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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 6  |  Page : 1880-1881

Intravenous Milrinone Infusion for Post Traumatic Cerebral Vasospasm

Department of Neurosurgery, National Institute of Mental, Health and Neurosciences (NIMHANS), Bangalore, Karnataka, India

Date of Submission04-Aug-2020
Date of Decision08-Sep-2021
Date of Acceptance20-Nov-2021
Date of Web Publication23-Dec-2021

Correspondence Address:
Dr. Dhaval Shukla
Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore - 560 029, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.333446

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How to cite this article:
Kulkarni AV, Uppar AM, Shukla D, Madhugiri V. Intravenous Milrinone Infusion for Post Traumatic Cerebral Vasospasm. Neurol India 2021;69:1880-1

How to cite this URL:
Kulkarni AV, Uppar AM, Shukla D, Madhugiri V. Intravenous Milrinone Infusion for Post Traumatic Cerebral Vasospasm. Neurol India [serial online] 2021 [cited 2022 Jan 26];69:1880-1. Available from:

Dear Sir,

Traumatic subarachnoid hemorrhage (tSAH) is the most common cause of SAH and is present in 19–68% of severe traumatic brain injuries (TBI).[1],[2] Within the first week of injury, 3.9–16.6% develop symptomatic delayed cerebral ischemia due to vasospasm.[2]

Intravenous milrinone infusion (IVM) has been described for aneurysmal subarachnoid haemorrhage (aSAH). We present two cases of successful treatment of post-traumatic vasospasm with milrinone.

Case 1

A 64-year-old man presented in the Glasgow coma scale (GCS) 15 following a road traffic accident. On evaluation, he was found to have diffuse thick cisternal and cortical SAH. He was managed medically. After 6 days of injury, he developed right side limb weakness with power 4/5 in the upper and lower limbs. There was no loss of consciousness or any other neurological deficits. The magnetic resonance imaging of the brain showed restricted diffusion in the right posterior temporal and left anterior region. Digital subtraction angiography showed diffuse vasospasm for which intra-arterial nimodipine (IAN) infusion for 4 days was given [Figure 1]. In the angiosuite, after the angiogram, IAN was injected as per the following protocol. Nimodipine 3 mg (15 mL) was diluted with normal saline so that the entire solution was 50 mL. It was infused intra-arterially in the cervical segment of both the carotid arteries over 30 min. One vessel was injected maximum of 3 mg and maximum of two vessels were injected per sitting. During the IAN injection, the mean arterial pressure was monitored throughout the procedure. The entire procedure in the angiosuite was done under conscious sedation. As he did not sustain improvement, he was managed with continuous intravenous milrinone (IVM) infusion for 7 days. In IVM protocol, the drug was infused intravenously in which 10 mL (1 mg/mL) vial was diluted with 40 mL normal saline making the solution to 50 mL, which was given initially at 7 mL/h. A further dose of IVM was increased or decreased according to the patient's clinical status (maximum 15 mL/h depending on the bodyweight). During IVM infusion, continuous electrocardiogram (ECG) monitoring and monitoring of the blood pressure were done. Additionally, the serum electrolytes levels were measured regularly, and accordingly, corrections were given if required.
Figure 1: CT scan of the brain at the time of admission showing thick SAH in the basal cisterns (a) and left parietal cortex (b). The MRI of the brain diffusion weightage imaging (c) showing restricted diffusion in the left anterior temporal and right posterior temporal lobes (d). Fluid attenuation inversion recovery sequence showing signal changes in in the left anterior temporal and right posterior temporal lobes. DSA of the right carotid injection (e) and left carotid injection (f) showing diffuse vasospasm. DSA after intra-arterial nimodipine infusion of the right carotid injection (g) and left carotid injection (h) showing improvement in the vasospasm, relatively better on the right side.

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At discharge, he was conscious without neurological deficits. At 9 months after injury, he had a good recovery on the Glasgow outcome scale (GOS), i.e., GOS-5.

Case 2

A 34-year-old man presented in GCS 15 following a road traffic accident. On evaluation, he was found to have acute subdural hematoma with Sylvian SAH. He was managed medically. After 5 days of injury, he deteriorated to GCS 10 and developed left hemiplegia with power 0/5 in the upper and lower limbs. Computerized tomographic angiography (CTA) revealed vasospasm of the right middle cerebral artery without infarction. He was treated with continuous IVM infusion for 10 days. The protocol of IVM was the same as for the previous patient. The patient improved after the IVM therapy. At discharge, he was conscious, and his power in the left upper limb was 3/5 and in the left lower limb was 4/5. At 3 months after injury, he had a good recovery, i.e., GOS-5.

Milrinone is a selective phosphodiesterase III enzyme inhibitor. Through a cyclic adenosine monophosphate (cAMP)-related cascade, it decreases the smooth muscle tone in the cerebral vessels causing vasodilation. The inotropic effect is due to increased cardiac contractility, decreased afterload, and decreased systemic vascular resistance.[3] We followed the Montreal Neurological Hospital protocol.[3] The efficacy of this protocol to treat post-traumatic vasospasm has been described in two cases earlier.[4],[5] A recent systematic review of the effect of milrinone in the treatment of delayed cerebral ischemia (DCI) following aneurysmal SAH revealed clinical resolution of DCI in 375/424 (88%) and angiographic response in 165/234 (71%). Hypotension (70/303, 23%) and hypokalemia (31/287, 11%) were common adverse effects. Four cases (0.5%) of drug intolerance occurred. A good functional outcome was achieved in 271/364 (74%) patients. Cerebral infarction attributable to DCI occurred in 47/250 (19%). The authors concluded that the IVM is a safe and feasible therapy for DCI. However, the utility of IVM in traumatic vasospasm is limited to two case reports.

IVM has a role in the management of vasospasm, especially in critically ill patients who cannot be shifted to endovascular suites for intraarterial vasodilator therapy.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kramer DR, Winer JL, Pease BA, Amar AP, Mack WJ. Cerebral vasospasm in traumatic brain injury. Neurol Res Int 2013;2013:1-7. doi: 10.1155/2013/415813.  Back to cited text no. 1
Servadei F, Murray GD, Teasdale GM, Dearden M, Iannotti F, Lapierre F, et al. Traumatic subarachnoid hemorrhage: Demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery 2002;50:261-7; discussion 267-9.  Back to cited text no. 2
Lannes M, Teitelbaum J, del Pilar Cortés M, Cardoso M, Angle M. Milrinone and homeostasis to treat cerebral vasospasm associated with subarachnoid hemorrhage: The Montreal neurological hospital protocol. Neurocrit Care 2012;16:354-62.  Back to cited text no. 3
Lasry O, Marcoux J. The use of intravenous Milrinone to treat cerebral vasospasm following traumatic subarachnoid hemorrhage. Springerplus 2014;3:1-7.  Back to cited text no. 4
Castle-Kirszbaum M, Lai L, Maingard J, Asadi H, Danks RA, Goldschlager T, et al. Intravenous milrinone for treatment of delayed cerebral ischaemia following subarachnoid haemorrhage: A pooled systematic review. Neurosurg Rev 2021;44:3107-24.  Back to cited text no. 5


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