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Pulmonary embolism in the traumatic brain injured adolescent: Report of two cases
362
Pulmonary Embolism in the Traumatic Brain Injured Adolescent: Report of Two Cases Kerstin M. Sobus, MD, Michael F. Cawley, MD, Michael A. Alexander, MD ABSTRACT. Sobus KM, Cawley MF, Alexander MA. Pulmonary embolism in the traumatic brain iqjured adolescent: report of two cases. Arch Phys Med Rehabil 1994;75:362-4. l Deep venous thrombosis @VT) and pulmonary embolus (PE) are known to occur with significant frequency in the adult population but are believed to be rare in children. Our experience during a 26 month period would challenge this thought. Five of 60 adolescent patients developed an acute DVT and/or PE after severe traumatic brain iqjury. Clinical presentation of pulmonary embolus in two of three patients was similar to acute pneumonia. Prophylaxis for DVT and PE may be necessary to those adolescent patients who are likely to remain immobile for an extended period of time. 0 1994 bv the American Conpress of Rehabilitation Medicine and the American Academy of Physical Medicine and ., Rehabilitkon ”
Pulmonary embolism (PE) is thought to be a disease of adulthood but a rarity in childhood. A literature review finds the disease to be more common than would be expected in the pediatric population. Pulmonary embolism in children in the past has been described as a complication in association with otitis media, meningitis, mastoiditis, measles, diphtheria, pleural empyema, appendiceal abscess, rheumatic carditis, bacterial endocarditis, bacillary dysentery, septicemia, pertussis, and pneumonia.lW3Three case reports of PE following trauma have been reported in children between 2 and 10 years of age.4-6 METHOD
Review of our admissions to the rehabilitation units from January 1, 1990 to March 30, 1992 revealed 115 patients admitted after severe traumatic brain injury (TBI). All children were comatose for more than 6 hours. No child under the age of 13 years developed clinical evidence of a deep venous thrombosis (DVT) or PE. However, there were 60 children age 13 years or older 5 of whom developed clinical evidence of a DVT and three of these had an acute PE. The two children who had a DVT without PE also had heterotopic ossification in the same lower extremity as the DVT. One child who developed a DVT with PE did so during his acute hospitalization prior to transfer to the rehabilitation unit. This child had a Greenfield filter placed. The other two children who developed a PE and DVT did not have clinical evidence of a DVT at the time of the pulmonary embolism but did so later during the rehabilitation course. Two of these cases are presented. CASE REPORTS Case 1 A 17-year-old boy was involved in a motor vehicle accident with resultantant severe TBI. Initial Glascow Coma Scale score From Alfred I. duPont Institute, Wilmington, DE. Submitted for publication January 12, 1993. Accepted in revised form July 20, 1993. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Kerstin M. Sobus, MD, Alfred I. duPont Institute, 1600 Rockland Road, PO Box 69, Wilmington, DE 1989. 0 1994 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/94/7503-0094$3.00/O Arch Phys Med Rehabil Vol75,
March 1994
was 3. A computed axial tomography (CAT) scan revealed a subarachnoid hemorrhage, cerebral edema, petechial hemorrhages, and compressed ventricles. Additional trauma included a right Salter II radial fracture, right lower lobe contusion, and a small right pneumothorax. Three weeks after injury the child was transferred to an acute inpatient pediatric rehabilitation hospital. At the time of transfer he demonstrated increased tone and decerebrate posturing in all four extremities. His Ranch0 Coma Scale level was II. Six weeks after injury, still in the same state of coma, he became febrile with temperature to 40 degrees C. Physical examination showed tachyphnea at 40 breaths/minute, tachycardia at 150 beats/ minute, and increased quantity of blood-tinged tracheal secretions. O2 saturation was 97% on 31% F,02. Breath sounds were decreased to ausculation in the left lung base. A chest x-ray demonstrated left lower lobe consolidation. Antibiotic treatment for a presumed pneumonia was initiated. Repeat chest x-ray was consistent with a left lower lobe pneumonia. He continued to need supplemental O2 to maintain saturation in the high 90s. Five days after starting antibiotics, a another chest x-ray revealed increasing consolidation and moderate effusion in the left pleural base. Hemoglobin had decreased to 9.7g/dl. A thoracentesis revealed bloody fluid. Seven weeks after injury he underwent diagnostic studies to evaluate a possible PE and a DVT, although the lower extremities showed no edema. Doppler ultrasound to the level of the iliac vessels revealed normal flow and good venous compressibility. However, the lung perfusion study was abnormal with high probability of a PE. A pulmonary arteriogram demonstrated a definite clot in the main descending branch of the left pulmonary artery.
Case 2 A 14-year-old boy was riding a dirt bike when he was hit by a car. Initial Glascow Coma Scale was 4. Initial CAT scan revealed a severe TBI with hemorrhagic contusion of the left cerebellum, right pons, right basal ganglia, subarachnoid hemorrhage at the left tentorial region, left temporal contusion with subarachnoid hemorrhage, and left basilar skull fracture. Intracranial pressure monitoring showed peaks over 40mmHg intermittently. Two weeks after injury, a tracheostomy, gastrostomy, and jejunostomy were performed. Associated medical problems included aspiration pneumonia, pancreatitis, and pansinusitis. The patient remained comatose with no visual focusing or tracking, no localization to sound, and no response to painful stimuli. His muscle tone was hypotonic and no voluntary movement was noted. Six weeks after injury, he was transferred to the rehabilitation unit. He remained a Ranch0 II level state. Two months after the injury, he was noted to be febrile with a
363
PULMONARY EMBOLISM IN THE TBI ADOLESCENT, Sobus temperature of 39.5 degrees C. Other vital signs at that time included a blood pressure of 152192, respirations 36, pulse 122. His oxygenation needs increased to 2L of oxygen per minute via nasal cannula to maintain hemoglobin in the high 90s. Physical examination revealed the heart rate to be regular without murmur. There were coarse rhonchi noted in both lower lung fields right greater than left. A chest x-ray revealed left lower lobe infiltrate and questionable pleural effusion. He was believed to have a pneumonia and was started on ticarcillin-clavulanate and albuterol. Oxygen needs increased to 3L of oxygenlmin via nasal cannula and he remained febrile. Both lower extremities remained nonedematous. He underwent a ventilation perfusion scan that suggested a high probability of PE. He was started on IV heparin. Eleven weeks after injury, he was noted to have an asymmetrical swelling of his right lower extremity. A Doppler ultrasound revealed extensive DVT of this extremity, including the iliac, femoral, and popliteal veins.
radiotracer introduced intravenously extremities obstruction.
into the distal lower
and follows the venous flow to detect The most conclusive test is the iodine
venous
venous contrast study with the material introduced distally in a vein that can be seen radiographically. It does involve a risk of allergic reaction to the contrast material. Diagnostic evaluation for PE also requires medical imaging. A chest radiograph is usually obtained and is used to alert the possibility of localized pulmonary pathology or regional obstructive pulmonary disease. The addition of a ventilation and perfusion lung scan can reveal pulmonary disorders in which there is an impairment of function. The perfusion scan is central in the evaluation because of its high sensitivity to perfusion defects caused by a PE. The probability of a PE is based on the size of the defects. whether they are matched or mismatched with the scans or plain radiograph. Definitive examination is a pulmonary DISCUSSION angiogram, which involves a risk of allergic reaction to the contrast material. Traditional teaching states that DVT and PE are common If a DVT and/or PE is documented, definitive treatment occurrences in adults during rehabilitation but it is a rarity in the pediatric age group. Our recent experience has chal- needs to be initiated to prevent additional PE or extension lenged this thought. Perhaps with the advent of better acute of the clot. However, in a patient with TBI, the risk of bleeding from multiple trauma and recent brain injury must emergency management of the TBI, we are experiencing the survival of children who are more severely injured and be evaluated. Recent associated skeletal fracture sites, soft medically complicated than in previous years who remain tissue injury, abdominal or pelvic organ injury, subdural or comatose often for several days to weeks. Immobility sec- intracranial bleeding, or neurosurgical procedures are potenondary to coma with associated central or peripheral lower tial sources for hemorrhage. Repeated magnetic resonance imaging or CAT scans of the brain may be necessary immeextremity paralysis can lead to venous stasis. These children diately prior to the start of treatment to carefully evaluate may also have other associated soft tissue trauma or skeletal fractures, particularly in the legs, which may predispose to the risk of bleeding with anticoagulation. If the secondary risk for bleeding is too great, a Greenfield filter should be development of DVT. considered to prevent additional PEs.” Clinical findings for a DVT/PE are generally nonspecific If anticoagulation can be started, IV heparin is the initial and insensitive.’ Evaluation may be complicated by the child being unable to respond to questions because of age, coma, treatment. For actively developing DVT and recent PE, an or communicative or cognitive impairment. Signs of DVT initial single IV bolus of heparin at 5OUikg should be given. ” may include pain or tenderness, swelling, Homans sign, su- This is followed immediately with SOOU/kg per 24 hours. Larger doses, up to l,OU/kg, should be considered for acute perficial venous distention, palpable cord, or fever.’ These PE to minimize the release of vasoactive and bronchoconsigns may also be present with soft tissue injury, skeletal fracture, or heterotopic ossification. Clinical features associ- strictor agents.14 The goal is to achieve a steady state plasma ated with PE may mimic pulmonary or cardiac disease. heparin level of 0.3 to 0.4U/mL or an activated partial thromSymptoms may include tachypnea, tachycardia, pallor, cya- boplastin time and thrombin time value of one and a half to twice the control value.r4 Traditionally, heparin is continued nosis, weakness, altered mental status, pulmonary consolidafor approximately 1 week and then oral warfarin is started. tion, rales, hemoptysis, pleuritic chest pain, pleural friction rub, pleural effusion, fall in blood pressure, and/or fever.397 Recent studies in adult population have indicated that a Sday course of heparin is as effective as a lo-day course in The child may need additional oxygen to maintain oxygen saturation in the normal range. Adult patients may present treating DVT and warfarin may be started soon after initiation of heparin. Major bleeding episodes were not increased with acute pulmonary decompensation secondary to occlusion of a main pulmonary artery; however, it is rare to see with this short-term treatment program.“.‘6 For patients with this in a child. More commonly, children present with a extremely high risk of bleeding, such as those in the intensive care unit with multiple invasive lines or recent multiple clinical picture that resembles an acute respiratory infection, often diagnosed as pneumonia, with short, shallow, painful trauma, it may be wise to delay starting oral anticoagulation respirations, dry, nonproductive cough, or hemoptysis and with warfarin.ls Heparin can be stopped immediately and decreasing oxygen saturation.3z8,9 reversed quickly with protamine sulfate, whereas it may take Diagnostic evaluation for suspected DVT requires medical 6 to 12 hours to reverse the effects of warafin with Vitamin K. 15,18Oral anticoagulation should be continued for 3 to 6 imaging. The Doppler ultrasound is a noninvasive technique that senses blood flow by analyzing the shift in frequency months. caused in a continuous wave signal transmitted by moving When treating with heparin, the platelet count should be red blood cells. Manual compression of the extremity aug- periodically monitored because thrombocytopenia may dements the flow of red blood cells and can provide informavelop in as many as 5% of cases. Additionally, this drugtion about occlusion and incompetence of the deep veins induced thrombocytopenia may be complicated by life-andin the lower extremities.” Radionuclide venogram uses a limb threatening arterial thrombosis. Fortunately, this serious Arch Phys Med Rehabil Vol 75, March 1994
PULMONARY EMBOLISM IN THE TBI ADOLESCENT, Sobus
complication is rare.” It can be detected in adults between 3 and 15 days after institution of heparin. This phenomenon is usually reversible with discontinuation of heparin and is generally benign. Thrombocytopenia may be avoided when heparin treatment is limited to 5 to 6 days.’ The rehabilitation program only needs temporary modification when treating for an acute DVT or PE. If the patient is medically stable, he may continue to receive therapy initially at bedside and resume gait training and active therapy 24 hours after heparin is initiated.’ Finally, the question of prophylaxis and who is truly at risk for a DVT and/or PE should be raised. Few studies have focused on DVT and PE in children and the issue of prevention is rarely raised. Radecki reported on children with spinal cord injury and did not believe prophylactic heparin was warranted in the prepubescent age group. He noted a 5% incidence of DVT in patients under 15 years. There were no deaths and no children developed postphlebitic syndrome.” Our experience would suggest that children after severe TBI who remain in a prolonged coma and are immobile, either with flaccid or spastic lower extremities, are at increased risk for DVT and/or PE. Perhaps hormonal changes with puberty may represent a risk factor, as opposed to age itself. Two of the three adolescents who developed a PE were Tanner stage IV and V. The third young man was Tanner stage II. For those children who are expected to remain immobile for a prolonged period of time, prophylactic treatment may be warranted.” Prophylaxis may be given as subcutaneous dose of 5,OU per dose every 8 to 12 hours until ambulation is achieved.13 Small heparin doses may also be used at a continuous IV infusion in lOOU/kg per 24 hours.14 Elastic stocking or compression boots may be useful. Further investigation in this area is necessary. CONCLUSION Although traditional teaching is that DVT and PE are rare in children, in our experience it is more common than assumed and should not be overlooked. Acute pulmonary embolus in adolescent patients may mimic an acute pneumonia and should be considered in the differential diagnosis, narticularlv if there is no resuonse to medical treatment for
Arch Phys Med Rehabil Vol75,
March 1994
a presumed pneumonia. Prophylaxis for a deep venous thrombosis and or PE may be necessary for those adolescent patients after severe TBI who are likely to remain immobile for an extended period of time. References 1. Stevenson G, Stevenson F, Wayne F. Pulmonary embolism in childhood. J Ped 1949;34:62-9. 2. Stulik C, Rust B. Pulmonary embolism in infancy. Am J Dis Child 1929;37: 1246-50. 3. Zuschlag E. Infarction of the lung in children. Am J Dis Child 1947;74:399-416. 4. Loschner. Phlebitis venae cruralis sinistrae, per&et myocarditis, embolia et Oedema pulmonum, Jahrb. f. Kinderh 1861;4:66. 5. Curtin RG. Pulmonary hemorrhagic infarction in a child following injury to the leg. Am J Dis Woman and Child 1878;11:611-12. 6. Rosenbloom H, Henderson RJ. Pulmonary infarct in a child, Br Med J 1935;2:64. 7. Brandstater M, Roth E, Siebens H. Venous thromboembolism in stroke: literature review and implications for clinical practice. Arch Phys Med Rehabil 1992;73:S-379-91. 8. Emery J. Pulmonary embolism in children. Arch Dis Child 1962;37:591-5. 9. Jones DRB, Macintyre MC. Venous thromboembolism in infancy and childhood. Arch Dis Child 1975;50: 153-5. 10. Sigel B, Felix R, Popky G, Ipsen J. Diagnosis of lower limb venous thrombosis by Doppler ultrasound technique. Arch Surg 1972;104: 17483. II. Alderson P, Martin E. Pulmonary embolism: diagnosis with multiple imaging modalities. Radiology 1987:164:297-3 12. 12. Greenfield L, Michna B. Twelve-year clinical experience with Greenfield vena caval filter. Surgery 1988;104:706-12. 13. Grigorian M, editor. The Harriet Lane Handbook: A manual for pediatric house officers. 12th ed. St Louis: Mosby Year Book, 1991, p 190. 14. Matthew D, Levin M. Pulmonary thromboembolism in children. Intensive Care Med 1986;12:404-6. 15. Hull R, Raskob G, Rosenbloom D, Panju A, Brill-Edwards P, Ginsberg J. Heparin for 5 days as compared with 10 days in the initial treatment of proximal venous thrombosis. N Engl J Med 1990;322:1260-4. 16. Gallus A. Tillett J, Jackmara J, Mills W, Wycherley A. Safety and efficacy of warfarin started early after submassive venous thrombosis or pulmonary embolism. Lancet 1986;2:1293-6. 17. Warkentin T, Kelton J. Heparin-induced thrombocytopenia. Ann Rev Med 1989;40:31-44. of anticoagulant therapy, 18. Levin M, Hirsh J. Hemorrhagic complications Semin Thromb Hemost 1986;12:39-57. 19. Radecki RT. Deep venous thrombosis in the pediatric disabled patient. Arch Phys Med Rehabil 1988;69:743-4. 20. Buck J, Connors R, Coon W, Weintraub W, Wesley J, Coran A. Pulmonary embolism in children. J Ped Surg 1981;16:385-91.
Pulmonary Embolism in the Traumatic Brain Injured Adolescent: Report of Two Cases Kerstin M. Sobus, MD, Michael F. Cawley, MD, Michael A. Alexander, MD ABSTRACT. Sobus KM, Cawley MF, Alexander MA. Pulmonary embolism in the traumatic brain iqjured adolescent: report of two cases. Arch Phys Med Rehabil 1994;75:362-4. l Deep venous thrombosis @VT) and pulmonary embolus (PE) are known to occur with significant frequency in the adult population but are believed to be rare in children. Our experience during a 26 month period would challenge this thought. Five of 60 adolescent patients developed an acute DVT and/or PE after severe traumatic brain iqjury. Clinical presentation of pulmonary embolus in two of three patients was similar to acute pneumonia. Prophylaxis for DVT and PE may be necessary to those adolescent patients who are likely to remain immobile for an extended period of time. 0 1994 bv the American Conpress of Rehabilitation Medicine and the American Academy of Physical Medicine and ., Rehabilitkon ”
Pulmonary embolism (PE) is thought to be a disease of adulthood but a rarity in childhood. A literature review finds the disease to be more common than would be expected in the pediatric population. Pulmonary embolism in children in the past has been described as a complication in association with otitis media, meningitis, mastoiditis, measles, diphtheria, pleural empyema, appendiceal abscess, rheumatic carditis, bacterial endocarditis, bacillary dysentery, septicemia, pertussis, and pneumonia.lW3Three case reports of PE following trauma have been reported in children between 2 and 10 years of age.4-6 METHOD
Review of our admissions to the rehabilitation units from January 1, 1990 to March 30, 1992 revealed 115 patients admitted after severe traumatic brain injury (TBI). All children were comatose for more than 6 hours. No child under the age of 13 years developed clinical evidence of a deep venous thrombosis (DVT) or PE. However, there were 60 children age 13 years or older 5 of whom developed clinical evidence of a DVT and three of these had an acute PE. The two children who had a DVT without PE also had heterotopic ossification in the same lower extremity as the DVT. One child who developed a DVT with PE did so during his acute hospitalization prior to transfer to the rehabilitation unit. This child had a Greenfield filter placed. The other two children who developed a PE and DVT did not have clinical evidence of a DVT at the time of the pulmonary embolism but did so later during the rehabilitation course. Two of these cases are presented. CASE REPORTS Case 1 A 17-year-old boy was involved in a motor vehicle accident with resultantant severe TBI. Initial Glascow Coma Scale score From Alfred I. duPont Institute, Wilmington, DE. Submitted for publication January 12, 1993. Accepted in revised form July 20, 1993. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Kerstin M. Sobus, MD, Alfred I. duPont Institute, 1600 Rockland Road, PO Box 69, Wilmington, DE 1989. 0 1994 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/94/7503-0094$3.00/O Arch Phys Med Rehabil Vol75,
March 1994
was 3. A computed axial tomography (CAT) scan revealed a subarachnoid hemorrhage, cerebral edema, petechial hemorrhages, and compressed ventricles. Additional trauma included a right Salter II radial fracture, right lower lobe contusion, and a small right pneumothorax. Three weeks after injury the child was transferred to an acute inpatient pediatric rehabilitation hospital. At the time of transfer he demonstrated increased tone and decerebrate posturing in all four extremities. His Ranch0 Coma Scale level was II. Six weeks after injury, still in the same state of coma, he became febrile with temperature to 40 degrees C. Physical examination showed tachyphnea at 40 breaths/minute, tachycardia at 150 beats/ minute, and increased quantity of blood-tinged tracheal secretions. O2 saturation was 97% on 31% F,02. Breath sounds were decreased to ausculation in the left lung base. A chest x-ray demonstrated left lower lobe consolidation. Antibiotic treatment for a presumed pneumonia was initiated. Repeat chest x-ray was consistent with a left lower lobe pneumonia. He continued to need supplemental O2 to maintain saturation in the high 90s. Five days after starting antibiotics, a another chest x-ray revealed increasing consolidation and moderate effusion in the left pleural base. Hemoglobin had decreased to 9.7g/dl. A thoracentesis revealed bloody fluid. Seven weeks after injury he underwent diagnostic studies to evaluate a possible PE and a DVT, although the lower extremities showed no edema. Doppler ultrasound to the level of the iliac vessels revealed normal flow and good venous compressibility. However, the lung perfusion study was abnormal with high probability of a PE. A pulmonary arteriogram demonstrated a definite clot in the main descending branch of the left pulmonary artery.
Case 2 A 14-year-old boy was riding a dirt bike when he was hit by a car. Initial Glascow Coma Scale was 4. Initial CAT scan revealed a severe TBI with hemorrhagic contusion of the left cerebellum, right pons, right basal ganglia, subarachnoid hemorrhage at the left tentorial region, left temporal contusion with subarachnoid hemorrhage, and left basilar skull fracture. Intracranial pressure monitoring showed peaks over 40mmHg intermittently. Two weeks after injury, a tracheostomy, gastrostomy, and jejunostomy were performed. Associated medical problems included aspiration pneumonia, pancreatitis, and pansinusitis. The patient remained comatose with no visual focusing or tracking, no localization to sound, and no response to painful stimuli. His muscle tone was hypotonic and no voluntary movement was noted. Six weeks after injury, he was transferred to the rehabilitation unit. He remained a Ranch0 II level state. Two months after the injury, he was noted to be febrile with a
363
PULMONARY EMBOLISM IN THE TBI ADOLESCENT, Sobus temperature of 39.5 degrees C. Other vital signs at that time included a blood pressure of 152192, respirations 36, pulse 122. His oxygenation needs increased to 2L of oxygen per minute via nasal cannula to maintain hemoglobin in the high 90s. Physical examination revealed the heart rate to be regular without murmur. There were coarse rhonchi noted in both lower lung fields right greater than left. A chest x-ray revealed left lower lobe infiltrate and questionable pleural effusion. He was believed to have a pneumonia and was started on ticarcillin-clavulanate and albuterol. Oxygen needs increased to 3L of oxygenlmin via nasal cannula and he remained febrile. Both lower extremities remained nonedematous. He underwent a ventilation perfusion scan that suggested a high probability of PE. He was started on IV heparin. Eleven weeks after injury, he was noted to have an asymmetrical swelling of his right lower extremity. A Doppler ultrasound revealed extensive DVT of this extremity, including the iliac, femoral, and popliteal veins.
radiotracer introduced intravenously extremities obstruction.
into the distal lower
and follows the venous flow to detect The most conclusive test is the iodine
venous
venous contrast study with the material introduced distally in a vein that can be seen radiographically. It does involve a risk of allergic reaction to the contrast material. Diagnostic evaluation for PE also requires medical imaging. A chest radiograph is usually obtained and is used to alert the possibility of localized pulmonary pathology or regional obstructive pulmonary disease. The addition of a ventilation and perfusion lung scan can reveal pulmonary disorders in which there is an impairment of function. The perfusion scan is central in the evaluation because of its high sensitivity to perfusion defects caused by a PE. The probability of a PE is based on the size of the defects. whether they are matched or mismatched with the scans or plain radiograph. Definitive examination is a pulmonary DISCUSSION angiogram, which involves a risk of allergic reaction to the contrast material. Traditional teaching states that DVT and PE are common If a DVT and/or PE is documented, definitive treatment occurrences in adults during rehabilitation but it is a rarity in the pediatric age group. Our recent experience has chal- needs to be initiated to prevent additional PE or extension lenged this thought. Perhaps with the advent of better acute of the clot. However, in a patient with TBI, the risk of bleeding from multiple trauma and recent brain injury must emergency management of the TBI, we are experiencing the survival of children who are more severely injured and be evaluated. Recent associated skeletal fracture sites, soft medically complicated than in previous years who remain tissue injury, abdominal or pelvic organ injury, subdural or comatose often for several days to weeks. Immobility sec- intracranial bleeding, or neurosurgical procedures are potenondary to coma with associated central or peripheral lower tial sources for hemorrhage. Repeated magnetic resonance imaging or CAT scans of the brain may be necessary immeextremity paralysis can lead to venous stasis. These children diately prior to the start of treatment to carefully evaluate may also have other associated soft tissue trauma or skeletal fractures, particularly in the legs, which may predispose to the risk of bleeding with anticoagulation. If the secondary risk for bleeding is too great, a Greenfield filter should be development of DVT. considered to prevent additional PEs.” Clinical findings for a DVT/PE are generally nonspecific If anticoagulation can be started, IV heparin is the initial and insensitive.’ Evaluation may be complicated by the child being unable to respond to questions because of age, coma, treatment. For actively developing DVT and recent PE, an or communicative or cognitive impairment. Signs of DVT initial single IV bolus of heparin at 5OUikg should be given. ” may include pain or tenderness, swelling, Homans sign, su- This is followed immediately with SOOU/kg per 24 hours. Larger doses, up to l,OU/kg, should be considered for acute perficial venous distention, palpable cord, or fever.’ These PE to minimize the release of vasoactive and bronchoconsigns may also be present with soft tissue injury, skeletal fracture, or heterotopic ossification. Clinical features associ- strictor agents.14 The goal is to achieve a steady state plasma ated with PE may mimic pulmonary or cardiac disease. heparin level of 0.3 to 0.4U/mL or an activated partial thromSymptoms may include tachypnea, tachycardia, pallor, cya- boplastin time and thrombin time value of one and a half to twice the control value.r4 Traditionally, heparin is continued nosis, weakness, altered mental status, pulmonary consolidafor approximately 1 week and then oral warfarin is started. tion, rales, hemoptysis, pleuritic chest pain, pleural friction rub, pleural effusion, fall in blood pressure, and/or fever.397 Recent studies in adult population have indicated that a Sday course of heparin is as effective as a lo-day course in The child may need additional oxygen to maintain oxygen saturation in the normal range. Adult patients may present treating DVT and warfarin may be started soon after initiation of heparin. Major bleeding episodes were not increased with acute pulmonary decompensation secondary to occlusion of a main pulmonary artery; however, it is rare to see with this short-term treatment program.“.‘6 For patients with this in a child. More commonly, children present with a extremely high risk of bleeding, such as those in the intensive care unit with multiple invasive lines or recent multiple clinical picture that resembles an acute respiratory infection, often diagnosed as pneumonia, with short, shallow, painful trauma, it may be wise to delay starting oral anticoagulation respirations, dry, nonproductive cough, or hemoptysis and with warfarin.ls Heparin can be stopped immediately and decreasing oxygen saturation.3z8,9 reversed quickly with protamine sulfate, whereas it may take Diagnostic evaluation for suspected DVT requires medical 6 to 12 hours to reverse the effects of warafin with Vitamin K. 15,18Oral anticoagulation should be continued for 3 to 6 imaging. The Doppler ultrasound is a noninvasive technique that senses blood flow by analyzing the shift in frequency months. caused in a continuous wave signal transmitted by moving When treating with heparin, the platelet count should be red blood cells. Manual compression of the extremity aug- periodically monitored because thrombocytopenia may dements the flow of red blood cells and can provide informavelop in as many as 5% of cases. Additionally, this drugtion about occlusion and incompetence of the deep veins induced thrombocytopenia may be complicated by life-andin the lower extremities.” Radionuclide venogram uses a limb threatening arterial thrombosis. Fortunately, this serious Arch Phys Med Rehabil Vol 75, March 1994
PULMONARY EMBOLISM IN THE TBI ADOLESCENT, Sobus
complication is rare.” It can be detected in adults between 3 and 15 days after institution of heparin. This phenomenon is usually reversible with discontinuation of heparin and is generally benign. Thrombocytopenia may be avoided when heparin treatment is limited to 5 to 6 days.’ The rehabilitation program only needs temporary modification when treating for an acute DVT or PE. If the patient is medically stable, he may continue to receive therapy initially at bedside and resume gait training and active therapy 24 hours after heparin is initiated.’ Finally, the question of prophylaxis and who is truly at risk for a DVT and/or PE should be raised. Few studies have focused on DVT and PE in children and the issue of prevention is rarely raised. Radecki reported on children with spinal cord injury and did not believe prophylactic heparin was warranted in the prepubescent age group. He noted a 5% incidence of DVT in patients under 15 years. There were no deaths and no children developed postphlebitic syndrome.” Our experience would suggest that children after severe TBI who remain in a prolonged coma and are immobile, either with flaccid or spastic lower extremities, are at increased risk for DVT and/or PE. Perhaps hormonal changes with puberty may represent a risk factor, as opposed to age itself. Two of the three adolescents who developed a PE were Tanner stage IV and V. The third young man was Tanner stage II. For those children who are expected to remain immobile for a prolonged period of time, prophylactic treatment may be warranted.” Prophylaxis may be given as subcutaneous dose of 5,OU per dose every 8 to 12 hours until ambulation is achieved.13 Small heparin doses may also be used at a continuous IV infusion in lOOU/kg per 24 hours.14 Elastic stocking or compression boots may be useful. Further investigation in this area is necessary. CONCLUSION Although traditional teaching is that DVT and PE are rare in children, in our experience it is more common than assumed and should not be overlooked. Acute pulmonary embolus in adolescent patients may mimic an acute pneumonia and should be considered in the differential diagnosis, narticularlv if there is no resuonse to medical treatment for
Arch Phys Med Rehabil Vol75,
March 1994
a presumed pneumonia. Prophylaxis for a deep venous thrombosis and or PE may be necessary for those adolescent patients after severe TBI who are likely to remain immobile for an extended period of time. References 1. Stevenson G, Stevenson F, Wayne F. Pulmonary embolism in childhood. J Ped 1949;34:62-9. 2. Stulik C, Rust B. Pulmonary embolism in infancy. Am J Dis Child 1929;37: 1246-50. 3. Zuschlag E. Infarction of the lung in children. Am J Dis Child 1947;74:399-416. 4. Loschner. Phlebitis venae cruralis sinistrae, per&et myocarditis, embolia et Oedema pulmonum, Jahrb. f. Kinderh 1861;4:66. 5. Curtin RG. Pulmonary hemorrhagic infarction in a child following injury to the leg. Am J Dis Woman and Child 1878;11:611-12. 6. Rosenbloom H, Henderson RJ. Pulmonary infarct in a child, Br Med J 1935;2:64. 7. Brandstater M, Roth E, Siebens H. Venous thromboembolism in stroke: literature review and implications for clinical practice. Arch Phys Med Rehabil 1992;73:S-379-91. 8. Emery J. Pulmonary embolism in children. Arch Dis Child 1962;37:591-5. 9. Jones DRB, Macintyre MC. Venous thromboembolism in infancy and childhood. Arch Dis Child 1975;50: 153-5. 10. Sigel B, Felix R, Popky G, Ipsen J. Diagnosis of lower limb venous thrombosis by Doppler ultrasound technique. Arch Surg 1972;104: 17483. II. Alderson P, Martin E. Pulmonary embolism: diagnosis with multiple imaging modalities. Radiology 1987:164:297-3 12. 12. Greenfield L, Michna B. Twelve-year clinical experience with Greenfield vena caval filter. Surgery 1988;104:706-12. 13. Grigorian M, editor. The Harriet Lane Handbook: A manual for pediatric house officers. 12th ed. St Louis: Mosby Year Book, 1991, p 190. 14. Matthew D, Levin M. Pulmonary thromboembolism in children. Intensive Care Med 1986;12:404-6. 15. Hull R, Raskob G, Rosenbloom D, Panju A, Brill-Edwards P, Ginsberg J. Heparin for 5 days as compared with 10 days in the initial treatment of proximal venous thrombosis. N Engl J Med 1990;322:1260-4. 16. Gallus A. Tillett J, Jackmara J, Mills W, Wycherley A. Safety and efficacy of warfarin started early after submassive venous thrombosis or pulmonary embolism. Lancet 1986;2:1293-6. 17. Warkentin T, Kelton J. Heparin-induced thrombocytopenia. Ann Rev Med 1989;40:31-44. of anticoagulant therapy, 18. Levin M, Hirsh J. Hemorrhagic complications Semin Thromb Hemost 1986;12:39-57. 19. Radecki RT. Deep venous thrombosis in the pediatric disabled patient. Arch Phys Med Rehabil 1988;69:743-4. 20. Buck J, Connors R, Coon W, Weintraub W, Wesley J, Coran A. Pulmonary embolism in children. J Ped Surg 1981;16:385-91.