Keywords
massive pulmonary embolism - alteplase - traumatic head injury - thrombolysis
Introduction
Trauma patients have a high risk of venous thromboembolism, with the incidence of
deep vein thrombosis (DVT) reaching as high as 58% in case of traumatic head injury.[1] Pulmonary embolism (PE) is a known complication in neurocritical care intensive
care unit (ICU) where patients have low Glasgow coma scale (GCS) score, with limited
mobility and hesitation by clinicians in initiating pharmacoprophylaxis to prevent
DVT. Massive PE is a life-threatening situation with intravenous tissue plasminogen
activator (tPA) thrombolysis or urgent mechanical thrombectomy as only options. Mortality
rate from massive PE varies from 50 to 100%.[2] When appropriate expertise and resources are available, catheter-guided retrieval
of thrombus is suggested over no treatment, when high risk of bleeding exists and
the patient has acute PE with hypotension.[3]
Case Description
A 40-year-old man, road traffic accident victim, with no known/existing comorbidities,
was brought to the hospital with an arrival GCS score of E2M4Vt. Noncontrast computed
tomography (CT) of the head was suggestive of multiple frontal bone fractures, anterior
cranial fossa fractures, multiple hemorrhagic contusions, subarachnoid hemorrhage
(SAH), and pneumocephalus in bilateral frontal and basifrontal lobes ([Fig. 1]). CT of the whole spine was normal. The patient had multiple rib fractures but no
long bone fractures. Complete blood count, liver and renal function tests, and two-dimensional
(2D) echo were normal with ejection fraction of 65%. Sequential compression stockings
were applied as per the ICU protocol to prevent DVT.
Fig. 1 The non-contrast computed tomography (NCCT) of the head with 3D reconstruction shows
multiple frontal bone fractures, anterior cranial fossa fractures, multiple hemorrhagic
contusions bilateral frontal and basifrontal lobes (black arrow). SAH in bilateral
frontoparietal lobes. Intraventricular hemorrhage present. Pneumocephalus (black star)
in bilateral frontal and temporal lobes. 3D, three-dimensional; SAH, subarachnoid
hemorrhage.
On day 1, the patient underwent bifrontal craniotomy, right frontal contusectomy,
anterior cranial fossa repair (by neurosurgical team), and open reduction and internal
fixation of the frontal, zygomatic and maxillary bones (by plastic surgery team).
On day 2, he underwent redo bilateral frontal craniotomy for hematoma evacuation.
From days 3 to 12, he had intermittent fever spikes (for which he underwent cerebrospinal
fluid [CSF] analysis by lumbar puncture on days 5 and 11, and meningitis was ruled
out) and one episode of seizures on day 5. GCS score during this time fluctuated between
E2VtM3 and E2VtM2. Enoxaparin at 40 mg once daily for thromboembolism prophylaxis
was started on day 12. By day 15, the patient was successfully weaned off ventilator
to T-piece for 48 hours. Fever spikes (up to 38.9°C) intermittently continued.
On day 16 morning, the patient had fever (39°C), was tachypneic (respiratory rate
≈ 25 breaths/min) and was started on continuous positive airway pressure (CPAP) support.
Systolic blood pressure (SBP) was low (≈ 90–100 mm Hg) that responded to fluid boluses.
At this time, 2D echo was normal with no obvious lower limb swellings. Serum procalcitonin
was measured (suspecting a new-onset infection), which came 1.0 ng/mL (similar to
the value 4 days back). In the evening, however, the patient suddenly became severely
tachypneic (respiratory rate ≈ 35–40 breaths/min), with desaturation (SpO2 up to 92% on FiO2 50%) and needed progressively higher ventilatory and inotropic support. At this time,
2D echo done was suggestive of severe pulmonary hypertension, dilated right atrium
and ventricle, and right ventricular ejection fraction (RVEF) 35%. CT pulmonary angiography
was suggestive of bilateral pulmonary artery thrombosis in the main, ascending, descending,
and subsegmental branches ([Fig. 2]). CT venography showed partial filling defect of the left common femoral, popliteal,
and tibial veins and right superficial femoral and popliteal vein.
Fig. 2 The CT pulmonary angiography showing filling defect (white arrows) of right and left
main pulmonary artery, its ascending, descending, and subsegmental branches. CT, computed
tomography.
As the patient's hemodynamics became progressively unstable (SBP ≈ 60 mm Hg on triple
inotropes), he was considered unsuitable for mechanical thrombectomy or catheter guided
thrombolysis. With no better alternative other than intravenous thrombolysis, after
consulting and explaining the eventuality to family including high risk of intracranial
bleed, the patient was started on alteplase 100 mg over 6 hours followed by heparin
infusion for 24 hours. His blood pressure (BP) gradually improved over 6 hours, and
he was off inotropes in next 24 hours. GCS was E1VtM1 for next 3 days but then gradually
improved. The patient underwent vena cava filter (IVC) filter placement on day 17
and was later started on rivaroxaban. He was shifted to the ward from ICU on day 35
with GCS of E3VtM5 where his GCS improved to E3VtM6 by day 60.
Discussion
The authors believe that the use of alteplase for thrombolysis in case of traumatic
brain injury with recent decompressive craniectomy for massive PE has not been described
previously in the literature. A significant head trauma in previous 3 months, history
of intracranial hemorrhage, and recent intracranial surgery are (absolute) exclusion
criteria for alteplase administration after acute stroke[4]
[5] because of the risk of worsening intracranial hemorrhage. Therefore, massive PE
in neurocritical care unit becomes a challenging situation.
Heparinization followed by warfarinization for PE has been done successfully previously
in case of a traumatic brain injury with nephrotic syndrome by Akimoto et al.[6] They noticed slight increase in the hemorrhagic contusions with this therapy. Bottinor
et al used tPA in case of a massive PE to save life of a 60-year-old who had suffered
from hemorrhagic stroke 8 weeks prior.[2] Their daring trial achieved much-needed appreciation, so we should not follow the
guidelines blindly but must also make clinical judgments as per the need of situation.[7] Similarly, thrombolytic bolus was successful in saving a patient's life following
intracranial surgery for glioblastoma multiforme who suffered from cardiac arrest
while being prepared for the mechanical thrombolysis via ultrasonography for pulmonary
embolus dissolution.[8]
With this case report, we wish to highlight that although intravenous thrombolysis
is contraindicated in cases of recent head injury and intracranial bleed, even this
absolute contraindication should be considered relative in case of an eventually dying
patient.[5]
[9] We were left with no option to save the patient's life but to try intravenous thrombolysis.[3] In this case, our patient fortunately recovered from PE with no complication of
thrombolysis. Having said that, we acknowledge the wait in starting enoxaparin early
and diagnosing PE earlier where we could have stepped up our antithrombotic measures.
Therefore, one must be more vigilant in suspecting PE in neurosurgical ICU where antithrombotic
measures are usually delayed or underdosed.[1]
[10] Fever, a consistent sign in our patient was probably due to DVT, and its association
carries worse outcome.[11]
Conclusion
We thus recommend that every effort must be made for prevention and early diagnosis
of DVT and PE in neurocritical care unit, as role of thrombolysis in case of massive
PE is limited. If, however, a dire situation arises to save a patient, all the absolute
contraindications for thrombolysis become relative (as recent intracranial surgery
and cerebral contusions in this case). The clinician must not be hesitant in counseling
the family and taking the best possible course at that moment.
