Orthopedics

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Case Reports 

Compartment Syndrome Following Intraosseous Infusion

Todd C. Moen, MD; John F. Sarwark, MD

Abstract

Initially described by Drinker et al1 in 1922, intraosseous infusion is a valuable technique in the resuscitation of critically ill pediatric patients in whom vascular access has proved otherwise impossible. Although it is well-established as a safe and reliable means of emergent access and is being used more frequently in both children and adults,2,3 intraosseous infusion is not without danger, nor complication.4-9 One of the rare yet most grave complications of intraosseous access is compartment syndrome. This article presents a case of compartment syndrome as a result of intraosseous infusion in a 6-year-old girl.

A 6-year-old otherwise healthy girl presented to our institution’s pediatric intensive care unit following emergent resuscitation for a prolonged cardiac arrest. Approximately 1 hour following an uneventful soccer practice, without any antecedent cardiopulmonary symptoms or complaints, the patient collapsed and was unresponsive, not breathing, and pulseless. Cardiopulmonary resuscitation (CPR) was initiated by the patient’s father at the scene, and local emergency medical services were called. The patient was found by the responding paramedics to be in a pulseless ventricular tachyarrhythmia, refractory to defibrillation by an automated external defibrillator. The patient was emergently transferred to a community hospital, and in the course of resuscitation, right and left tibial intraosseous lines were started. After 30 minutes of resuscitation, with multiple rounds of lidocaine and epinephrine infused through the intraosseous lines, a sustained perfusing rhythm was established. The patient was admitted to the intensive care unit, peripheral intravenous access was established, and approximately 1 hour after initial insertion, both intraosseous lines were removed. The patient was then transferred to our institution’s pediatric intensive care unit.

The patient presented to our institution approximately 9 hours after the initial cardiopulmonary collapse and resuscitation. Upon presentation to our institution, the patient was intubated, not sedated, and responsive only to vigorous painful stimuli. She could not actively follow commands. Physical examination was significant for a swollen right lower extremity, palpable but faint dorsalis pedis and posterior tibialis pulses, and diminished capillary refill when compared with the contralateral extremity. Over the course of the next 3 hours, the patient’s extremity examination deteriorated with a loss of pedal pulses, and the orthopedic surgery service was ultimately consulted approximately 12 hours following the initial cardiopulmonary event.

Initial examination by the orthopedic surgery service revealed an intubated, nonresponsive patient, with hemodynamics maintained with 3 vasopressors. Physical examination was notable for a swollen right lower extremity, taut anterior and posterior compartments, nondetectable pedal pulses by both palpation and Doppler, and diminished capillary refill throughout the foot. The patient could not follow commands, but passive flexion and extension of the ankle and toes elicited a withdrawal response. Compartment pressures were as follows: anterior, 81 mm Hg; lateral, 95 mm Hg; deep posterior, 75 mm Hg; superficial posterior, 22 mm Hg. Diastolic blood pressure ranged from 60 to 70 mm Hg.

Acute compartment syndrome was diagnosed, and a 4-compartment fasciotomy was planned. The patient was not sufficiently stable for transport to the operating room; therefore, at the patient’s bedside a popliteal nerve block was administered, and the patient was sedated as her hemodynamics allowed. Through anterolateral and posteromedial incisions, all 4 fascial compartments were released. Intraoperatively, the muscular tissue of the deep posterior compartment appeared ischemic and mottled and was not contractile with stimulation. The tissues of the superficial posterior, anterior, and lateral compartments also appeared ischemic, but were contractile with stimulation. Following release, the wounds were left open and packed with wet-to-dry dressings.

On postoperative day 1, pedal pulses had returned and capillary refill had improved. On postoperative day 2, plastic surgery was consulted for wound management, and they…

Initially described by Drinker et al1 in 1922, intraosseous infusion is a valuable technique in the resuscitation of critically ill pediatric patients in whom vascular access has proved otherwise impossible. Although it is well-established as a safe and reliable means of emergent access and is being used more frequently in both children and adults,2,3 intraosseous infusion is not without danger, nor complication.4-9 One of the rare yet most grave complications of intraosseous access is compartment syndrome. This article presents a case of compartment syndrome as a result of intraosseous infusion in a 6-year-old girl.

Case Report

A 6-year-old otherwise healthy girl presented to our institution’s pediatric intensive care unit following emergent resuscitation for a prolonged cardiac arrest. Approximately 1 hour following an uneventful soccer practice, without any antecedent cardiopulmonary symptoms or complaints, the patient collapsed and was unresponsive, not breathing, and pulseless. Cardiopulmonary resuscitation (CPR) was initiated by the patient’s father at the scene, and local emergency medical services were called. The patient was found by the responding paramedics to be in a pulseless ventricular tachyarrhythmia, refractory to defibrillation by an automated external defibrillator. The patient was emergently transferred to a community hospital, and in the course of resuscitation, right and left tibial intraosseous lines were started. After 30 minutes of resuscitation, with multiple rounds of lidocaine and epinephrine infused through the intraosseous lines, a sustained perfusing rhythm was established. The patient was admitted to the intensive care unit, peripheral intravenous access was established, and approximately 1 hour after initial insertion, both intraosseous lines were removed. The patient was then transferred to our institution’s pediatric intensive care unit.

The patient presented to our institution approximately 9 hours after the initial cardiopulmonary collapse and resuscitation. Upon presentation to our institution, the patient was intubated, not sedated, and responsive only to vigorous painful stimuli. She could not actively follow commands. Physical examination was significant for a swollen right lower extremity, palpable but faint dorsalis pedis and posterior tibialis pulses, and diminished capillary refill when compared with the contralateral extremity. Over the course of the next 3 hours, the patient’s extremity examination deteriorated with a loss of pedal pulses, and the orthopedic surgery service was ultimately consulted approximately 12 hours following the initial cardiopulmonary event.

Initial examination by the orthopedic surgery service revealed an intubated, nonresponsive patient, with hemodynamics maintained with 3 vasopressors. Physical examination was notable for a swollen right lower extremity, taut anterior and posterior compartments, nondetectable pedal pulses by both palpation and Doppler, and diminished capillary refill throughout the foot. The patient could not follow commands, but passive flexion and extension of the ankle and toes elicited a withdrawal response. Compartment pressures were as follows: anterior, 81 mm Hg; lateral, 95 mm Hg; deep posterior, 75 mm Hg; superficial posterior, 22 mm Hg. Diastolic blood pressure ranged from 60 to 70 mm Hg.

Acute compartment syndrome was diagnosed, and a 4-compartment fasciotomy was planned. The patient was not sufficiently stable for transport to the operating room; therefore, at the patient’s bedside a popliteal nerve block was administered, and the patient was sedated as her hemodynamics allowed. Through anterolateral and posteromedial incisions, all 4 fascial compartments were released. Intraoperatively, the muscular tissue of the deep posterior compartment appeared ischemic and mottled and was not contractile with stimulation. The tissues of the superficial posterior, anterior, and lateral compartments also appeared ischemic, but were contractile with stimulation. Following release, the wounds were left open and packed with wet-to-dry dressings.

On postoperative day 1, pedal pulses had returned and capillary refill had improved. On postoperative day 2, plastic surgery was consulted for wound management, and they ultimately placed a vacuum assisted closure (VAC). The patient’s extremity examination continued to improve, as did the appearance of the fasciotomy wounds, and a delayed primary closure was performed on postoperative day 8. While the condition of the patient’s extremity improved, the overall clinical condition of the patient did not. The patient had sustained an ischemic neurologic insult due to the prolonged cardiac arrest, and the insult was felt to be unrecoverable. The patient died 1 month following the initial event.

Discussion

Intraosseous infusion is used increasingly in both pediatric and adult emergency care.10-13 Although an invaluable technique in emergent resuscitation, intraosseous infusion can be prone to complication with improper technique.4-9,14-16 One of the most serious complications is compartment syndrome. Given the increased use of intraosseous infusion, this case provides a relevant opportunity to review the pertinent anatomy of pediatric long bones, fundamentals of the technique of intraosseous infusion and, more importantly, the principles of diagnosis and treatment of compartment syndrome.

The anatomy of the intraosseous space of the proximal tibia and the proper indications and correct technique for intraosseous access are well-described.17,18 The intramedullary canal of pediatric long bones creates a compelling target for emergent vascular access, as the vascularity of the intramedullary canal in children is supported by a bony architecture, allowing them to remain patent in the face of cardiovascular collapse. Fluids administered to cancellous bone are absorbed by the microvasculature, ultimately enter the systemic circulation via a number of routes,17-19 and can be administered more quickly than those administered peripherally.20

Broadly, intraosseous access is indicated for children younger than 6 years in need of vascular access in whom 3 attempts at peripheral access have failed, or after 90 seconds, whichever arrives first. Several commercially available devices can be used to obtain intraosseous access.21 Regardless of the device, the needle used should be strong enough to penetrate cortical bone and have a large enough lumen to avoid obstruction from osseous material. In the tibia, the needle should be inserted from the anteromedial aspect, directed away from the epiphysis. Appropriate placement does not require radiographic conformation, but requires aspiration of bone marrow prior to the initiation of infusion. Only 1 penetration of the cortex should be attempted, and once access has been obtained, the needle should be strongly secured to a splint to prevent iatrogenic removal and dislodgement of the catheter. Multiple cortical perforations, dislodgement of the catheter, or other technical errors can lead to the extravasation of fluid into the leg, which can in turn lead to compartment syndrome.2,3,17,18

Compartment syndrome is defined as a condition in which the pressure of a minimally distensible osseofascial muscular compartment reaches an elevated level such that the perfusion gradient across capillary beds is significantly diminished, leading to tissue hypoxia, ischemia, and death. A fracture, bleeding disorder, contusion, burn, or other local insult to a muscular compartment induces local inflammation and edema. The fascial and bony compartments surrounding the local insult have a limited capacity to expand their volume, and thus as the local edema increases, so does the local compartment pressure. The exact mechanism of how systemic blood pressure and local interstitial pressure interact to cause compartment syndrome is unknown. However, recent literature suggests that when the absolute pressure gradient between systemic blood pressure and intracompartmental pressure decreases below a certain level, compartment syndrome ensues.22-24 The precise critical pressure gradient varies with pressures, local metabolic activity, and vascular resistance,25,26 and is between 20 and 30 mm Hg.

Compartment syndrome is primarily a clinical diagnosis. A pressured, tight compartment should elicit a suspicion for compartment syndrome, and dogma has stressed that the 6 Ps—pressure, pain, pulselessness, paresthesias, paralysis, and pallor—are the keys in identifying this syndrome. Of these 6, pressure and pain are the most useful. Pain out of proportion to an inciting event and pain with passive flexion and extension are the most sensitive symptom and sign, respectively, of compartment syndrome. When there is sufficient clinical suspicion, direct measurement of intracompartmental pressures with commercially available pressure monitors or modified arterial line apparatuses can aid in ruling in or ruling out the diagnosis. Although the specific pressure threshold at which compartment syndrome develops is controversial, absolute compartment pressures above 30 mm Hg or within 20 to 30 mm Hg of diastolic blood pressure are indications for emergent fasciotomy.

In a patient for whom there is a suspicion of compartment syndrome but for whom a reliable clinical and neurovascular examination cannot be elicited, such as a critically ill or obtunded patient, it becomes more challenging to make the diagnosis of compartment syndrome, and a greater emphasis must be placed on compartmental pressure measurements. However, compartment pressure measurements can be inaccurate.23 Most authors would argue that in a patient, obtunded or otherwise, with an extremity with a tight myofascial compartment and evidence of distal microvascular compromise, but normal or equivocal compartment pressure measurements, a diagnosis of compartment syndrome could still be made, and surgical intervention would be indicated.

Four-compartment fasciotomy of the lower extremity is ideally performed in the controlled environment of an operating room. However, if the patient is too unstable for transport, fasciotomy may be performed at bedside. Regardless of the location of the procedure, fasciotomy of all 4 compartments of the lower extremity may be performed via a 1- or 2-incision technique, with the 2-incision technique being preferred. In the 2-incision technique, the fascia of anterior and lateral compartments are released via an anterolateral incision, and the fascia of the deep and superficial compartments are released via a posteromedial incision. In the 1-incision technique, all 4 compartments are released via a direct lateral incision and approach. Along with fascial release, any frankly necrotic or nonviable tissue is debrided. Following the release, the wounds are left open to allow for full decompression, and a delayed closure is performed when the compartments are suitable.

The case described here highlights the fundamental principles regarding the use of intraosseous infusion and the diagnosis and management of compartment syndrome in critically ill patients. Intraosseous infusion is a potentially life-saving method to achieve vascular access, but given the risk of intracompartmental fluid extravasation, it should only be used until other access routes are secured. Once intraosseous access has been discontinued, the involved extremity must be vigilantly observed and assessed for signs of compartment syndrome or neurovascular compromise, particularly in the critically ill patient. There must be a low threshold to measure compartment pressures in a patient in which compartment syndrome is suspected, and once the diagnosis of compartment syndrome has been made, emergent fasciotomy, either in the operating room or at the bedside, must be performed. Failure to do this may result in loss of significant extremity function or even loss of the extremity itself,6,8 while prompt compartment release can allow for an eventual return to full recovery.4,14,16

References

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Authors

Dr Moen is from the Department of Orthopedic Surgery, Northwestern University Feinberg School of Medicine, and Dr Sarwark is from the Division of Pediatric Orthopedic Surgery, Children’s Memorial Hospital, Chicago, Illinois.

Drs Moen and Sarwark have no relevant financial relationships to disclose.

Correspondence should be addressed to: John F. Sarwark, MD, Children’s Memorial Hospital, Division of Pediatric Orthopedic Surgery, 2300 Children’s Plaza, Chicago, IL 60614-3363.

10.3928/01477447-20080801-17

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