in the journal Neurosurgery in 2005, there has been some unsavory back and forths between the NFL’s Mild Traumatic Brain Injury Committee and Dr. Omalu that I learned about in the Wall Street Journal (“The Doctor the NFL Tried to Silence,” by Jeanne Marie Laskas, Nov 24, 2015). The doctor’s side of the story has been published in a book, “Concussion” (New York: Penguin Random House, 2015). “Concussion,” the movie based on the book, was slated for release in December.

The tangle of he said – our experts don’t agree has involved the University of Michigan and Boston University, and the smell of conflict of interest hangs over the NFL’s choice of experts and its decisions to publish or not publish the results of various studies. It now appears that Dr. Omalu’s discovery was the tip of an iceberg of undetermined size. As happens far too often, assumptions and attributions have been made in haste based on scanty evidence from small studies that have surely failed to control for all of the possible contributors.

Considering the results of the autopsies on a few NFL players, it is probably reasonable to suspect that there is something in the culture surrounding professional football that makes some of the players vulnerable to central nervous system damage. And blows to the head are likely to be one of those factors. However, leaping to the conclusion that parents shouldn’t allow their young children to play football is another story. But that is just what Dr. Omalu has done in an op-ed piece that has appeared in the New York Times (“Don’t Let Kids Play Football,” Dec 7, 2015).

Relying heavily on the analogy with cumulative effects of cigarette smoking, Dr. Omalu continues to fan the flame that he ignited with his initial autopsy finding. The timing of the piece is interesting in light of the movie’s release date of Dec. 25. While his discovery of CTE in a professional player is important, Dr. Omalu’s case for prohibiting children from playing football is rife with half-truths and unwarranted conclusions.

For example, he states that in his 30 years as a neuropathologist he has yet to see a “neuron that naturally creates a new neuron to regenerate itself.” True, but he fails to report that there is new evidence that the long-held dictum that neurons can’t heal themselves may be wrong.

Dr. Omalu observes that “if a child who plays football is subjected to advanced radiological and neurocognitive studies during the season and several months after there can be evidence of brain damage at the cellular level even if there were no documented concussions or reported symptoms.” It took some time, but I eventually found the study to which I assume he is referring, by Dr. Christopher T. Whitlow of Wake Forest University, Winston-Salem, N.C., presented at the Radiological Society of North America meeting in December of 2014. Its lead author is careful to state that conclusions should not be drawn from this small preliminary study and observes, “it is unclear whether or not these effects will be associated with any long-term consequences.” However, Dr. Omalu asserts that “If that child continues to play over many seasons, these cellular injuries accumulate to cause irreversible brain damage.” He states this as fact without any supporting evidence.

Fortunately, the American Academy of Pediatrics has presented a more balanced perspective on allowing children to participate in football in light of what we are learning about the health of professional players (“Tackling in Youth Football” [Pediatrics. 2015;136(5)e1419-31]). Dr. William P. Meehan III and Dr. Gregory L. Landry, speaking for the Council on Sports Medicine and Fitness, point out that serious head and neck injury in young football players is very unlikely, and that by teaching proper tackling technique, these injuries can be further decreased.

The real solution to the problem that Dr. Omalu first brought to light in 2002 lies with zero tolerance for the practice of tackling headfirst at all levels of football. Although the NFL has made some feeble attempts to discipline its teams, there is still more that should be done. Every professional and college football game is being video recorded, often from multiple angles. Retrospective analysis of these images should be used to discipline players whose injury-threatening tactics have not been detected by the officials during the game. Multiple game suspensions meted out promptly, and without possibility of appeal, would go a long way to return football to being the safer sport it was when leather helmets discouraged players from using their heads as lethal weapons.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

I try to avoid revisiting a subject I have pontificated on in the recent past, but when I encounter a situation in which scientists are behaving unscientifically it is hard to remain silent. In 2002, a Pittsburgh neuropathologist named Bennet Omalu performed an autopsy on Mike Webster, a former National Football League (NFL) lineman who had died in his 50s. Webster had been exhibiting bizarre behaviors and was developing dementia. What Dr. Omalu found in Webster’s brain was a collection of changes that have become known as chronic traumatic encephalopathy (CTE).

In the decade following the publication of Dr. Omalu’s findings in the journal Neurosurgery in 2005, there has been some unsavory back and forths between the NFL’s Mild Traumatic Brain Injury Committee and Dr. Omalu that I learned about in the Wall Street Journal (“The Doctor the NFL Tried to Silence,” by Jeanne Marie Laskas, Nov 24, 2015). The doctor’s side of the story has been published in a book, “Concussion” (New York: Penguin Random House, 2015). “Concussion,” the movie based on the book, was slated for release in December.

The tangle of he said – our experts don’t agree has involved the University of Michigan and Boston University, and the smell of conflict of interest hangs over the NFL’s choice of experts and its decisions to publish or not publish the results of various studies. It now appears that Dr. Omalu’s discovery was the tip of an iceberg of undetermined size. As happens far too often, assumptions and attributions have been made in haste based on scanty evidence from small studies that have surely failed to control for all of the possible contributors.

Considering the results of the autopsies on a few NFL players, it is probably reasonable to suspect that there is something in the culture surrounding professional football that makes some of the players vulnerable to central nervous system damage. And blows to the head are likely to be one of those factors. However, leaping to the conclusion that parents shouldn’t allow their young children to play football is another story. But that is just what Dr. Omalu has done in an op-ed piece that has appeared in the New York Times (“Don’t Let Kids Play Football,” Dec 7, 2015).

Relying heavily on the analogy with cumulative effects of cigarette smoking, Dr. Omalu continues to fan the flame that he ignited with his initial autopsy finding. The timing of the piece is interesting in light of the movie’s release date of Dec. 25. While his discovery of CTE in a professional player is important, Dr. Omalu’s case for prohibiting children from playing football is rife with half-truths and unwarranted conclusions.

For example, he states that in his 30 years as a neuropathologist he has yet to see a “neuron that naturally creates a new neuron to regenerate itself.” True, but he fails to report that there is new evidence that the long-held dictum that neurons can’t heal themselves may be wrong.

Dr. Omalu observes that “if a child who plays football is subjected to advanced radiological and neurocognitive studies during the season and several months after there can be evidence of brain damage at the cellular level even if there were no documented concussions or reported symptoms.” It took some time, but I eventually found the study to which I assume he is referring, by Dr. Christopher T. Whitlow of Wake Forest University, Winston-Salem, N.C., presented at the Radiological Society of North America meeting in December of 2014. Its lead author is careful to state that conclusions should not be drawn from this small preliminary study and observes, “it is unclear whether or not these effects will be associated with any long-term consequences.” However, Dr. Omalu asserts that “If that child continues to play over many seasons, these cellular injuries accumulate to cause irreversible brain damage.” He states this as fact without any supporting evidence.

Fortunately, the American Academy of Pediatrics has presented a more balanced perspective on allowing children to participate in football in light of what we are learning about the health of professional players (“Tackling in Youth Football” [Pediatrics. 2015;136(5)e1419-31]). Dr. William P. Meehan III and Dr. Gregory L. Landry, speaking for the Council on Sports Medicine and Fitness, point out that serious head and neck injury in young football players is very unlikely, and that by teaching proper tackling technique, these injuries can be further decreased.

The real solution to the problem that Dr. Omalu first brought to light in 2002 lies with zero tolerance for the practice of tackling headfirst at all levels of football. Although the NFL has made some feeble attempts to discipline its teams, there is still more that should be done. Every professional and college football game is being video recorded, often from multiple angles. Retrospective analysis of these images should be used to discipline players whose injury-threatening tactics have not been detected by the officials during the game. Multiple game suspensions meted out promptly, and without possibility of appeal, would go a long way to return football to being the safer sport it was when leather helmets discouraged players from using their heads as lethal weapons.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

I try to avoid revisiting a subject I have pontificated on in the recent past, but when I encounter a situation in which scientists are behaving unscientifically it is hard to remain silent. In 2002, a Pittsburgh neuropathologist named Bennet Omalu performed an autopsy on Mike Webster, a former National Football League (NFL) lineman who had died in his 50s. Webster had been exhibiting bizarre behaviors and was developing dementia. What Dr. Omalu found in Webster’s brain was a collection of changes that have become known as chronic traumatic encephalopathy (CTE).

In the decade following the publication of Dr. Omalu’s findings in the journal Neurosurgery in 2005, there has been some unsavory back and forths between the NFL’s Mild Traumatic Brain Injury Committee and Dr. Omalu that I learned about in the Wall Street Journal (“The Doctor the NFL Tried to Silence,” by Jeanne Marie Laskas, Nov 24, 2015). The doctor’s side of the story has been published in a book, “Concussion” (New York: Penguin Random House, 2015). “Concussion,” the movie based on the book, was slated for release in December.

The tangle of he said – our experts don’t agree has involved the University of Michigan and Boston University, and the smell of conflict of interest hangs over the NFL’s choice of experts and its decisions to publish or not publish the results of various studies. It now appears that Dr. Omalu’s discovery was the tip of an iceberg of undetermined size. As happens far too often, assumptions and attributions have been made in haste based on scanty evidence from small studies that have surely failed to control for all of the possible contributors.

Considering the results of the autopsies on a few NFL players, it is probably reasonable to suspect that there is something in the culture surrounding professional football that makes some of the players vulnerable to central nervous system damage. And blows to the head are likely to be one of those factors. However, leaping to the conclusion that parents shouldn’t allow their young children to play football is another story. But that is just what Dr. Omalu has done in an op-ed piece that has appeared in the New York Times (“Don’t Let Kids Play Football,” Dec 7, 2015).

Relying heavily on the analogy with cumulative effects of cigarette smoking, Dr. Omalu continues to fan the flame that he ignited with his initial autopsy finding. The timing of the piece is interesting in light of the movie’s release date of Dec. 25. While his discovery of CTE in a professional player is important, Dr. Omalu’s case for prohibiting children from playing football is rife with half-truths and unwarranted conclusions.

For example, he states that in his 30 years as a neuropathologist he has yet to see a “neuron that naturally creates a new neuron to regenerate itself.” True, but he fails to report that there is new evidence that the long-held dictum that neurons can’t heal themselves may be wrong.

Dr. Omalu observes that “if a child who plays football is subjected to advanced radiological and neurocognitive studies during the season and several months after there can be evidence of brain damage at the cellular level even if there were no documented concussions or reported symptoms.” It took some time, but I eventually found the study to which I assume he is referring, by Dr. Christopher T. Whitlow of Wake Forest University, Winston-Salem, N.C., presented at the Radiological Society of North America meeting in December of 2014. Its lead author is careful to state that conclusions should not be drawn from this small preliminary study and observes, “it is unclear whether or not these effects will be associated with any long-term consequences.” However, Dr. Omalu asserts that “If that child continues to play over many seasons, these cellular injuries accumulate to cause irreversible brain damage.” He states this as fact without any supporting evidence.

Fortunately, the American Academy of Pediatrics has presented a more balanced perspective on allowing children to participate in football in light of what we are learning about the health of professional players (“Tackling in Youth Football” [Pediatrics. 2015;136(5)e1419-31]). Dr. William P. Meehan III and Dr. Gregory L. Landry, speaking for the Council on Sports Medicine and Fitness, point out that serious head and neck injury in young football players is very unlikely, and that by teaching proper tackling technique, these injuries can be further decreased.

The real solution to the problem that Dr. Omalu first brought to light in 2002 lies with zero tolerance for the practice of tackling headfirst at all levels of football. Although the NFL has made some feeble attempts to discipline its teams, there is still more that should be done. Every professional and college football game is being video recorded, often from multiple angles. Retrospective analysis of these images should be used to discipline players whose injury-threatening tactics have not been detected by the officials during the game. Multiple game suspensions meted out promptly, and without possibility of appeal, would go a long way to return football to being the safer sport it was when leather helmets discouraged players from using their heads as lethal weapons.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

Blount disease (tibia vara) is an angular tibia deformity that includes varus, increased posterior slope, and internal rotation. This deformity was first described in 1922 by Erlacher1 in Germany. In 1937, Walter Blount2 reported on it in the United States. It is the most common cause of pathologic genu varum in adolescence and childhood.

An oblique incomplete closing wedge osteotomy of the proximal tibial metaphysis was described by Wagner³ for the treatment of unicompartmental osteoarthrosis of the knee in adults. Laurencin and colleagues⁴ applied this technique to the treatment of pediatric tibia vara with favorable results. They spared the medial cortex of the tibia in their incomplete closing wedge osteotomy technique. In each of the 9 cases we treated and describe here, we accidentally completed the tibial osteotomy when attempting the Laurencin technique. Given that the osteotomy was completed, we modified the Laurencin technique by using a 6-hole, 4.5-mm compression plate rather than a 5-hole semitubular plate, and added a large oblique screw from the medial side to compress the osteotomy site and to protect the plate from fracture. In addition, in 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability. In this article, we report the outcomes of correcting adolescent tibia vara with a complete closing wedge tibial osteotomy and an oblique fibular osteotomy.

Materials and Methods

This study was approved by the Institutional Review Board at Pennsylvania State University. Between 2009 and 2012, we performed 9 complete oblique proximal tibial lateral closing wedge osteotomies on 8 patients (2 girls, 6 boys). In each case, the primary diagnosis was Blount disease. One patient also had renal dysplasia and was receiving dialysis. Mean age at time of operation was 15 years (range, 13-17 years). Mean preoperative weight was 215 pounds (range, 119-317 lb). Mean weight gain at follow-up was 4.39 pounds (range, –10 to 19 lb). Mean body mass index (BMI) was 38 (range, 25-48) (Table). All patients had varus angulation of the proximal tibia before surgery. Mean preoperative varus on standing films was 22° (range, 10°-36°). Because of the patients’ size, we used standing long-leg radiographs, on individual cassettes, for each leg.

Surgical Technique

Before surgery, we use paper cutouts to template the osteotomy wedge. We also use perioperative antibiotics and a standard time-out. For visualization of the entire leg for accurate correction, we prepare and drape the entire leg. A sterile tourniquet is used. At the midshaft of the fibula, a 4-cm incision is made, and dissection is carefully carried down to the fibula. Subperiosteal dissection is performed about the fibula, allowing adequate clearance for an oblique osteotomy. The osteotomy removes about 1 cm of fibula, which is to be used as bone graft for the tibial osteotomy. In addition, a lateral compartment fasciotomy is performed to prevent swelling-related complications. The wound is irrigated and injected with bupivacaine and closed in routine fashion.

We then make an inverted hockey-stick incision over the proximal tibia, centered down to the tibial tubercle. After dissecting down to the anterior compartment, we perform a fasciotomy of about 8 cm to accommodate swelling. Subperiosteal dissection is then performed around the proximal tibia. The medial soft tissues are left attached to increase blood supply and healing. During subperiosteal dissection, soft elevators are used to gently retract the lateral soft tissues along with the inferior and posterior structures. We use fluoroscopic imaging to guide the osteotomy as well as screw and plate placement. We use a 6-hole, 4.5-mm compression plate and screws for fixation. The 2 proximal screws of the plate are predrilled in place to allow for application of the plate after completion of the osteotomy. The plate is then rotated out of position on 1 screw, and the osteotomy is identified under fluoroscopy with the appropriate position distal to the second hole of the 6-hole plate.

An oscillating saw and osteotomes are used to perform the oblique osteotomy. The pre-estimated bone wedge is removed. Wedge size is adjusted, if needed. The bone wedge is morselized for bone graft. The osteotomy is then closed, correcting both varus and internal tibial torsion. Our goal is 5° valgus. After correction is obtained, the plate is placed, and the proximal screw is snugly seated. Three cortical screws are placed distally to hold the plate in place under compression mode, and a cancellous screw is placed superiorly at the proximal portion of the plate for additional fixation. The screw placed proximal to the osteotomy site is a fully threaded cortical screw with excellent compression. Correction and proper placement of hardware are verified with fluoroscopy.

The wound is irrigated and injected with bupivacaine. Bone graft is then placed at the osteotomy site. Additional bone graft is placed posteriorly between the osteotomy site and the muscle mass to stimulate additional healing. Another screw is placed obliquely from the medial side across the osteotomy site to provide additional fixation (Figure 1).

Copyright belongs to the authors

A deep drain is placed and connected to bulb suction for 24 hours after surgery. The wound is then closed in routine fashion. In 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability (Figure 2).

Copyright belongs to the authors

Postoperative Care

The incisions are dressed with antibiotic ointment and 4×4-in bandages and then wrapped with sterile cotton under-cast padding. The leg is placed into a well-padded cylinder cast with the knee flexed 10°. The leg is aligned to about 5° valgus. The cast is then split on the side and spread to allow for swelling and to prevent compartment syndrome.⁵ We also use a drain hooked to bulb suction, which is removed 24 hours after surgery. Toe-touch weight-bearing with crutches is allowed immediately after surgery. The cast is removed at 6 weeks, and a hinged range-of-motion knee brace is worn for another 6 weeks. All patients are allowed to resume normal activity after 4 months. In our 2 external-fixator cases, a cast was not used, and toe-touch weight-bearing and knee motion were allowed immediately. The external fixators were removed at about 10 weeks.

Results

Mean postoperative mechanical femoral-tibial angle was 3°, and mean correction was 26° (range, 16°-43°) (Table). Lateral distal femoral angle did not show significant femoral deformity in our sample. Mean medial proximal tibial angle was 74° (range, 63°-79°). In each case, the varus deformity was primarily in the tibia. Mean tourniquet time was 88 minutes (range, 50-119 min). Our complication rate was 11% (1 knee). In our first case, in which we did not use an extra medial screw, the 4.5-mm plate fractured at the osteotomy site 2.5 months after surgery. The 250-pound patient subsequently lost 17° of correction, and valgus alignment was not achieved. Preoperative varus was 25°, and postoperative alignment was 8° varus. This plate fracture led us to use an extra medial screw for additional stability in all subsequent cases and to consider using an external fixator for patients weighing more than 250 pounds. After the first case, there were no other plate fractures. A potential problem with closing wedge osteotomy is shortening, but varus correction restores some length. Mean postoperative leg-length difference was 10 mm (range, 0-16 mm). No patient complained of leg-length difference during the postoperative follow-up.

Eight and a half months after surgery, 1 patient had hardware removed, at the family’s request. No patient experienced perioperative infection or neurovascular damage. Our overall patient population was obese—mean BMI was 38 (range, 25-48), and mean postoperative weight was 219 pounds. Three of our 8 patients were overweight (BMI, 25-30), and 5 were obese (BMI, >30). For prevention of plate failure, we recommend using an extra oblique screw in all patients and considering an external fixator for patients who weigh more than 250 pounds.

Discussion

Correction of adolescent tibia vara can be challenging because of patient obesity. The technique described here—a modification of the technique of Laurencin and colleagues⁴—is practical and reproducible in this population. The goals in performing osteotomy are to correct the deformity, restore joint alignment, preserve leg length, and prevent recurrent deformity and other complications, such as neurovascular injury, nonunion, and infection.^3,6-8 Our technique minimizes the risk for these complications. For example, the fasciotomy provides excellent decompression of the anterior and lateral compartments, minimizing neurovascular ischemia and the risk for compartment syndrome. During cast placement, splitting and spreading reduce the risk for compartment syndrome as well.⁵

Wagner3,9 demonstrated the utility of a closing wedge proximal tibial osteotomy in adults. Laurencin and colleagues4 showed this technique is effective in correcting tibia vara in a pediatric population. However, they did not specify patient weight and used a small semitubular plate for fixation, and some of their patients had infantile Blount disease. We modified the technique in 3 ways. First, we performed a complete osteotomy. Second, because our patients were adolescents and very large, we used a 6-hole, 4.5-mm compression plate and screws. Third, we used an external fixator for increased stability in patients who weighed more than 250 pounds.

The reported technique, using an oblique metaphyseal closing wedge osteotomy with internal fixation in obese patients, is practical, safe, and reliable. This technique is a useful alternative to an external fixator. We used it on 9 knees with tibia vara, and it was completely successful in 8 cases and partially successful in 1 (hardware breakage occurred). An external fixator was used to prevent hardware breakage in 2 patients who weighed more than 250 pounds. This technique is a valuable treatment option for surgical correction, especially in obese patients.

Blount disease (tibia vara) is an angular tibia deformity that includes varus, increased posterior slope, and internal rotation. This deformity was first described in 1922 by Erlacher1 in Germany. In 1937, Walter Blount2 reported on it in the United States. It is the most common cause of pathologic genu varum in adolescence and childhood.

An oblique incomplete closing wedge osteotomy of the proximal tibial metaphysis was described by Wagner³ for the treatment of unicompartmental osteoarthrosis of the knee in adults. Laurencin and colleagues⁴ applied this technique to the treatment of pediatric tibia vara with favorable results. They spared the medial cortex of the tibia in their incomplete closing wedge osteotomy technique. In each of the 9 cases we treated and describe here, we accidentally completed the tibial osteotomy when attempting the Laurencin technique. Given that the osteotomy was completed, we modified the Laurencin technique by using a 6-hole, 4.5-mm compression plate rather than a 5-hole semitubular plate, and added a large oblique screw from the medial side to compress the osteotomy site and to protect the plate from fracture. In addition, in 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability. In this article, we report the outcomes of correcting adolescent tibia vara with a complete closing wedge tibial osteotomy and an oblique fibular osteotomy.

Materials and Methods

This study was approved by the Institutional Review Board at Pennsylvania State University. Between 2009 and 2012, we performed 9 complete oblique proximal tibial lateral closing wedge osteotomies on 8 patients (2 girls, 6 boys). In each case, the primary diagnosis was Blount disease. One patient also had renal dysplasia and was receiving dialysis. Mean age at time of operation was 15 years (range, 13-17 years). Mean preoperative weight was 215 pounds (range, 119-317 lb). Mean weight gain at follow-up was 4.39 pounds (range, –10 to 19 lb). Mean body mass index (BMI) was 38 (range, 25-48) (Table). All patients had varus angulation of the proximal tibia before surgery. Mean preoperative varus on standing films was 22° (range, 10°-36°). Because of the patients’ size, we used standing long-leg radiographs, on individual cassettes, for each leg.

Surgical Technique

Before surgery, we use paper cutouts to template the osteotomy wedge. We also use perioperative antibiotics and a standard time-out. For visualization of the entire leg for accurate correction, we prepare and drape the entire leg. A sterile tourniquet is used. At the midshaft of the fibula, a 4-cm incision is made, and dissection is carefully carried down to the fibula. Subperiosteal dissection is performed about the fibula, allowing adequate clearance for an oblique osteotomy. The osteotomy removes about 1 cm of fibula, which is to be used as bone graft for the tibial osteotomy. In addition, a lateral compartment fasciotomy is performed to prevent swelling-related complications. The wound is irrigated and injected with bupivacaine and closed in routine fashion.

We then make an inverted hockey-stick incision over the proximal tibia, centered down to the tibial tubercle. After dissecting down to the anterior compartment, we perform a fasciotomy of about 8 cm to accommodate swelling. Subperiosteal dissection is then performed around the proximal tibia. The medial soft tissues are left attached to increase blood supply and healing. During subperiosteal dissection, soft elevators are used to gently retract the lateral soft tissues along with the inferior and posterior structures. We use fluoroscopic imaging to guide the osteotomy as well as screw and plate placement. We use a 6-hole, 4.5-mm compression plate and screws for fixation. The 2 proximal screws of the plate are predrilled in place to allow for application of the plate after completion of the osteotomy. The plate is then rotated out of position on 1 screw, and the osteotomy is identified under fluoroscopy with the appropriate position distal to the second hole of the 6-hole plate.

An oscillating saw and osteotomes are used to perform the oblique osteotomy. The pre-estimated bone wedge is removed. Wedge size is adjusted, if needed. The bone wedge is morselized for bone graft. The osteotomy is then closed, correcting both varus and internal tibial torsion. Our goal is 5° valgus. After correction is obtained, the plate is placed, and the proximal screw is snugly seated. Three cortical screws are placed distally to hold the plate in place under compression mode, and a cancellous screw is placed superiorly at the proximal portion of the plate for additional fixation. The screw placed proximal to the osteotomy site is a fully threaded cortical screw with excellent compression. Correction and proper placement of hardware are verified with fluoroscopy.

The wound is irrigated and injected with bupivacaine. Bone graft is then placed at the osteotomy site. Additional bone graft is placed posteriorly between the osteotomy site and the muscle mass to stimulate additional healing. Another screw is placed obliquely from the medial side across the osteotomy site to provide additional fixation (Figure 1).

Copyright belongs to the authors

A deep drain is placed and connected to bulb suction for 24 hours after surgery. The wound is then closed in routine fashion. In 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability (Figure 2).

Copyright belongs to the authors

Postoperative Care

The incisions are dressed with antibiotic ointment and 4×4-in bandages and then wrapped with sterile cotton under-cast padding. The leg is placed into a well-padded cylinder cast with the knee flexed 10°. The leg is aligned to about 5° valgus. The cast is then split on the side and spread to allow for swelling and to prevent compartment syndrome.⁵ We also use a drain hooked to bulb suction, which is removed 24 hours after surgery. Toe-touch weight-bearing with crutches is allowed immediately after surgery. The cast is removed at 6 weeks, and a hinged range-of-motion knee brace is worn for another 6 weeks. All patients are allowed to resume normal activity after 4 months. In our 2 external-fixator cases, a cast was not used, and toe-touch weight-bearing and knee motion were allowed immediately. The external fixators were removed at about 10 weeks.

Results

Mean postoperative mechanical femoral-tibial angle was 3°, and mean correction was 26° (range, 16°-43°) (Table). Lateral distal femoral angle did not show significant femoral deformity in our sample. Mean medial proximal tibial angle was 74° (range, 63°-79°). In each case, the varus deformity was primarily in the tibia. Mean tourniquet time was 88 minutes (range, 50-119 min). Our complication rate was 11% (1 knee). In our first case, in which we did not use an extra medial screw, the 4.5-mm plate fractured at the osteotomy site 2.5 months after surgery. The 250-pound patient subsequently lost 17° of correction, and valgus alignment was not achieved. Preoperative varus was 25°, and postoperative alignment was 8° varus. This plate fracture led us to use an extra medial screw for additional stability in all subsequent cases and to consider using an external fixator for patients weighing more than 250 pounds. After the first case, there were no other plate fractures. A potential problem with closing wedge osteotomy is shortening, but varus correction restores some length. Mean postoperative leg-length difference was 10 mm (range, 0-16 mm). No patient complained of leg-length difference during the postoperative follow-up.

Eight and a half months after surgery, 1 patient had hardware removed, at the family’s request. No patient experienced perioperative infection or neurovascular damage. Our overall patient population was obese—mean BMI was 38 (range, 25-48), and mean postoperative weight was 219 pounds. Three of our 8 patients were overweight (BMI, 25-30), and 5 were obese (BMI, >30). For prevention of plate failure, we recommend using an extra oblique screw in all patients and considering an external fixator for patients who weigh more than 250 pounds.

Discussion

Correction of adolescent tibia vara can be challenging because of patient obesity. The technique described here—a modification of the technique of Laurencin and colleagues⁴—is practical and reproducible in this population. The goals in performing osteotomy are to correct the deformity, restore joint alignment, preserve leg length, and prevent recurrent deformity and other complications, such as neurovascular injury, nonunion, and infection.^3,6-8 Our technique minimizes the risk for these complications. For example, the fasciotomy provides excellent decompression of the anterior and lateral compartments, minimizing neurovascular ischemia and the risk for compartment syndrome. During cast placement, splitting and spreading reduce the risk for compartment syndrome as well.⁵

Wagner3,9 demonstrated the utility of a closing wedge proximal tibial osteotomy in adults. Laurencin and colleagues4 showed this technique is effective in correcting tibia vara in a pediatric population. However, they did not specify patient weight and used a small semitubular plate for fixation, and some of their patients had infantile Blount disease. We modified the technique in 3 ways. First, we performed a complete osteotomy. Second, because our patients were adolescents and very large, we used a 6-hole, 4.5-mm compression plate and screws. Third, we used an external fixator for increased stability in patients who weighed more than 250 pounds.

The reported technique, using an oblique metaphyseal closing wedge osteotomy with internal fixation in obese patients, is practical, safe, and reliable. This technique is a useful alternative to an external fixator. We used it on 9 knees with tibia vara, and it was completely successful in 8 cases and partially successful in 1 (hardware breakage occurred). An external fixator was used to prevent hardware breakage in 2 patients who weighed more than 250 pounds. This technique is a valuable treatment option for surgical correction, especially in obese patients.

Blount disease (tibia vara) is an angular tibia deformity that includes varus, increased posterior slope, and internal rotation. This deformity was first described in 1922 by Erlacher1 in Germany. In 1937, Walter Blount2 reported on it in the United States. It is the most common cause of pathologic genu varum in adolescence and childhood.

An oblique incomplete closing wedge osteotomy of the proximal tibial metaphysis was described by Wagner³ for the treatment of unicompartmental osteoarthrosis of the knee in adults. Laurencin and colleagues⁴ applied this technique to the treatment of pediatric tibia vara with favorable results. They spared the medial cortex of the tibia in their incomplete closing wedge osteotomy technique. In each of the 9 cases we treated and describe here, we accidentally completed the tibial osteotomy when attempting the Laurencin technique. Given that the osteotomy was completed, we modified the Laurencin technique by using a 6-hole, 4.5-mm compression plate rather than a 5-hole semitubular plate, and added a large oblique screw from the medial side to compress the osteotomy site and to protect the plate from fracture. In addition, in 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability. In this article, we report the outcomes of correcting adolescent tibia vara with a complete closing wedge tibial osteotomy and an oblique fibular osteotomy.

Materials and Methods

This study was approved by the Institutional Review Board at Pennsylvania State University. Between 2009 and 2012, we performed 9 complete oblique proximal tibial lateral closing wedge osteotomies on 8 patients (2 girls, 6 boys). In each case, the primary diagnosis was Blount disease. One patient also had renal dysplasia and was receiving dialysis. Mean age at time of operation was 15 years (range, 13-17 years). Mean preoperative weight was 215 pounds (range, 119-317 lb). Mean weight gain at follow-up was 4.39 pounds (range, –10 to 19 lb). Mean body mass index (BMI) was 38 (range, 25-48) (Table). All patients had varus angulation of the proximal tibia before surgery. Mean preoperative varus on standing films was 22° (range, 10°-36°). Because of the patients’ size, we used standing long-leg radiographs, on individual cassettes, for each leg.

Surgical Technique

Before surgery, we use paper cutouts to template the osteotomy wedge. We also use perioperative antibiotics and a standard time-out. For visualization of the entire leg for accurate correction, we prepare and drape the entire leg. A sterile tourniquet is used. At the midshaft of the fibula, a 4-cm incision is made, and dissection is carefully carried down to the fibula. Subperiosteal dissection is performed about the fibula, allowing adequate clearance for an oblique osteotomy. The osteotomy removes about 1 cm of fibula, which is to be used as bone graft for the tibial osteotomy. In addition, a lateral compartment fasciotomy is performed to prevent swelling-related complications. The wound is irrigated and injected with bupivacaine and closed in routine fashion.

We then make an inverted hockey-stick incision over the proximal tibia, centered down to the tibial tubercle. After dissecting down to the anterior compartment, we perform a fasciotomy of about 8 cm to accommodate swelling. Subperiosteal dissection is then performed around the proximal tibia. The medial soft tissues are left attached to increase blood supply and healing. During subperiosteal dissection, soft elevators are used to gently retract the lateral soft tissues along with the inferior and posterior structures. We use fluoroscopic imaging to guide the osteotomy as well as screw and plate placement. We use a 6-hole, 4.5-mm compression plate and screws for fixation. The 2 proximal screws of the plate are predrilled in place to allow for application of the plate after completion of the osteotomy. The plate is then rotated out of position on 1 screw, and the osteotomy is identified under fluoroscopy with the appropriate position distal to the second hole of the 6-hole plate.

An oscillating saw and osteotomes are used to perform the oblique osteotomy. The pre-estimated bone wedge is removed. Wedge size is adjusted, if needed. The bone wedge is morselized for bone graft. The osteotomy is then closed, correcting both varus and internal tibial torsion. Our goal is 5° valgus. After correction is obtained, the plate is placed, and the proximal screw is snugly seated. Three cortical screws are placed distally to hold the plate in place under compression mode, and a cancellous screw is placed superiorly at the proximal portion of the plate for additional fixation. The screw placed proximal to the osteotomy site is a fully threaded cortical screw with excellent compression. Correction and proper placement of hardware are verified with fluoroscopy.

The wound is irrigated and injected with bupivacaine. Bone graft is then placed at the osteotomy site. Additional bone graft is placed posteriorly between the osteotomy site and the muscle mass to stimulate additional healing. Another screw is placed obliquely from the medial side across the osteotomy site to provide additional fixation (Figure 1).

Copyright belongs to the authors

A deep drain is placed and connected to bulb suction for 24 hours after surgery. The wound is then closed in routine fashion. In 2 patients who weighed more than 250 pounds, we used an external fixator for additional stability (Figure 2).

Copyright belongs to the authors

Postoperative Care

The incisions are dressed with antibiotic ointment and 4×4-in bandages and then wrapped with sterile cotton under-cast padding. The leg is placed into a well-padded cylinder cast with the knee flexed 10°. The leg is aligned to about 5° valgus. The cast is then split on the side and spread to allow for swelling and to prevent compartment syndrome.⁵ We also use a drain hooked to bulb suction, which is removed 24 hours after surgery. Toe-touch weight-bearing with crutches is allowed immediately after surgery. The cast is removed at 6 weeks, and a hinged range-of-motion knee brace is worn for another 6 weeks. All patients are allowed to resume normal activity after 4 months. In our 2 external-fixator cases, a cast was not used, and toe-touch weight-bearing and knee motion were allowed immediately. The external fixators were removed at about 10 weeks.

Results

Mean postoperative mechanical femoral-tibial angle was 3°, and mean correction was 26° (range, 16°-43°) (Table). Lateral distal femoral angle did not show significant femoral deformity in our sample. Mean medial proximal tibial angle was 74° (range, 63°-79°). In each case, the varus deformity was primarily in the tibia. Mean tourniquet time was 88 minutes (range, 50-119 min). Our complication rate was 11% (1 knee). In our first case, in which we did not use an extra medial screw, the 4.5-mm plate fractured at the osteotomy site 2.5 months after surgery. The 250-pound patient subsequently lost 17° of correction, and valgus alignment was not achieved. Preoperative varus was 25°, and postoperative alignment was 8° varus. This plate fracture led us to use an extra medial screw for additional stability in all subsequent cases and to consider using an external fixator for patients weighing more than 250 pounds. After the first case, there were no other plate fractures. A potential problem with closing wedge osteotomy is shortening, but varus correction restores some length. Mean postoperative leg-length difference was 10 mm (range, 0-16 mm). No patient complained of leg-length difference during the postoperative follow-up.

Eight and a half months after surgery, 1 patient had hardware removed, at the family’s request. No patient experienced perioperative infection or neurovascular damage. Our overall patient population was obese—mean BMI was 38 (range, 25-48), and mean postoperative weight was 219 pounds. Three of our 8 patients were overweight (BMI, 25-30), and 5 were obese (BMI, >30). For prevention of plate failure, we recommend using an extra oblique screw in all patients and considering an external fixator for patients who weigh more than 250 pounds.

Discussion

Correction of adolescent tibia vara can be challenging because of patient obesity. The technique described here—a modification of the technique of Laurencin and colleagues⁴—is practical and reproducible in this population. The goals in performing osteotomy are to correct the deformity, restore joint alignment, preserve leg length, and prevent recurrent deformity and other complications, such as neurovascular injury, nonunion, and infection.^3,6-8 Our technique minimizes the risk for these complications. For example, the fasciotomy provides excellent decompression of the anterior and lateral compartments, minimizing neurovascular ischemia and the risk for compartment syndrome. During cast placement, splitting and spreading reduce the risk for compartment syndrome as well.⁵

Wagner3,9 demonstrated the utility of a closing wedge proximal tibial osteotomy in adults. Laurencin and colleagues4 showed this technique is effective in correcting tibia vara in a pediatric population. However, they did not specify patient weight and used a small semitubular plate for fixation, and some of their patients had infantile Blount disease. We modified the technique in 3 ways. First, we performed a complete osteotomy. Second, because our patients were adolescents and very large, we used a 6-hole, 4.5-mm compression plate and screws. Third, we used an external fixator for increased stability in patients who weighed more than 250 pounds.

The reported technique, using an oblique metaphyseal closing wedge osteotomy with internal fixation in obese patients, is practical, safe, and reliable. This technique is a useful alternative to an external fixator. We used it on 9 knees with tibia vara, and it was completely successful in 8 cases and partially successful in 1 (hardware breakage occurred). An external fixator was used to prevent hardware breakage in 2 patients who weighed more than 250 pounds. This technique is a valuable treatment option for surgical correction, especially in obese patients.