Cerebral Venous Thrombosis – A Case Study

 

Mr. L Anand¹, Shruti Shirke²

¹Associate Professor, Dept. of Nursing, AIIMS, Bhubaneswar.

²M.Sc Nursing, Neuroscience, AIIMS, Bhubaneswar.

 

ABSTRACT:

This case study presents a descriptive scenario and disease progress in patient with cerebral venous sinus thrombosis, the key objectives of this case study is to highlight the disease process, problem faced by patient with CVST and nursing care for the patient suffering with CVST, through literature review was done to present epidemiology of disease, rationally explain each symptoms. study further explains the anatomy and physiology in relation with pathophysiology and sign and symptoms, also describes proposed algorithm for the management of CVST, given by ASA. This case study recommends comprehensive and rational based care to the patient with cerebral venous sinus thrombosis, early detection, considering family history and educating people regarding simple measures of prevention like keeping our-self hydrated, periodic health checkups. Etc.

 

 

INTRODUCTION:

In today’s scenario where non-communicable diseases are increasing day by day and comorbidities are becoming part of life among general population, 15 million people suffer stroke worldwide each year of these 5million die and another 5 million are permanently disabled, out of all these cases approx. 1-5% of cases of stroke is due to cerebral venous sinus thrombosis (CVST)¹

 

CVST is a vascular disease of cerebrum in which blood clot forms in the brains venous sinuses from where venous blood and CSF drains into jugular vein, ultimately increasing intracranial pressure and is characterized by headache, papilledema, seizures and altered mental status.

 

Cerebral venous sinus thrombosis (CVST) is an uncommon condition with the incidence of 1-5% of all strokes, and it is initially often goes misdiagnosed due to its vague manifestations of sign and symptoms ranges from headache to focal neurological signs. CVST is slightly more common in women, particularly in the age group of 20-35.²

 

This case study of Mr. Rakesh khilwar was undertaken to describe the detailed medical history, sociodemographic, personal factors, clinical features, diagnostic and comprehensive medical and nursing care provided to this patient.

 

PRESENTATION OF CASE:

A 38 years old man admitted with the complaint of headache localized more in the right parito-occipital region with VAS score of 8/10, aggravated by sneezing, coughing, Valsalva maneuver and in lying down position and not relieved by taking oral analgesics, slightly relieved by sitting position and also complained of episodes of blurring of vision and 2 episodes of vomiting on the same day. On admission patient vital signs was stable except patient is presented with sinus tachycardia, patient was conscious and oriented, no evidence of cranial nerve involvement and intact reflexes, motor and sensory functions. Systemic examination was also came to be relatively normal, Initial medications started was prophylactic antibiotic inj. ceftriaxone along with tab. pantoprazole, tab ultracet sos prescribed by physician.  Routine investigations was done including CBC, RFT, PTINR, APTT, ECG, ABG, Viral marker, RTPCR for covid 19, additionally to this D-DIMER Assay, lipid profile, glycosylated hb % and radiologic investigations i.e. MRI (T2) Brain, MRV was also done.

 

Present medical history as told by patient, Patient was apparently fine 2 months back, when he travelled from one state to another around 320kms through bicycle to home during complete lockdown due to corono pandemic, once patient was reached after 3 days developed light headache VAS score of 4/10 which gradually progressed within 1 month and become severe thunderclap holocranial headache VAS Score of round 8-9/10, that time patient came to hospital and admitted for further evaluation and treatment. Patient’s last three generation family history does not revealed anything contributory to the patient current condition, by socioeconomically patient belongs to middle class family, and is cook by profession, and dietary pattern was satisfactory but had a history of chronic constipation and skin tag. He was occasional drinker and smoker and was having no sleep disturbances.

 

Patient’s Hematologic test report was relatively normal, viral marker and has negative covid status, normal glycosylated hb% with 6.1%, D-Dimer values was slightly raised indication of thrombus 1.64microgram/L FEU and lipid profile showed HDL was 26mg/dl, MRI (T2) of the brain showed pachymeningeal enhancement and MRV revealed features of right mastoiditis, acute thrombosis involving bilateral transverse sinuses, right sigmoid sinus, other sinuses are relatively fine. As per ASA guidelines³ (Figure 1) patient immediately started with heparin (anticoagulant) infusion at the rate of 1500IU/hour, Inj mannitol 20% kept as sos and ophthalmic consultation was advised, which evidenced B/L papilledema. Within 24 hours of heparin infusion patient symptoms of headache was reduced upto VAS score of 5-6/10, Heparin infusion continued for one week and APTT therapeutic range was maintained after one week of heparin infusion, inj. LMWX 0.6mg OD started there was a progressive decrease in the headache in a gap to 16-24 hours and finally reached 2/10 and then 0/10 VAS score in the period of 20 days. Finally the patient was discharged after 20 days of admission with the advice to take tablet acitrom 2mg OD for atleast 1 month and to come for follow-up.

 

PATHOPHYSIOLOGY:

The formation of a thrombus in the cerebral venous circulation (Figure 2), leads to increase in hydrostatic pressure in the veins and capillaries upstream of the occlusion. Because of the anatomical circuits/ Monro-Kellie hypothesis (Figure 3) increase venous pressure is compensated to some extent, it can cause blood brain barrier disruption, extravasation of fluids into the cerebral parenchyma and consequent localized edema.^4,5

 

Edema will decrease arterial supply to the brain and may cause, ischemic damage to the brain, if not treated may leads to haemorrhagic infarct, ultimately increases intracranial pressure, characterized by headache (88.8%) papilledema, paresis, and mental status alteration. Headache is featured as thunderclap outbreak mimicking subarachnoid haemorrhage, intensity of pain increase with lying down position, Valsalva maneuver, sneezing and coughing.   Seizures are focal in quarter of patients or it can be generalized to the whole body^6,7,8. Focal neurological deficit such as paresis, dysarthria and aphasia due to localized damage in the cerebral cortex secondary to venous infarction. Papilledema is the consequence of increase intracranial pressure can cause diplopia, vision loss, proptosis, orbital pain, chemosis, opthalamoplegia secondary to palsy of III, IV, VI cranial nerves. Altered mental status may features with amnesia, mutism, confusion or delirium rarely coma and death.

 

NURSING IMPLICATON:

Nurses’ role begins with the admission of the patient from receiving till discharge, to provide comprehensive nursing care in all aspect it requires adequate knowledge and critical thinking to prevent further complications, measures to promote the effectiveness of drug therapy and to achieve ultimate patient outcome, by adequately assessing physical, mental and neurological condition of the patient.

 

Throughout the course of treatment nurse look after several things including all medications assisting in diagnostic procedure and physical and psychological support to the patient.

 

Managing headache with non-pharmacological as well as pharmacological approach, maintaining sitting positing and daily activities as much as possible to manage headache, decrease periorbital and facial edema and prevention of complication by promoting venous drainage. Taking all bleeding precautions as the patient will be on thrombolytic therapy, avoiding unnecessary pricks, advising high fiber diet to prevent anal fissure due to constipation, maintaining adequate hydration maintaining intake and output, withholding heparin infusion at least 6 hours prior to LP and bone marrow aspiration procedure for the diagnostic purpose, maintaining therapeutic range of APTT. Looking forward any other side effects due to medication and prevention from nosocomial infection and identifying early signs of infection, following all standard operating protocol in providing patient care. Additional to this patient was advised to take picture of himself every morning to make better day by day comparison of trend of increasing and decreasing facial and periorbital edema. 

 

 

Figure 1: Proposed algorithm for the management of CVT by ASA

(https://www.ahajournals.org/doi/pdf/10.1161/STR.0b013e31820a8364)

 

Figure 2: The anatomy and terminology of the cerebral and sinus veins.

(https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.008018)

 

Figure 3: Monro-kellie hypothesis in case of increase ICP and hydrocephalus, compromising arterial and venous blood and compressed brain parenchyma and CSF

(https://www.researchgate.net/figure/Monro-Kellie-hypothesis-in-case-of-increase-intracranial-pressure-and-hydrocephalus_fig2_224831155)

 

 

CONCLUSION:

Cerebral venous sinus thrombosis is one of the life threatening neurological condition, Treatment at early onset has been proven successful with rehydration and intravenous anticoagulants. Like any disease processes, potential complications grow with severity and location of the patient. Patient as well as familial education is important for stroke patients of any kind. Understanding of both modifiable and non-modifiable risk factors are imperative for treatment and prevention of additional clotting secondary effects. This case study also emphasised that the onset of disease is progressed after long period of dehydration and exhaustion which need to be taken under consideration as a major risk factor. Day to day progress report and assessment is also an essential part to check the effectiveness of treatment plan, overall patient preferences, consent and satisfaction was also given importance. Comprehensive nursing care also has a positive significant difference by providing care throughout patient stay for the successful delivery of treatment and prevention of complication.^{9, 10}

 

REFERENCE:

1.     Mokri B. The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001; 56(12): 1746-1748. doi:10.1212/wnl.56.12.1746

2.     Miranda B, Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F, Scoditti U; ISCVT Investigators. Venous thromboembolic events after cerebral vein thrombosis.Stroke. 2010; 41: 1901–1906.LinkGoogle Scholar

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4.     Role of Dexamethasone in Meningitis - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/Monro-Kellie-hypothesis-in-case-of-increase-intracranial-pressure-and-hydrocephalus_fig2_224831155 [accessed 17 Sep, 2020]

5.     Yamamoto A, Hattammaru Y, Uezono S. Spontaneous intracranial hypotension associated with cerebral venous thrombosis detected by a sudden seizure: a case report. JA Clin Rep. 2020;6(1):59. Published 2020 Aug 4. doi:10.1186/s40981-020-00362-3

6.     Perry A, Graffeo CS, Brinjikji W, Copeland WR, Rabinstein AA, Link MJ. Spontaneous occult intracranial hypotension precipitating life-threatening cerebral venous thrombosis: case report. J Neurosurg Spine. 2018; 28(6): 669-678. doi:10.3171/2017.10.SPINE17806

7.     Taksande A, Meshram R, Yadav P, Lohakare A. Rare presentation of cerebral venous sinus thrombosis in a child. J Pediatr Neurosci [serial online] 2017 [cited 2020 Sep 17];12: 389-92. Available from: http://www.pediatricneurosciences.com/text.asp?2017/12/4/389/227966

8.     Beer-Furlan A, de Almeida CC, Noleto G, Paiva W, Ferreira AA, Teixeira MJ. Dural sinus and internal jugular vein thrombosis complicating a blunt head injury in a pediatric patient. Childs Nerv Syst 2013; 29: 1231-4.

9.     Einhäupl KM, Villringer A, Meister W, Mehraein S, Garner C, Pellkofer M, et al. Heparin treatment in sinus venous thrombosis. Lancet 1991; 338: 597-600.

10.  Ries S, Steinke W, Neff KW. Echocontrast-enhanced transcranial color-coded sonography for the diagnosis of transverse sinus venous thrombosis. Stroke 1997; 28: 696-700

 

 

 

 

Received on 26.09.2020          Modified on 05.12.2020

Accepted on 08.02.2021      ©AandV Publications All right reserved