- Email: [email protected]
Intraosseous Extravasation Complication Reports
CASE REPORT
Intraosseous Extravasation Complication Reports From the Departmentsof Emergency Medicine* and Pediatrics,~ Loma Linda University School of Medicine, Loma Linda, California.
C Michael Simmons, MD* N Eric Johnson,MD, MPH, FACEP* Ronald M Perkin, MD, FCCMt David van Stralen, MDt
Receivedfor publication September8, 1992. Acceptedfor publication May 27, 1993.
We report two cases of severe complications from intraosseous infusions. One child was a sudden infant death syndrome patient who developed severe tissue necrosis after intraosseous placement. The second child was a near drowning who developed a compartment syndrome requiring fasciotomy. Extravasation is a potentially major complication that resulted in these limb-threatening events. Intraosseous infusion remains an important resuscitation modality, but great care must be taken to avoid these results. Strategies for avoiding extravasation are discussed. [Simmons CM, Johnson NE, Perkin RM, van Stralen D: Intraosseous extravasation complication reports. Ann Emerg Med February 1994;23:363-366.] INTRODUCTION Rediscovery and popularization of intraosseous infusion represent a major advance in pediatric resuscitation practice within the past five years. Orlowski's lament, "My kingdom for an IV" is no longer cried, as intraosseous infusion has proven to be an effective initial pediatric vascular access strategy in emergencies.1 We report two cases of severe intraosseous extravasation injury. Opportunities for improvement in technique that minimize extravasation risk are discussed, particularly as taught by advanced life support curricula.
CASE REPORT 1 A 27-month-old boy who was found face-down in a cold Jacuzzi with an estimated down-time of 30 minutes presented to a local emergency department by paramedic ambulance. On arrival, the patient was pulseless and apneic. The patient was intubated and attempts at IV access were made, which included multiple punctures of both tibiae with eventual successful placement of a proximal left tibial intraosseous line. Laboratory evaluation revealed a pH of 6.8; Pco 2, 40; Po2,494; and base excess, -28. Sodium was 134; potassium, 2.7; chloride, 90; and
FEBRUARY 1994 23:2 ANNALS OF EMERGENCY MEDICINE
363
INTRAOSSEOUS EXTRAVASATION Simmons et al
Co 2, 8.7. Subsequently, through the intraosseous line the patient received atropine (0.25 mg), NaHCO 3 (5.0 mEq), epinephrine (1.0 mg), followed by epinephrine (10.0 mg) and methylprednisolone. The resuscitation efforts resulted in return of a blood pressure and pulse. On initial examination by the transport physician, the patient was intubated, sedated, and paralyzed. The extremities revealed good pulses and perfusion. The patient's left lower extremity was purple and swollen. The patient was transported and admitted to Loma Linda University Medical Center pediatric ICU. Examination the following day revealed multiple puncture sites on both tibiae proximally and distally. The left leg was markedly edematous and tense, with loss of the dorsalis pedis and posterotibial pulses. The patient reacted vigorously to passive dorsiflexion of the foot. Orthopedics consultation was sought, and compartment pressures were measured. The anterior and posterior compartment pressures were more than 100 mm Hg; the lateral compartment pressure was normal at 15 mm Hg. Four-compartment fasciotomy was performed, with the patient undergoing delayed primary closure four days later. The patient eventually was transferred to a neurologic rehabilitation center. At the time of transfer, the patient had a remaining severe anoxic encephalopathy with decorticate posturing in the upper extremities and extensor posturing in the lower extremities with a residual foot drop on the left side. CASE REPORT 2
A 3-month-old, apparently healthy girl was found unresponsive 30 minutes after being laid supine in bed, asleep. No bystander CPR was performed; CPR was performed during ten minutes of police transport. Advanced life support, including endotracheal ventilation and intraosseous cannulation, was initiated on ED arrival. ECG monitoring revealed initial asystole. Initial blood gas revealed a pH of 6.78; Pco 2, 40; base excess, -32; and Pox, 600. The sodium was 127 and the potassium was 4.2. The patient was treated with epinephrine (0.2 mg x five), atropine (0.1 mg x two), NaHCO 3 (4.0 mL) and lidocaine (4.0 mg) administered by intraosseous push. Ventricular fibrillation resulted, converting to sinus tachycardia with multiple defibrillations after 27 minutes of advanced life support. Multiple bilateral tibial intraosseous cannulations infiltrated and were discontinued before subclavian cannulation was achieved. The infant was transferred to Loma Linda University Medical Center in a coma.
364
On arrival, the right proximal pretibial area was ecchymotic and edematous, with two puncture wounds. Multiple left pretibial puncture wounds also were noted. During the next 48 hours, bullae formed over the right intraosseous wounds, with serosanguinous fluid leakage. On declaration of brain death, donor cardiac and hepatic harvest was completed before life support termination. An autopsy was not performed. Had the patient survived, surgical intervention (debridement, skin grafting) would have been required. DISCUSSION
The resurgence of the intraosseous technique in the emergency setting has added greatly to the resuscitation armamentarium of medical personnel. Drinker and Drinker2 published their first work on circulation of the mammalian bone marrow in 1916 in the AmericanJournal of Physiology when they demonstrated vasomotor control of the marrow vessels of the dog tibia. This was expanded in 1922, further outlining the vasomotor control of the marrow vessels. 3 Tocantins4 demonstrated the rapid absorption of intraosseous injections and popularized the intraosseous technique. Thereafter, the literature is replete with case reports of intraosseous infusion and the attendant complicationsJ later, the technique was largely forgotten with the advent of improved IV devices and increased skill in their use. For the most part, this technique has been attended by few and reasonably minor complications. One case of tissue necrosis resulting from an intraosseous infusion was reported by Pillar 6 in a patient who had a levarterenol infusion. Rosetti et al 7 reviewed 4,270 cases in the intraosseous literature and found a 0.6% incidence of osteomyelitis, by far the most frequent complication. However, these resulted only from prolonged infusions. A few cases of mediastinitis from sternal puncture as well as several subcutaneous abscesses were noted. 7 Since that review, bilateral tibia fractures have been reported in a 3month-old infant as well as a compartment syndrome in a 5-week-old boy. Skin necrosis has been reported in a 3month-old boy and in an 1 l-month-old boy. A compartment syndrome requiring amputation has been reported in a 3-month-old boy.8-1E Growth plate injury, a potential complication that has long concerned researchers, has not been substantiated by animal studies or reports from the literature. 12,13 The only instances of growth plate abnormalities have been in patients with severe osteomyelitis. 13 A second concern has been fat emboli.14-16 Fat emboli do occur
ANNALS OF EMER6ENCY MEDICINE
23:2
FEBRUARY 1994
INTRAOSSEOUS EXTRAVASATION Simmons et al
microscopically, but they are so small as to be not clinically relevant. The only problem with modern, emergent intraosseous technique that, as demonstrated above, can have severe clinical relevance is extravasation into the subcutaneous tissues. This potential complication is documented frequently, but the serious sequelae rarely have been identified specifically. With the exception of recent case reports, compartment syndrome and necrosis of the skin generally are not recognized as the devastating end result of extravasation into the subcutaneous tissues.r,9-11,1 r-2o From the two cases presented, we can conclude that second attempts at intraosseous line placement in the same bone can result in extravasation with potentially disastrous results. We can only surmise that poor insertion technique may have contributed as well. The first patient received atropine, NaHCO 3 epinephrine, and methylprednisolone. In the second' patient, the necrosis appeared on the right side where epinephrine, NaHCO3, atropine, and lidocaine were all infused as opposed to the left side where only epinephrine was infused. Of the patients with compartment syndrome previously reported, one received normal saline, NaHCO 3, epinephrine, calcium gluconate, and atropine, whereas the other received atropine, epinephrine, 0.25% NaC1, and NaHCO3.9,z 1 Of the patients with skin necrosis previously reported, one patient received levarterenol; one received epinephrine, atropine, NaHCO3, and isoproterenol; and the third received lactated Ringer's solution, epinephrine, and atropine. 6,1° Many IV drugs have been implicated in tissue necrosis including chemotherapeutic agents, heparin, KC1, hyperalimentation, some antibiotics, epinephrine, norepinephrine, dobutamine, dopamine, radiographic contrast agents, hypertonic glucose, calcium, and NaHCO3 .21-31 A compartment syndrome has been reported in a patient with an IV line that infiltrated while being infused by a pressurized infusion pump. The IV line contained 5% dextrose and 0.25% NaC1 with 20 mEq of KC1 added. 32 Both of the patients reported here had drugs infused that have reported tissue toxicity. However, it is difficult to determine which drug is the actual culprit and, in the case of the compartment syndrome, whether this resulted from drugs or if it was secondary solely to the mechanical effects of pressurized fluid infusion. Extravasation risk may result from several technical errors, some of which inadvertently may be promoted in current advanced life support curricula. Insertion error may arise from misplacement in the soft tissue by failure
FEBRUARY 1994 23:2 ANNALS OF EMERGENCY MEDICINE
to penetrate the cortex completely or by overpenetration through the opposite cortex. Insertion error also may occur from wobbly insertion technique. This may be a complication of poor operator technique or from dull needle tips requiring greater pressure for insertion. Another cause of extravasation is cortical disruption. This can result when previous insertion attempts are ignored, as illustrated by the cases discussed here, or by an unrecognized previous fracture or by fracture of the extremity when placing the line. This cortical disruption may also result in less drug bioavailability as demon-strated by Brickman et aP 3 in their study on phenobarbital levels in single versus multiple attempts at intraosseous infusions. A final source of error can occur after the intraosseous cannula has been placed successfully. If the limb is not splinted, movement of the patient may result in loosening or dislodgment of the intraosseous needle. If the IV tubing is not secured adequately, tugging on it may result in loosening or dislodgment of the needle. It is important always to remain alert for extravasation by monitoring the infusion site. If the site is obscured by a dressing, then the risk of unrecognized and continuing extravasation is increased greatly. Screw designs and improved tip and shaft materials under development may improve future shaft continence. Meanwhile, the following strategies should be considered: 1. Use sharp needles requiring less pressure for cortical perforation. 2. Use needles with strong metal resistant to damage during penetration effort. 3. Emphasize rotary motion with stabilizing fingertips on insertion surface, rather than downward pressure with high shaft center of gravity. 4. Avoid direct aspiration/infusion syringe tests of placement (use injection sites of IV tubing). 5. Avoid dressings on site. 6. Stabilize tubing and limb (not needle shaft) to minimize accidental dislodgment or traumatic loosening. 7. Monitor continuously for signs of extravasation. 8. Discontinue infusion on accomplishing other venous access. CONCLUSION
Severe complications from extravasation during intraosseous infusion can occur. Further development of the infusion devices is needed. In the meantime, intraosseous infusion should not be abandoned; however, strategies that reduce the risk of extravasation should be used.
365
INTRAOSSEOUS EXTRAVASATION Simmons et aZ
REFERENCES 1. Orlowski J: My kingdom for an intravenous line. Am J Ois Child1984;138:803. 2. Drinker CK, Drinker KR: A method for maintaining an artificial circulation through the tibia of the dog, with a demonstration of the vasomotor control of the marrow vessels. Am J Physiol 1916; XL:514-521. 3. Drinker CK, Drinker KR, Lund CC: The circulation in the mammalian bone-marrow. Am J Physio11922;62:1-92. 4. Tocantins LM: Rapid absorption of substances injected into the bone marrow. ProcSac Exp Biol Med 1940;45:292-296. 5. Fiser DH: Intraosseus infusion. NEnglJMed1990;322:1579-1581. 6. Pillar S: Re-emphasis on bone marrow as a medium for administration of fluid. N EnglJ Med 1954;251:846-851. 7. Rosetti VA, Thompson BM, Miller J, et al: An alternative route of pediatric intravascular access. Ann EmergMed 1985;14:885-888. 8. La Fleche FR, Slepin M J, Vargas J, et al: latrogenic bilateral tibial fractures after intraosseous infusion attempts in a 3-month-old infant. Ann EmergMeal1989;18:1099-1101. g. Rimar S, Westry J, Rodriguez R: Compartment syndrome in an infant following emergency intraosseous infusion. ClinPediatr1988;27:259-260.
30. Reed W, Newman KA, Applefeld MM, et el: Drug extravasation as a complication of venous access ports. Ann InternMed1985;102:788-789. 31. Yosowitz P, Eldand DA, Shaw RC, et al: Peripheral intravenous infiltration necrosis. Ann Surg 1975;182:553-556. 32. Handler E: Superficial compartment of the foot after infiltration of intravenous fluid. Arch PhysMed Rehabil 1990;71:58-59. 33. Brickman K, Rega P, Choa M, et al: Comparison of serum phenobarbital levels after single versus multiple attempts at intraosseous infusion. Ann EmergMed1990;19:31-33.
Reprint no. 47/1/32822 Address for reprints: C MichaelSimmons,MD Department of Emergency Medicine Baystate Medical Center Springfield, Massachusetts 01199 413-784-5375
10. Christensen DW, Vernon DD, Banner W, et al: Skin necrosis complicating intraosseous infusion. PediatrEmergCare1991;7:289-290. 11. Moscati R, Moore P: Compartment syndrome with resultant amputation following intraosseous infusion. Am J EmergMed 1990;8:470-471. 12. Brickman KR, Rega P, Koltz M, et al: Analysis of growth plate abnormalities following emergency intraosseous infusion through the proximal tibial epiphysis in pigs. Ann EmergMed 1988;17:121-123. 13. Heinild S, Sendergard T, Tudvad F: Bone marrow infusion in childhood. Experiences from a thousand infusions. J Pediatr1947;30:400-411. 14. Orlowski JP, Jusius CJ, Petras RE, et ah The safety of intraosseous infusions: Risks of fat and bone marrow emboli to the lungs. Ann EmergMed 1989;18:1062-1067. 15. Plewa MC, Kaplan RM, LaCovey D, et al: Fat embolism following intraosseous infusion. Ann EmergMed 1988;17:407. 16. Wile UJ, Schamberg IL: Pulmonary fat embolism following infusions via the bone marrow. J InvestOermatol1942; 5:173-177. 17. Massey LWC: Bone marrow infusion: Intratibial and intravenous routes compared. Br Med J 1950;2:197-198. 18. Meola F: Bone marrow infusions as a routine procedure in children. J Pediatr1944;25:13-16. 19. Quilligan J J, Turkel H: Bone marrow infusions and its complications. Am J Dis Child 1946;71:457-465. 20. Smith RJ, Keseg DP, Menley LK, et al: Intraosseaus infusions by prehaspital personnel in critically ill pediatric patients. Ann EmergMed1988;17:491-495. 21. Behnia R, Wilkinson C: Lidocaine treatment of experimental cutaneous lesions from potassium chloride injection. Anesthesiology1977;47:428-429. 22. grown A, Hoelzer D, Piercy S: Skin necrosis from extravasation of intravenous fluids in children. PlastReconstrSurg1979;64:145-150. 23. gurk R Ill, Serafin D, Klitzman B: Toxic effects of catecholamines on skin. PlastReconstrSurg 1990;85:92-99. 24. Close A, Frackelton W: Cutaneous necrosis due to norepinephrine: Analysis of reported cases and surgical treatment. Wis MealJ1958;127-132. 25. Close A: Phentolamine hydrochloride in prevention of cutaneous necrosis due to levarterenol. JAMA 1959;170:1916-1917. 26.6aze N: Tissue necrosis caused by commonly used intravenous infusions. Lancet1978;:417419. 27. Heft J, Beatty P, Wade J: Dermal necrosis from dobutamine. N EnglJ Med 1979;1280. 28. Jackson I, Robinson D: Severe tissue damage following accidental subcutaneous infusion of bicarbonate solution. ScotMed J 1976;21:200-201. 29. Lath T, Eversmann W Jr: Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248-254.
366
ANNALS OF EMERGENCY MEDICINE 23:2 FEBRUARY 1994
Intraosseous Extravasation Complication Reports From the Departmentsof Emergency Medicine* and Pediatrics,~ Loma Linda University School of Medicine, Loma Linda, California.
C Michael Simmons, MD* N Eric Johnson,MD, MPH, FACEP* Ronald M Perkin, MD, FCCMt David van Stralen, MDt
Receivedfor publication September8, 1992. Acceptedfor publication May 27, 1993.
We report two cases of severe complications from intraosseous infusions. One child was a sudden infant death syndrome patient who developed severe tissue necrosis after intraosseous placement. The second child was a near drowning who developed a compartment syndrome requiring fasciotomy. Extravasation is a potentially major complication that resulted in these limb-threatening events. Intraosseous infusion remains an important resuscitation modality, but great care must be taken to avoid these results. Strategies for avoiding extravasation are discussed. [Simmons CM, Johnson NE, Perkin RM, van Stralen D: Intraosseous extravasation complication reports. Ann Emerg Med February 1994;23:363-366.] INTRODUCTION Rediscovery and popularization of intraosseous infusion represent a major advance in pediatric resuscitation practice within the past five years. Orlowski's lament, "My kingdom for an IV" is no longer cried, as intraosseous infusion has proven to be an effective initial pediatric vascular access strategy in emergencies.1 We report two cases of severe intraosseous extravasation injury. Opportunities for improvement in technique that minimize extravasation risk are discussed, particularly as taught by advanced life support curricula.
CASE REPORT 1 A 27-month-old boy who was found face-down in a cold Jacuzzi with an estimated down-time of 30 minutes presented to a local emergency department by paramedic ambulance. On arrival, the patient was pulseless and apneic. The patient was intubated and attempts at IV access were made, which included multiple punctures of both tibiae with eventual successful placement of a proximal left tibial intraosseous line. Laboratory evaluation revealed a pH of 6.8; Pco 2, 40; Po2,494; and base excess, -28. Sodium was 134; potassium, 2.7; chloride, 90; and
FEBRUARY 1994 23:2 ANNALS OF EMERGENCY MEDICINE
363
INTRAOSSEOUS EXTRAVASATION Simmons et al
Co 2, 8.7. Subsequently, through the intraosseous line the patient received atropine (0.25 mg), NaHCO 3 (5.0 mEq), epinephrine (1.0 mg), followed by epinephrine (10.0 mg) and methylprednisolone. The resuscitation efforts resulted in return of a blood pressure and pulse. On initial examination by the transport physician, the patient was intubated, sedated, and paralyzed. The extremities revealed good pulses and perfusion. The patient's left lower extremity was purple and swollen. The patient was transported and admitted to Loma Linda University Medical Center pediatric ICU. Examination the following day revealed multiple puncture sites on both tibiae proximally and distally. The left leg was markedly edematous and tense, with loss of the dorsalis pedis and posterotibial pulses. The patient reacted vigorously to passive dorsiflexion of the foot. Orthopedics consultation was sought, and compartment pressures were measured. The anterior and posterior compartment pressures were more than 100 mm Hg; the lateral compartment pressure was normal at 15 mm Hg. Four-compartment fasciotomy was performed, with the patient undergoing delayed primary closure four days later. The patient eventually was transferred to a neurologic rehabilitation center. At the time of transfer, the patient had a remaining severe anoxic encephalopathy with decorticate posturing in the upper extremities and extensor posturing in the lower extremities with a residual foot drop on the left side. CASE REPORT 2
A 3-month-old, apparently healthy girl was found unresponsive 30 minutes after being laid supine in bed, asleep. No bystander CPR was performed; CPR was performed during ten minutes of police transport. Advanced life support, including endotracheal ventilation and intraosseous cannulation, was initiated on ED arrival. ECG monitoring revealed initial asystole. Initial blood gas revealed a pH of 6.78; Pco 2, 40; base excess, -32; and Pox, 600. The sodium was 127 and the potassium was 4.2. The patient was treated with epinephrine (0.2 mg x five), atropine (0.1 mg x two), NaHCO 3 (4.0 mL) and lidocaine (4.0 mg) administered by intraosseous push. Ventricular fibrillation resulted, converting to sinus tachycardia with multiple defibrillations after 27 minutes of advanced life support. Multiple bilateral tibial intraosseous cannulations infiltrated and were discontinued before subclavian cannulation was achieved. The infant was transferred to Loma Linda University Medical Center in a coma.
364
On arrival, the right proximal pretibial area was ecchymotic and edematous, with two puncture wounds. Multiple left pretibial puncture wounds also were noted. During the next 48 hours, bullae formed over the right intraosseous wounds, with serosanguinous fluid leakage. On declaration of brain death, donor cardiac and hepatic harvest was completed before life support termination. An autopsy was not performed. Had the patient survived, surgical intervention (debridement, skin grafting) would have been required. DISCUSSION
The resurgence of the intraosseous technique in the emergency setting has added greatly to the resuscitation armamentarium of medical personnel. Drinker and Drinker2 published their first work on circulation of the mammalian bone marrow in 1916 in the AmericanJournal of Physiology when they demonstrated vasomotor control of the marrow vessels of the dog tibia. This was expanded in 1922, further outlining the vasomotor control of the marrow vessels. 3 Tocantins4 demonstrated the rapid absorption of intraosseous injections and popularized the intraosseous technique. Thereafter, the literature is replete with case reports of intraosseous infusion and the attendant complicationsJ later, the technique was largely forgotten with the advent of improved IV devices and increased skill in their use. For the most part, this technique has been attended by few and reasonably minor complications. One case of tissue necrosis resulting from an intraosseous infusion was reported by Pillar 6 in a patient who had a levarterenol infusion. Rosetti et al 7 reviewed 4,270 cases in the intraosseous literature and found a 0.6% incidence of osteomyelitis, by far the most frequent complication. However, these resulted only from prolonged infusions. A few cases of mediastinitis from sternal puncture as well as several subcutaneous abscesses were noted. 7 Since that review, bilateral tibia fractures have been reported in a 3month-old infant as well as a compartment syndrome in a 5-week-old boy. Skin necrosis has been reported in a 3month-old boy and in an 1 l-month-old boy. A compartment syndrome requiring amputation has been reported in a 3-month-old boy.8-1E Growth plate injury, a potential complication that has long concerned researchers, has not been substantiated by animal studies or reports from the literature. 12,13 The only instances of growth plate abnormalities have been in patients with severe osteomyelitis. 13 A second concern has been fat emboli.14-16 Fat emboli do occur
ANNALS OF EMER6ENCY MEDICINE
23:2
FEBRUARY 1994
INTRAOSSEOUS EXTRAVASATION Simmons et al
microscopically, but they are so small as to be not clinically relevant. The only problem with modern, emergent intraosseous technique that, as demonstrated above, can have severe clinical relevance is extravasation into the subcutaneous tissues. This potential complication is documented frequently, but the serious sequelae rarely have been identified specifically. With the exception of recent case reports, compartment syndrome and necrosis of the skin generally are not recognized as the devastating end result of extravasation into the subcutaneous tissues.r,9-11,1 r-2o From the two cases presented, we can conclude that second attempts at intraosseous line placement in the same bone can result in extravasation with potentially disastrous results. We can only surmise that poor insertion technique may have contributed as well. The first patient received atropine, NaHCO 3 epinephrine, and methylprednisolone. In the second' patient, the necrosis appeared on the right side where epinephrine, NaHCO3, atropine, and lidocaine were all infused as opposed to the left side where only epinephrine was infused. Of the patients with compartment syndrome previously reported, one received normal saline, NaHCO 3, epinephrine, calcium gluconate, and atropine, whereas the other received atropine, epinephrine, 0.25% NaC1, and NaHCO3.9,z 1 Of the patients with skin necrosis previously reported, one patient received levarterenol; one received epinephrine, atropine, NaHCO3, and isoproterenol; and the third received lactated Ringer's solution, epinephrine, and atropine. 6,1° Many IV drugs have been implicated in tissue necrosis including chemotherapeutic agents, heparin, KC1, hyperalimentation, some antibiotics, epinephrine, norepinephrine, dobutamine, dopamine, radiographic contrast agents, hypertonic glucose, calcium, and NaHCO3 .21-31 A compartment syndrome has been reported in a patient with an IV line that infiltrated while being infused by a pressurized infusion pump. The IV line contained 5% dextrose and 0.25% NaC1 with 20 mEq of KC1 added. 32 Both of the patients reported here had drugs infused that have reported tissue toxicity. However, it is difficult to determine which drug is the actual culprit and, in the case of the compartment syndrome, whether this resulted from drugs or if it was secondary solely to the mechanical effects of pressurized fluid infusion. Extravasation risk may result from several technical errors, some of which inadvertently may be promoted in current advanced life support curricula. Insertion error may arise from misplacement in the soft tissue by failure
FEBRUARY 1994 23:2 ANNALS OF EMERGENCY MEDICINE
to penetrate the cortex completely or by overpenetration through the opposite cortex. Insertion error also may occur from wobbly insertion technique. This may be a complication of poor operator technique or from dull needle tips requiring greater pressure for insertion. Another cause of extravasation is cortical disruption. This can result when previous insertion attempts are ignored, as illustrated by the cases discussed here, or by an unrecognized previous fracture or by fracture of the extremity when placing the line. This cortical disruption may also result in less drug bioavailability as demon-strated by Brickman et aP 3 in their study on phenobarbital levels in single versus multiple attempts at intraosseous infusions. A final source of error can occur after the intraosseous cannula has been placed successfully. If the limb is not splinted, movement of the patient may result in loosening or dislodgment of the intraosseous needle. If the IV tubing is not secured adequately, tugging on it may result in loosening or dislodgment of the needle. It is important always to remain alert for extravasation by monitoring the infusion site. If the site is obscured by a dressing, then the risk of unrecognized and continuing extravasation is increased greatly. Screw designs and improved tip and shaft materials under development may improve future shaft continence. Meanwhile, the following strategies should be considered: 1. Use sharp needles requiring less pressure for cortical perforation. 2. Use needles with strong metal resistant to damage during penetration effort. 3. Emphasize rotary motion with stabilizing fingertips on insertion surface, rather than downward pressure with high shaft center of gravity. 4. Avoid direct aspiration/infusion syringe tests of placement (use injection sites of IV tubing). 5. Avoid dressings on site. 6. Stabilize tubing and limb (not needle shaft) to minimize accidental dislodgment or traumatic loosening. 7. Monitor continuously for signs of extravasation. 8. Discontinue infusion on accomplishing other venous access. CONCLUSION
Severe complications from extravasation during intraosseous infusion can occur. Further development of the infusion devices is needed. In the meantime, intraosseous infusion should not be abandoned; however, strategies that reduce the risk of extravasation should be used.
365
INTRAOSSEOUS EXTRAVASATION Simmons et aZ
REFERENCES 1. Orlowski J: My kingdom for an intravenous line. Am J Ois Child1984;138:803. 2. Drinker CK, Drinker KR: A method for maintaining an artificial circulation through the tibia of the dog, with a demonstration of the vasomotor control of the marrow vessels. Am J Physiol 1916; XL:514-521. 3. Drinker CK, Drinker KR, Lund CC: The circulation in the mammalian bone-marrow. Am J Physio11922;62:1-92. 4. Tocantins LM: Rapid absorption of substances injected into the bone marrow. ProcSac Exp Biol Med 1940;45:292-296. 5. Fiser DH: Intraosseus infusion. NEnglJMed1990;322:1579-1581. 6. Pillar S: Re-emphasis on bone marrow as a medium for administration of fluid. N EnglJ Med 1954;251:846-851. 7. Rosetti VA, Thompson BM, Miller J, et al: An alternative route of pediatric intravascular access. Ann EmergMed 1985;14:885-888. 8. La Fleche FR, Slepin M J, Vargas J, et al: latrogenic bilateral tibial fractures after intraosseous infusion attempts in a 3-month-old infant. Ann EmergMeal1989;18:1099-1101. g. Rimar S, Westry J, Rodriguez R: Compartment syndrome in an infant following emergency intraosseous infusion. ClinPediatr1988;27:259-260.
30. Reed W, Newman KA, Applefeld MM, et el: Drug extravasation as a complication of venous access ports. Ann InternMed1985;102:788-789. 31. Yosowitz P, Eldand DA, Shaw RC, et al: Peripheral intravenous infiltration necrosis. Ann Surg 1975;182:553-556. 32. Handler E: Superficial compartment of the foot after infiltration of intravenous fluid. Arch PhysMed Rehabil 1990;71:58-59. 33. Brickman K, Rega P, Choa M, et al: Comparison of serum phenobarbital levels after single versus multiple attempts at intraosseous infusion. Ann EmergMed1990;19:31-33.
Reprint no. 47/1/32822 Address for reprints: C MichaelSimmons,MD Department of Emergency Medicine Baystate Medical Center Springfield, Massachusetts 01199 413-784-5375
10. Christensen DW, Vernon DD, Banner W, et al: Skin necrosis complicating intraosseous infusion. PediatrEmergCare1991;7:289-290. 11. Moscati R, Moore P: Compartment syndrome with resultant amputation following intraosseous infusion. Am J EmergMed 1990;8:470-471. 12. Brickman KR, Rega P, Koltz M, et al: Analysis of growth plate abnormalities following emergency intraosseous infusion through the proximal tibial epiphysis in pigs. Ann EmergMed 1988;17:121-123. 13. Heinild S, Sendergard T, Tudvad F: Bone marrow infusion in childhood. Experiences from a thousand infusions. J Pediatr1947;30:400-411. 14. Orlowski JP, Jusius CJ, Petras RE, et ah The safety of intraosseous infusions: Risks of fat and bone marrow emboli to the lungs. Ann EmergMed 1989;18:1062-1067. 15. Plewa MC, Kaplan RM, LaCovey D, et al: Fat embolism following intraosseous infusion. Ann EmergMed 1988;17:407. 16. Wile UJ, Schamberg IL: Pulmonary fat embolism following infusions via the bone marrow. J InvestOermatol1942; 5:173-177. 17. Massey LWC: Bone marrow infusion: Intratibial and intravenous routes compared. Br Med J 1950;2:197-198. 18. Meola F: Bone marrow infusions as a routine procedure in children. J Pediatr1944;25:13-16. 19. Quilligan J J, Turkel H: Bone marrow infusions and its complications. Am J Dis Child 1946;71:457-465. 20. Smith RJ, Keseg DP, Menley LK, et al: Intraosseaus infusions by prehaspital personnel in critically ill pediatric patients. Ann EmergMed1988;17:491-495. 21. Behnia R, Wilkinson C: Lidocaine treatment of experimental cutaneous lesions from potassium chloride injection. Anesthesiology1977;47:428-429. 22. grown A, Hoelzer D, Piercy S: Skin necrosis from extravasation of intravenous fluids in children. PlastReconstrSurg1979;64:145-150. 23. gurk R Ill, Serafin D, Klitzman B: Toxic effects of catecholamines on skin. PlastReconstrSurg 1990;85:92-99. 24. Close A, Frackelton W: Cutaneous necrosis due to norepinephrine: Analysis of reported cases and surgical treatment. Wis MealJ1958;127-132. 25. Close A: Phentolamine hydrochloride in prevention of cutaneous necrosis due to levarterenol. JAMA 1959;170:1916-1917. 26.6aze N: Tissue necrosis caused by commonly used intravenous infusions. Lancet1978;:417419. 27. Heft J, Beatty P, Wade J: Dermal necrosis from dobutamine. N EnglJ Med 1979;1280. 28. Jackson I, Robinson D: Severe tissue damage following accidental subcutaneous infusion of bicarbonate solution. ScotMed J 1976;21:200-201. 29. Lath T, Eversmann W Jr: Extravasation injuries in the upper extremity. Clin Orthop 1991;272:248-254.
366
ANNALS OF EMERGENCY MEDICINE 23:2 FEBRUARY 1994