Critical Care of Spinal Cord Injury: Perry A. Ball, MD
Critical Care of Spinal Cord Injury: Perry A. Ball, MD
Perry A. Ball, MD
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S28 Spine • Volume 26 • Number 24S • 2001
Table 1. Vasoactive Agents rine, to counter the loss of sympathetic tone and provide
chronotropic support to the heart (Table 1). An agent
Agent Common Dosage Ranges Comments
with purely ␣-adrenergic action such a phenylephrine
Dopamine 1–10 Has primarily ␣-adrenergic does not provide the needed chronotropic influence to
(g/kg/min) effects at low doses and the heart.
primarily -adrenergic The resolution of shock and restitution of tissue per-
effects at higher doses; a
commonly used agent in fusion is a clear goal: this can be demonstrated by ade-
SCI quate urine output, resolution of systemic acidosis, and
Dobutamine 5–15 Most prominent effect is normal mentation. The blood pressure and cardiac out-
(g/kg/min) augmentation of cardiac
performance but may put that will achieve this will vary from patient to
lower systemic blood patient.
pressure so generally a The appropriate end point for spinal cord perfusion is
less useful agent in SCI
Epinephrine 1–8 Both ␣- and -adrenergic less clear. Given that there is evidence for ischemic and
(g/min) effects, may promote vascular factors on secondary SCI, the appropriate blood
arrythmias pressure to perfuse the injured spinal cord is an impor-
Norepinephrine 1–20 Has some ␣-adrenergic but
(g/min) predominately - tant question. Unfortunately, there is little information
adrenergic effects; a on this subject and no clear way to measure spinal cord
useful agent for blood perfusion. Vale et al treated a series of patients with acute
pressure support,
especially in cervical and SCI with fluid and vasopressors to achieve a mean arte-
high thoracic SCI rial pressure of 85 mm Hg for a minimum of 7 days and
Phenylephrine 10–100 Exclusively -adrenergic reported favorable neurologic outcomes.27 In this un-
(g/min) agent; should be used
with caution in cervical controlled series the mean arterial pressure chosen was
SCI because of potential arbitrary and the optimal value is unknown.
for reflex bradycardia
Thromboembolic Disease
Hemodynamic Instability
Patients with spine and spinal cord injuries are clearly at
Acute SCIs, especially those occurring in the cervical re- high risk for venous thromboembolism. A recent meta-
gion, are often associated with hemodynamic instability. analysis of risk factors for the development of venous
This is because of interruption of the sympathetic fibers thromboembolism in trauma patients demonstrated that
that exit the spinal cord in the thoracic region and con- spine fractures increased the risk by twofold and that SCI
sequent unopposed parasympathetic outflow, which can increased the risk by threefold. Conversely, no such as-
result in cardiac arrhythmias and hypotension. sociation could be clearly demonstrated for the widely
The most common arrhythmia seen is bradycardia, assumed risk factors of head injury, pelvic fracture, and
although supraventricular tachycardia and ventricular long bone fracture.29
tachycardia can also be seen. Arrhythmias appear to be Given this substantial risk, there is a clear logic to
most common within the first 14 days after injury and begin prophylaxis in the acute phase in the intensive care
are more common and more severe in more severe unit. The methods available for prophylaxis are mechan-
injuries.21 ical devices, such as external pneumatic compression de-
The hypotension seen is due to loss of vasoconstrictor vices or compression stockings, and anticoagulants, such
tone in the peripheral arterioles and subsequent pooling as heparin, low molecular weight heparin, or warfarin.
of blood in the peripheral vasculature. The first line of Mechanical devices carry no clear risk but are not on
treatment for this is volume resuscitation. If the infusion their own sufficient prophylaxis in patients with spinal
of 1–2 L of intravenous fluid fails to bring the blood injury.14 Anticoagulants are effective in preventing ve-
pressure into the normal range, consideration should be nous thromboembolism in patients with spinal injuries
given to the placement of a pulmonary artery catheter. but carry the risk of bleeding.
The problem that can arise is that as extra volume is There is often reluctance to start anticoagulants
infused and the venous return increases, there needs to be acutely in the setting of a spinal fracture because of con-
an increase in cardiac output. Because the cardiac accel- cern for promoting bleeding at the injury site or the need
erator fibers have often been interrupted in cervical and for surgery. Studies of patients with spinal injuries have
upper thoracic lesions, the heart is not able to increase shown that without prophylaxis the risk of the develop-
the cardiac output by increasing the heart rate but must ment of deep vein thrombosis is quite low in the first 72
rely on an increased stroke volume that may not be at- hours after injury.14 In this initial period the use of me-
tainable. A pulmonary artery catheter allows the periph- chanical devices is a safe option. After this period me-
eral resistance and cardiac output to be measured di- chanical devices can be continued, but consideration
rectly and vasopressor therapy guided. The choice of a should be made of starting anticoagulation. Standard
vasopressor should be an agent that has both ␣- and mini-dose heparin twice a day does not appear to provide
-adrenergic actions, such as dopamine or norepineph- adequate prophylaxis in patients with spinal injuries.24
S30 Spine • Volume 26 • Number 24S • 2001
Adjusted-dose heparin to raise the partial thromboplas- 8. Fagon J, Chastre J, Hance AJ, et al. Nosocomial pneumonia in ventilated
patients: a cohort study evaluating attributable mortality and hospital stay.
tin time to 1.5⫻ control is effective but has a significant Am J Med 1993;94:281– 8.
bleeding risk.13 Low molecular weight heparin appears 9. Gardner BP, Watt JWH, Krishnan KK. The artificial ventilation of acute
to be safe and effective.16 The length of time for prophy- spinal cord damaged patients: a retrospective study of forty-four patients.
Paraplegia 1986;24:208 –20.
laxis to continue should be 8 weeks, less if the patient 10. Goldman JM, Rose LS, Williams SJ, et al. Effect of abdominal binders on
becomes ambulatory.12 breathing in tetraplegic subjects. Thorax 1986;41:940 –5.
The diagnosis or exclusion of deep vein thrombosis on 11. Grande CM, Barton CR, Stene JK. Appropriate techniques for airway man-
agement of emergency patients with suspected spinal cord injury. Anesth
clinical grounds is notoriously inaccurate. The use of Analg 1988;67:714 –5.
compression B mode ultrasound is a safe and reliable 12. Green D, Hull RD, Mammen EF. Deep vein thrombosis in spinal cord injury.
means of diagnosis and has largely replaced venography Chest 1992;102(suppl):633–5.
13. Green D, Lee MY, Ito VY. Fixed vs adjusted dose heparin in the prophylaxis
and 125I scanning. of thromboembolism in spinal cord injury. JAMA 1988;260:1255– 8.
The diagnosis of pulmonary embolism (PE) has al- 14. Green D, Rossi EC, Yao JST. Deep vein thrombosis in spinal cord injury:
ways been difficult. The pulmonary angiogram remains effect of prophylaxis with calf compression, aspirin, and dipyridamole. Para-
plegia 1982;20:227–34.
the reference standard for the diagnosis, but concerns 15. Grossman RF. Evidence-based assessment of diagnostic tests for ventilator-
over availability, cost, and complications have limited its associated pneumonia. Chest 2000;117(suppl):177– 81.
routine use. For many years ventilation/perfusion (V/Q) 16. Harris S, Chen D, Green D. Enoxaparin for thromboembolism prophylaxis
in spinal injury: preliminary report on experience with 105 patients. Am J
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18. Jerjes-Sanchez C, de Ramirez-Rivera A, Lourdes Garcia M. Streptokinase,
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tal branches of the pulmonary arteries. Comparison with 19. John DA, Tobey RE, Homer LD, et al. Onset of succinylcholine-induced
hyperkalemia following denervation. Anesthesia 1976;45:294 –9.
pulmonary angiography suggests that the sensitivity is 20. Ledsome JR, Sharp JM. Pulmonary function in acute cervical cord injury.
94% and the specificity is 96%.28 In patients with sus- Am Rev Respir Dis 1981;124:41– 4.
pected PE randomized to V/Q scan or spiral CT, the 21. Lehmann KG, Lane JG, Piepmeier JM, et al. Cardiovascular abnormalities
accompanying acute spinal cord injury in humans: incidence time course and
diagnosis was able to be established in a larger percent- severity. J Am Coll Cardiol 1987;10:46 –52.
age of patients with spiral CT.4 In the subset of patients 22. Mansel JK, Norman JR. Respiratory complications and management of spi-
who present with massive PE associated with hemody- nal cord injuries. Chest 1990;97:1446 –52.
23. McMichan JC, Michel L, Westbrook PR. Pulmonary dysfunction following
namic compromise, the use of echocardiography can of- traumatic quadriplegia. JAMA 1980;243:528 –31.
ten demonstrate clot in the proximal pulmonary artery. 24. Merli GJ, Herbison GJ, Ditunno JF. Deep vein thrombosis: prophylaxis in
The mainstay of treatment of patients with PE who acute spinal cord injured patients. Arch Phys Med Rehabil 1988;69:661– 4.
25. Rodriguez JL, Steinberg SM, Luchetti FA. Early tracheostomy for primary
are hemodynamically stable is anticoagulation with hep- airway management in the surgical critical care setting. Surgery 1990;108:
arin or low molecular weight heparin followed by war- 655–9.
farin. If anticoagulation is contraindicated because of 26. Shatney CH, Brunner RD, Nguyen TQ. The safety of orotracheal intubation
in patients with unstable cervical spine fracture or high spinal cord injury.
concerns for bleeding, a vena cava filter is an alternative. Am J Surg 1995;170:676 – 80.
In patients with massive PE and hemodynamic compro- 27. Vale FL, Burns J, Jackson AB, et al. Combined medical and surgical treat-
mise, the use of thrombolytic therapy appears to reduce ment after acute spinal cord injury: results of a prospective pilot study to
assess the merits of aggressive medical resuscitation and blood pressure mea-
mortality over anticoagulation.18 surement. J Neurosurg 1997;87:239 – 46.
28. van Russum AB, et al. Pulmonary embolism: validation of spiral CT angiog-
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