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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 4  |  Issue : 2  |  Page : 34-36

Unexpected upper limb compartment syndrome due to venous thrombosis in frontal glioma surgery: A case report


1 Department of Anaesthesiology, S.M.B.T Medical College and IMSRC, Igatpuri, Maharashtra, India
2 Department of Anaesthesiology, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, Maharashtra, India
3 Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Hospital, Homi Bhabha National University, Mumbai, Maharashtra, India

Date of Submission03-Feb-2020
Date of Decision24-May-2021
Date of Acceptance31-May-2021
Date of Web Publication29-Jul-2021

Correspondence Address:
Dr. Amit Mahadev Dalvi
Room 1002, Om Sai Krupa Apartment, Vasant Kunj, Near Lok Puram Thane (West), Mumbai - 400 610, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/glioma.glioma_4_20

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  Abstract 


Although it is well known that 49% cases of upper limb deep-vein thrombosis are due to malignancies and the likelihood of venous thromboembolism is increased in patients with high grade gliomas due to the heightened prothrombotic milieu, requisite preoperative laboratory coagulation studies are not performed routinely in these patients to decide whether appropriate antithrombotic medications are required preoperatively. In addition, it is controversial whether antithrombotic therapy should be initiated before neurosurgery in view of the risk of intraoperative bleeding. Here, we have described the case of a 29-year-old female with high grade frontal malignant astrocytoma who developed the extremely rare complication of upper limb compartment syndrome postoperatively. The patient had no history of thrombotic events, and her basic laboratory parameters were not deranged in the pre-operative period. This rare case, supported with a literature review, suggested that the risk of thrombosis is increased in high grade and large gliomas, making us rethink the overall battery of investigations and perioperative medical management of such cases. We strongly recommend peri-operative coagulation studies and appropriate antithrombotic measures along with vigilant perioperative monitoring to avoid thrombotic complication in this subset of patients.

Keywords: Antithrombotic medications, case report, coagulation profile, compartment syndrome, deep-venous thrombosis, glioma, solid neurological tumors, superficial venous thrombosis


How to cite this article:
Dalvi AM, Shetty AN, Gangakhedkar GR, Waghalkar P. Unexpected upper limb compartment syndrome due to venous thrombosis in frontal glioma surgery: A case report. Glioma 2021;4:34-6

How to cite this URL:
Dalvi AM, Shetty AN, Gangakhedkar GR, Waghalkar P. Unexpected upper limb compartment syndrome due to venous thrombosis in frontal glioma surgery: A case report. Glioma [serial online] 2021 [cited 2021 Dec 4];4:34-6. Available from: http://www.jglioma.com/text.asp?2021/4/2/34/322652




  Introduction Top


Solid tumors such as gliomas are known to be associated with complications such as deep-vein thrombosis and pulmonary embolism.[1] Patients with tumors such as meningiomas and gliomas may have a deranged hemostatic profile preoperatively; consequently, they are likely to develop significant postoperative hematological complications.[2] Such patients have heightened activity of both the thrombotic and fibrinolytic systems. Furthermore, surgery itself has a procoagulant effect by causing circulatory stasis. In neurosurgery, both the operation time and recovery period may be prolonged leading to longer duration of immobility and increased risk of thrombosis. Here, we present a case who developed the well-known but extremely rare complication of upper limb compartment syndrome due to superficial and deep venous thrombosis following glioma excision surgery.


  Case Report Top


A 29-year-old female was scheduled to undergo right frontal glioma excision. Her only symptom was seizures, with the last episode occurring 2 months prior to admission. On examination, she was awake and alert with a Glasgow Coma Scale score of 15/15, along with an unremarkable general and systemic examination. Her hematological and biochemical parameters were within the normal limits. Magnetic resonance imaging was suggestive of a lesion in the right frontal brain region. Her only medication was Phenytoin tablet 500 mg twice daily to control the seizures. Standard American Society of Anesthesiologists monitoring was performed using pulse oximetry, electrocardiography, temperature monitoring, and capnography. A noninvasive blood pressure monitor was attached to the right arm with measurements performed at 5-min intervals. The left radial artery was cannulated for invasive blood pressure monitoring. The patient was positioned in the supine position postinduction with padding of all pressure points. The surgery lasted for 3 h and was uneventful with minimal hemodynamic changes. However, the blood loss amounted to 1400 mL as it was a high grade tumor and large-sized glioma. Overall, 350 mL of packed red cell concentrate and 1 L of Ringer's lactate solution were transfused during the surgery. When the drapes were removed following extubation, we observed that the patient's right arm was cyanosed from the elbow to the finger tips. She also complained of pain in that arm. In comparison, the left arm showed no discoloration. Doppler examination to investigate the underlying cause revealed extensive superficial and deep-venous thrombosis along with compartment syndrome of the right wrist. In addition, there was reduced blood flow in the right ulnar artery due to the compartment syndrome. However, there was no evidence of extravasation at the site of intravenous cannulation. Compartment syndrome was treated with emergency fasciotomy, anticoagulants, and analgesics. The patient's condition improved in 3 days with resolution of the cyanosis. On the follow-up visit after a month, the patient did not exhibit any focal neurological deficit or functional impairment of the right arm.

After completion of the surgery, a tumor specimen was sent to histopathology for the pathological classification. The tumor was found to be a high-grade malignant astrocytoma (WHO Grade III) with diffuse brain infiltration [Figure 1]. Since the tumor was widespread and highly vascular, there was an intraoperative blood loss of 1400 mL.
Figure 1: Magnetic resonance imaging of the brain in a patient with high-grade malignant diffuse glioma (black arrows)

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The ethical approval and written consent were waived by the institutional review board of our hospital owing to the retrospective nature of this case report.


  Discussion Top


It has been recognized for a long time that solid tumors induce a hypercoagulable state in patients. Thrombosis is the most common complication of malignancy and the second most common cause of death in cancer patients.[1] In general, 20% of the incidence of deep-vein thrombosis can be attributed to malignancy.[2] In addition, 49% cases of upper limb deep vein thrombosis are due to malignancy.[2] Among neurological tumors, gliomas are very likely to cause venous thromboembolism. As per estimates, the incidence of postoperative venous thromboembolism in patients undergoing neurosurgery is anywhere between 3% and 20% based on the use of thromboprophylaxis and the method of detection.[3] In a prospective randomized controlled trial on low-molecular-weight heparin (LMWH) thromboprophylaxis in patients diagnosed with high-grade glioma, Perry et al. found a 17% cumulative probability of venous thromboembolism in the placebo group as compared to 10% cumulative probability in patients given LMWH group in a period of 6 months after diagnosis.[4] Marras et al.[5] identified a 1.5%–2% risk of venous thromboembolism per month of survival in patients with glioblastoma.

The causes of thrombosis in glioma patients are varied. They may be patient related, tumor related, treatment related, or humoral factors which induce a hypercoagulable environment in these patients. Patient-related factors include age more than 75 years, multiple comorbidities, obesity, and prior history of thromboembolism.[6] Glioma-related factors comprise high grade tumor, large sized tumor, recurrent disease, and postoperative residual disease.[7],[8] These factors, when added to the neurological disability at the time of disease presentation as well as perioperative immobility, further increase the propensity of venous thromboembolism in these patients. Tissue factor is the initiator of the extrinsic coagulation pathway and is found abundantly in gliomas. Moreover, the amount of tissue factor correlates with the grade of gliomas.[7],[8] Other factors which determine the occurrence of thrombosis include the type of cancer, stage of cancer, degree of ambulation, and the therapeutic interventions performed. Sawaya and Glas-Greenwalt[6] in their study concluded that 40% of the study participants with cerebral metastasis had low-tissue plasminogen activator activity levels and enhanced plasminogen inhibitor 1 expression. Furthermore, steroids used for the treatment of these tumors can also lead to a hypercoagulable state in the body.[9]

In a broad sense, the cause of thrombosis in glioma patients is the ability of the tumor cells to increase prothrombotic agents in the body. This eventually leads to activation of the fibrinolytic system to control the prothrombotic milieu in the body. This is accompanied by an inflammatory response in the body involving interactions between tumor cells, blood cells, and vascular endothelium. There is the generation of acute-phase reactants and abnormal protein production with the release of substances like thromboplastin due to tumor necrosis, surgery, hormonal therapy, chemotherapy, central venous catheters, and immobility due to the underlying neurological condition.[10]

The prothrombotic state in these patients necessitates perioperative coagulation studies and antithrombotic therapy depending on the results. However, it has been suggested that initiating antithrombotic treatment in such patients may lead to intracranial bleeding. Therefore, antithrombotic therapy in these patients is under research and is still not widely accepted.

In the present case, neither any preoperative coagulation studies were undertaken, nor any anticoagulant therapy was started preoperatively as the patient did not complain of any hemorrhagic or thrombotic symptoms and was ambulatory before surgery. However, subsequent development of superficial and deep-venous thrombosis in this patient suggested that she might have had a deranged coagulation profile before surgery, which led to the postoperative complications. Another factor that might have precipitated thrombosis could be the rise in pressure and eventual circulatory stasis caused by the noninvasive blood pressure monitoring cuff used throughout the surgery. There was no other obvious cause of thrombosis as there was no pressure on the left arm from any equipment attached to the table and the arm was also adequately padded. Further hematological studies failed to reveal any other cause of thrombosis such as autoimmune disease.

Based on this case and a literature review, we found that patients with such solid tumors have a high likelihood of developing thrombotic events. However, thrombosis in the upper extremities is rare with limited data available. There is a need to be more vigilant perioperatively to identify such events and to act swiftly to resolve them. We recommend conducting extended coagulation profile studies in patients with large sized and high-grade gliomas to start antithrombotic medications if needed. If invasive monitoring is being performed, it is advisable to check the cannulated artery postoperatively for patency or clot formation. The interval during noninvasive blood pressure monitoring should be increased or it should be avoided totally, if concomitant invasive blood pressure monitoring is also being performed.


  Conclusion Top


Surgery acts as a prothrombotic factor in patients with solid malignancies, especially large sized and high grade gliomas. Thrombotic events are possible in the perioperative period even when the patient has no past history of thrombotic events. Performing an extended coagulation profile in such patients can help to predict the likelihood of a thrombotic event. Accordingly, antithrombotic medication can be started in consultation with the neurosurgeon to prevent any thrombotic episodes. Importantly, it is necessary to be highly vigilant for the possibility of thrombotic events perioperatively and treat them as early as possible.

Financial support and sponsorship

Nil.

Institutional review board statement

IRB review was waived owing to the retrospective nature of this case report.

Declaration of participant consent

The authors certify that they have obtained the appropriate patient consent form. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Donati MB. Cancer and thrombosis: From phlegmasia alba dolens to transgenic mice. Thromb Haemost 1995;74:278-81.  Back to cited text no. 1
    
2.
Heil J, Miesbach W, Vogl T, Bechstein WO, Reinisch A. Deep vein thrombosis of the upper extremity. Dtsch Arztebl Int 2017;114:244-9.  Back to cited text no. 2
    
3.
Perry JR. Thromboembolic disease in patients with high-grade glioma. Neuro Oncol 2012;14 Suppl 4:iv73-80.  Back to cited text no. 3
    
4.
Perry JR, Julian JA, Laperriere NJ, Geerts W, Agnelli G, Rogers LR, et al. PRODIGE: A randomized placebo-controlled trial of dalteparin low-molecular-weight heparin thromboprophylaxis in patients with newly diagnosed malignant glioma. J Thromb Haemost 2010;8:1959-65.  Back to cited text no. 4
    
5.
Marras LC, Geerts WH, Perry JR. The risk of venous thromboembolism is increased throughout the course of malignant glioma: An evidence-based review. Cancer 2000;89:640-6.  Back to cited text no. 5
    
6.
Sawaya R, Glas-Greenwalt P. Postoperative venous thromboembolism and brain tumors: Part II. Hemostatic profile. J Neurooncol 1992;14:127-34.  Back to cited text no. 6
    
7.
Hamada K, Kuratsu J, Saitoh Y, Takeshima H, Nishi T, Ushio Y. Expression of tissue factor correlates with grade of malignancy in human glioma. Cancer 1996;77:1877-83.  Back to cited text no. 7
    
8.
Morozov VV. The coagulant and anticoagulant blood systems in brain tumors of supratentorial localization. Zh Nevropatol Psikhiatr Im S S Korsakova 1968;68:505-9.  Back to cited text no. 8
    
9.
Blei F, Wilson EL, Mignatti P, Rifkin DB. Mechanism of action of angiostatic steroids: Suppression of plasminogen activator activity via stimulation of plasminogen activator inhibitor synthesis. J Cell Physiol 1993;155:568-78.  Back to cited text no. 9
    
10.
Caine GJ, Stonelake PS, Lip GY, Kehoe ST. The hypercoagulable state of malignancy: Pathogenesis and current debate. Neoplasia 2002;4:465-73.  Back to cited text no. 10
    


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