22 Anticoagulation and Antiplatelet Therapy in the Neurosurgical Intensive Care Unit
Abstract
When, and how, to manage anticoagulation and antiplatelet therapy in the neurosurgical intensive care unit (NICU) is a recurring question. All NICU patients are at risk of developing deep vein thrombosis or pulmonary embolism, but many of them also have absolute or relative contraindications for prophylactic anticoagulation or antiplatelet therapy. We review contemporary evidence-based literature on this topic and discuss our own experience and management rationales of anticoagulation and antiplatelet therapy in the NICU.
Case Presentation
A 55-year-old Caucasian male undergoes craniotomy for evacuation of a traumatic subdural hematoma and is postoperatively managed in the neurosurgical intensive care unit of a tertiary care trauma center. Neurological exam on postoperative day 7 revealed a Glasgow Coma Scale (GCS) score of 12, muscle power was 3/5 on the left upper extremity, 4/5 on the right upper extremity, and 5/5 on lower extremities bilaterally. No sensory deficit was noted. He complained of vague discomfort in his left shoulder area. Physical exam revealed left upper-extremity edema with a difference in diameter of 4 cm between upper extremities. A venous catheter was located on the left upper extremity for administration of fluids.
See end of chapter for Case Management.
22.1 Introduction
Neurotrauma, stroke (both ischemic and hemorrhagic), and postneurosurgical patients make up the majority of patients in the neurosurgical intensive care unit (NICU). Each of these three categories of patients presents complex issues about timing, and extent of, anticoagulation and/or antiplatelet prophylaxis and therapy. For example, neurointensivists commonly face the difficult issue of how to treat deep vein thrombosis (DVT) or pulmonary embolism (PE) in patients who already have acute brain hemorrhage, are immediately postop craniotomy, or have indwelling ventriculostomy catheters. Serious consideration needs to be given to when it is safe to start medications that are the standard of care for the thrombosis, while knowingly increasing the risk of exacerbating the bleed from the treatment. Dural venous sinus thrombosis is the only known condition in which the defined treatment, even in the face of intracerebral bleed, is anticoagulation; for all other conditions involving actual or potential bleeding in the brain, anticoagulation and antiplatelet prophylaxis and therapy pose known risks to the patient, mandating a deliberate and systematic treatment plan, reinforced with very clear communications with the entire treatment team and patient/family.
22.2 Indications for Anticoagulation in the NICU: Prophylaxis
22.2.1 DVT prophylaxis
Neurosurgical and neurotrauma patients are at increased risk of DVT and consequent PE. DVT may be prevalent at around 18% in the general major trauma patients without prophylaxis; however, this number skyrocketed to 54% in patients with traumatic brain injury (TBI). 1 Even in patients with isolated TBI the incidence of venous thromboembolism may be as high as 25%. 2 Several factors may account for this significant risk, such as long operating times of many procedures, prolonged bed rest, immobility related to motor deficits, as well as release of significant amounts of brain tissue thromboplastin during surgery and trauma, diuretic therapy used to reduce cerebral edema, intravascular volume losses following subarachnoid hemorrhage, and cerebral salt wasting. 3
The 2007 guidelines for the management of severe TBI recommended the combination of mechanical and chemical (with low molecular weight heparin [LMWH] or unfractionated heparin) prophylaxis; however, in caution with an increased risk for expansion of intracranial hemorrhage (ICH). 4 Among hematomas and contusions, expansion occurs in about 38% of cases between the first and second computed tomographic (CT) scan, the risk of which is associated with the size of the initial ICH and the presence of a subarachnoid or subdural hemorrhage. 5 Venous thromboembolism prophylaxis halves the risk of DVT and PE, whereas it doubles the risk of ICH progression. 6
Based on the latest evidence, Abdel-Aziz et al 7 refined the recommendation by following the Parkland Protocol, 8 which categorizes NICU patients into low, moderate, or high risk of spontaneous hematoma progression (thus offering some guidance on which patients can receive chemoprophylaxis relatively safely). The “low-risk” category included patients with (nonoperative) epidural or subdural hematoma < 9 mm, cerebral contusion < 2 cm, single contusion per lobe, traumatic subarachnoid hemorrhage with negative CT angiography, and intraventricular hemorrhage < 2 cm in maximum diameter. The “moderate risk” category included nonsurgical patients with a greater degree of hemorrhage than the low-risk ICH. The “high-risk” category included patients requiring craniotomy or intracranial pressure monitor. Their recommendations include the following:
Chemoprophylaxis should be withheld for 3 days for spontaneous ICH patients, or for those with moderate or high risk for ICH progression.
Chemoprophylaxis is reasonable when low-risk patients have not developed ICH progression within 48 hours postinjury.
Chemoprophylaxis is acceptable after day 3 when low-risk patients develop ICH expansion within 48 hours postinjury.
Chemoprophylaxis is reasonable on day 4 in diffuse axonal injury (DAI) patients who have not developed ICH expansion within 72 hours.
Chemoprophylaxis should not be delayed beyond day 7, overall.
LMWH is preferred over unfractionated heparin for lower ICH expansion.
Siddiqi and colleagues at three trauma centers in southern California have been even more aggressive with chemoprophylaxis in a subset of head injury patients when specific DVT risk factors are involved, including patient (or family) history of DVT, known significant blood loss from trauma with resulting hypotension and hypovolemia, morbid obesity, and anticipated prolonged bed rest (as for example with polytrauma or obtunded/comatose patients) (Javed Siddiqi, personal communication, May 12, 2016).
Guided by some studies in the literature, 9 , 10 and with good outcomes, Siddiqi and team have initiated DVT chemoprophylaxis on high-risk DVT patients as early as posttrauma day 1, but only when there is no progression of intracerebral bleeding on repeat CT scans for 24 hours.
22.3 Indications for Anticoagulation in the NICU: Treatment
22.3.1 DVT treatment
The primary objectives of DVT treatment are to prevent PE, reduce morbidity, and decrease the risk of postthrombotic syndrome. The 2012 American College of Chest Physicians (ACCP) guidelines 11 recommended that distal DVT below the knee without severe symptoms or risk for extension should be observed with serial ultrasounds for 2 weeks. Distal DVT with severe symptoms or risk for extension (including positive D-dimer, extensive DVT or close to the proximal veins, no reversible provoking factor, active cancer, previous history of blood clots, and inpatient status) and proximal DVT should be treated with anticoagulants.
The principles of anticoagulation include the following:
Warfarin should be started on the same day as LMWH or unfractionated heparin therapy is started (Level I evidence).
Warfarin should be overlapped with heparin for 4 to 5 days, with discontinuation around 5 to 7 days.
Alternative medications include factor X inhibitors (such as dabigatran, rivaroxaban, apixaban, and edoxaban).
Inferior vena cava filters (IVCFs) provide an alternative to full anticoagulation in patients at high risk for catastrophic hemorrhagic complications only during the acute phase (securing the aneurysm or 1 to 2 weeks after intracranial surgery). Full anticoagulation should be reconsidered beyond the high-risk period.
First episode of DVT triggered by surgery should be treated with anticoagulants for 3 months, recurrent episodes should be treated for at least 12 months.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
