Cardiac Complications After Subarachnoid Hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome.

Acute cardiac complications frequently occur after subarachnoid hemorrhage (SAH). These complications include electrocardiogram (ECG) abnormalities, the release of cardiac biomarkers, and the development of acute stress-induced heart failure resembling Takotsubo cardiomyopathy 1) 2) 3) 4) 5) 6)

non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.



Lång et al. assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH in a prospective observational multicenter study. They included 192 patients treated for non traumatic subarachnoid hemorrhage. They performed ECG recordings, echocardiogram, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0-64.0) years, 44.3% were male and the median World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage score was 2 (IQR 1-4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak e’ velocity (E/e’) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. They found no demographic or SAH-related factors associated with 90 days cardiac dysfunction 7).


Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).


1)

Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999;44:34–39. doi: 10.1097/00006123-199901000-00013.
2)

Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35:548–551. doi: 10.1161/01.STR.0000114874.96688.54.
3)

Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15–20. doi: 10.3171/jns.2006.105.1.15.
4)

Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown JRD, Wijdicks EFM. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. doi: 10.3171/jns.2006.105.2.264.
5)

Oras J, Grivans C, Bartley A, Rydenhag B, Ricksten SE, Seeman-Lodding H. Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. Crit Care (Lond, Engl) 2016;20:11. doi: 10.1186/s13054-015-1181-5.
6)

van der Bilt IA, Hasan D, Vandertop WP, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72:635–642. doi: 10.1212/01.wnl.0000342471.07290.07.
7)

Lång M, Jakob SM, Takala R, Lyngbakken MN, Turpeinen A, Omland T, Merz TM, Wiegand J, Grönlund J, Rahi M, Valtonen M, Koivisto T, Røsjø H, Bendel S. The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022 Nov 22;12(1):20109. doi: 10.1038/s41598-022-24675-8. PMID: 36418906.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.

Cranioplasty for hydrocephalus prevention after decompressive craniectomy

Cranioplasty for hydrocephalus prevention after decompressive craniectomy

After decompressive craniectomy, the occurrence of hydrocephalus is reported with varying incidences (10–45%) mainly due to differences in diagnostic criteria 1) 2) 3) 4).

The management of Hydrocephalus after decompressive craniectomy in need of cranial reconstruction can be challenging and thus is not precisely defined. The debate mainly revolves around the timing of cerebrospinal fluid shunt with respect to the cranioplasty 5).


To prevent decompressive craniectomy complications, such as sinking skin flap syndrome, studies suggested early cranioplasty (CP). However, several groups reported higher complication rates in early CP. In a single-center observational cohort, study cranioplasty has high complication rates, 23%. Contrary to recent systematic reviews, early CP was associated with more complications (41%), explained by the higher incidence of pre-CP CSF flow disturbance and acute subdural hematoma as etiology of DC. CP in such patients should therefore be performed with the highest caution. 6).


Delayed time to cranioplasty is linked with the development of persistent hydrocephalus, necessitating permanent CSF diversion in some patients. Waziri et al., propose that early cranioplasty, when possible, may restore normal intracranial pressure dynamics and prevent the need for permanent CSF diversion 7).


Ozoner et al. showed that early cranioplasty within 2 months after decompressive craniectomy was associated with a lower rate of posttraumatic hydrocephalus 8)


The goal of the study of Sethi et al. was to ascertain the efficacysafety, and comparability of ultra-early cranioplasty (CP; defined here as <30 days from the original craniectomy) to conventional cranioplasty (defined here as >30 days from the original craniectomy). A retrospective review of CPs performed between January 2016 and July 2020 was performed. Craniectomies initially performed at other institutions were excluded. Seventy-seven CPs were included in the study. Ultra-early CP was defined as CP performed within 30 days of craniectomy whereas conventional CP occurred after 30 days. Post-operative wound infection rates, rate of return to the operating room (OR) with or without bone flap removal, operative length, and rate of post-CP hydrocephalus were compared between the two groups. Thirty-nine and 38 patients were included in the ultra-early and conventional CP groups, respectively. The average number of days to CP in the ultra-early group was 17.70 ± 7.75 days compared to 95.70 ± 65.60 days in the conventional group. The mean Glasgow Coma Scale upon arrival to the emergency room was 7.28 ± 3.90 and 6.92 ± 4.14 for the ultra-early and conventional groups, respectively. The operative time was shorter in the ultra-early cohort than that in the conventional cohort (ultra-early, 2.40 ± 0.71 h; conventional, 3.00 ± 1.63 h; p = 0.0336). The incidence of post-CP hydrocephalus was also lower in the ultra-early cohort (ultra-early, 10.3%; conventional, 31.6%; p = 0.026). No statistically significant differences were observed regarding post-operative infection, return to the OR, or bone flap removal. The study shows that ultra-early CP can significantly reduce the rate of post-CP hydrocephalus, as well as operative time in comparison to conventional CP. However, the timing of CP post-DC should remain a patient-centered consideration 9).


1)

De Bonis P, Pompucci A, Mangiola A, Rigante L, Anile C. Post-traumatic hydrocephalus after decompressive craniectomy: an underestimated risk factor. J Neurotrauma. (2010) 27:1965–70. 10.1089/neu.2010.1425
2)

Cooper DJ, Rosenfeld JV, Murray L, Arabi YM, Davies AR, D’Urso P, et al.. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. (2011) 364:1493–502. 10.1056/NEJMoa1102077
3)

Honeybul S, Ho KM. Incidence and risk factors for post-traumatic hydrocephalus following decompressive craniectomy for intractable intracranial hypertension and evacuation of mass lesions. J Neurotrauma. (2012) 29:1872–8. 10.1089/neu.2012.2356
4)

Takeuchi S, Takasato Y, Masaoka H, Hayakawa T, Yatsushige H, Nagatani K, et al.. Hydrocephalus following decompressive craniectomy for ischemic stroke. Acta Neurochir Suppl. (2013) 118:289–91. 10.1007/978-3-7091-1434-6_56
5)

Iaccarino C, Kolias AG, Roumy LG, Fountas K, Adeleye AO. Cranioplasty Following Decompressive Craniectomy. Front Neurol. 2020 Jan 29;10:1357. doi: 10.3389/fneur.2019.01357. PMID: 32063880; PMCID: PMC7000464.
6)

Goedemans T, Verbaan D, van der Veer O, Bot M, Post R, Hoogmoed J, Lequin MB, Buis DR, Vandertop WP, Coert BA, van den Munckhof P. Complications in cranioplasty after decompressive craniectomy: timing of the intervention. J Neurol. 2020 May;267(5):1312-1320. doi: 10.1007/s00415-020-09695-6. Epub 2020 Jan 17. PMID: 31953606; PMCID: PMC7184041.
7)

Waziri A, Fusco D, Mayer SA, McKhann GM 2nd, Connolly ES Jr. Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery. 2007 Sep;61(3):489-93; discussion 493-4. PubMed PMID: 17881960.
8)

Ozoner B, Kilic M, Aydin L, Aydin S, Arslan YK, Musluman AM, Yilmaz A. Early cranioplasty associated with a lower rate of post-traumatic hydrocephalus after decompressive craniectomy for traumatic brain injury. Eur J Trauma Emerg Surg. 2020 Aug;46(4):919-926. doi: 10.1007/s00068-020-01409-x. Epub 2020 Jun 3. PMID: 32494837.
9)

Sethi A, Chee K, Kaakani A, Beauchamp K, Kang J. Ultra-Early Cranioplasty versus Conventional Cranioplasty: A Retrospective Cohort Study at an Academic Level 1 Trauma Center. Neurotrauma Rep. 2022 Aug 1;3(1):286-291. doi: 10.1089/neur.2022.0026. PMID: 36060455; PMCID: PMC9438438.

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Cerebral venous sinus thrombosis after Vaccine-induced Immune Thrombotic Thrombocytopenia

Health care providers should be familiar with the clinical presentations, pathophysiology, diagnostic criteria, and management consideration of this rare but severe and potentially fatal complication of the SARS-COV2 vaccine


Cerebral venous sinus thrombosis (CVT) prior to the COVID pandemic was rare, responsible for 0.5 of all strokes, at the onset of the pandemic on the East Coast, overall cross-sectional imaging volumes declined due to maintaining ventilation, high levels of care and limiting disease spread, although COVID-19 patients have a 30-60 times greater risk of CVT compared to the general population, and vaccination is currently the best option to mitigate severe disease. In early 2021, reports of adenoviral vector COVID vaccines causing CTV and Vaccine-induced Immune Thrombotic Thrombocytopenia (VITT), led to a 39.65% increase in cross-sectional venography, however, in this study unvaccinated patients in 2021 had a higher incidence of CVT (10.1%), compared to the vaccinated patients (4.5%). Clinicians should be aware that VITT CVT may present with a headache 5-30 days post-vaccination with thrombosis best diagnosed on CTV or MRV. If thrombosis is present with thrombocytopenia, platelets <150 × 109, elevated D-Dimer >4000 FEU, and positive anti-PF4 ELISA assay, the diagnosis is definitive. VITT CVT resembles spontaneous autoimmune heparin-induced thrombocytopenia (HIT) and is postulated to occur from platelet factor 4 (PF4) binding to vaccine adenoviral vectors forming a novel antigen, anti-PF4 memory B-cells, and anti-PF4 (VITT) antibodies. 1).

Neurosurgical management involves treating intracranial hypertension however survival outcomes in a cohort were poor. In these series, decompression was performed in deteriorating patients however prophylactic decompression, in the presence of extensive venous sinus thrombosis, should be considered on a case-by-case basis. As vaccination programs accelerate across the world, neurosurgeons are likely to be increasingly involved in managing intracranial hypertension in patients with VITT-related sinus thromboses. 2).


A distinct clinical profile and a high mortality rate were observed in patients meeting the criteria for thrombocytopenia syndrome (TTS) after SARS-CoV-2 vaccination 3).


Non-heparin anticoagulants and immunoglobulin treatment might improve outcomes of VITT-associated cerebral venous thrombosis 4)

Sixty-two studies reporting 160 cases were included from 16 countries. Patients were predominantly females with a median age of 42.50 (22) years. AZD1222 was administered to 140 patients (87·5%). TTS onset occurred in a median of 9 (4) days after vaccination. Venous thrombosis was most common (61.0%). Most patients developed cerebral venous sinus thrombosis (CVST; 66.3%). CVST was significantly more common in female vs male patients (p = 0·001) and in patients aged <45 years vs ≥45 years (p = 0·004). The mortality rate was 36.2%, and patients with suspected TTS, venous thrombosis, CVST, pulmonary embolism, or intraneural complications, patients not managed with non-heparin anticoagulants or IVIG, patients receiving platelet transfusions, and patients requiring intensive care unit admission, mechanical ventilation, or inpatient neurosurgery were more likely to expire than recover. 5)

Cerebral venous thrombosis caused by vaccine-induced immune thrombotic thrombocytopenia (VITT-CVT) is a rare adverse effect of adenovirus-based SARS-COV2 vaccines. In March 2021, after autoimmune pathogenesis of VITT was discovered, treatment recommendations were developed. This comprised immunomodulation, nonheparin anticoagulants, and avoidance of platelet transfusion. The aim of the study was to evaluate adherence to these recommendations and their association with mortality.

Scutelnic et al. used data from an international prospective registry of patients with CVT after adenovirus-based SARS-CoV-2 vaccination. They analyzed possible, probable, or definite VITT-CVT cases included until 18 January 2022. Immunomodulation entailed the administration of intravenous immunoglobulins and/or plasmapheresis.

99 VITT-CVT patients from 71 hospitals in 17 countries were analyzed. Five of 38 (13%), 11/24 (46%), and 28/37 (76%) of patients diagnosed in March, April, and from May onwards, respectively, were treated in-line with VITT recommendations (p<0.001). Overall, treatment according to recommendations had no statistically significant influence on mortality (14/44 (32%) vs 29/55 (52%), adjusted OR 0.43 (95%CI 0.16-1.19)). However, patients who received immunomodulation had lower mortality (19/65 (29%) vs 24/34 (70%), adjusted OR 0.19 (95%CI 0.06-0.58)). Treatment with non-heparin anticoagulants instead of heparins was not associated with lower mortality (17/51 (33%) vs 13/35 (37%), adjusted OR 0.70 (95%CI 0.24-2.04)). Mortality was also not significantly influenced by platelet transfusion (17/27 (63%) vs 26/72 (36%), adjusted OR 2.19 (95%CI 0.74-6.54)).

In VITT-CVT patients, adherence to VITT treatment recommendations improved over time. Immunomodulation seems crucial for reducing mortality of VITT-CVT 6).


During a 2-week period, we encountered five cases presenting with a combination of cerebral venous thrombosis (CVT), intracerebral hemorrhage, and thrombocytopenia. A clinical hallmark was the rapid and severe progression of disease in spite of maximum treatment efforts, resulting in fatal outcomes for 4 out of 5 patients. All cases had received the ChAdOx1 nCov-19 vaccine 1-2 weeks earlier and developed a characteristic syndrome thereafter. The rapid progressive clinical course and high fatality rate of CVT in combination with thrombocytopenia in such a cluster and in otherwise healthy adults is a recent phenomenon. Cerebral autopsy findings were those of venous hemorrhagic infarctions and thrombi in dural venous sinuses, including thrombus material apparently rich in thrombocytes, leukocytes, and fibrin. Vessel walls were free of inflammation. Extra-cerebral manifestations included leech-like thrombi in large veins, fibrin clots in small venules, and scattered hemorrhages on skin and membranes. CVT with thrombocytopenia after adenovirus vectored COVID-19 vaccination is a new clinical syndrome that needs to be recognized by clinicians is challenging to treat and seems associated with a high mortality rate 7)

A patient was rapidly treated with steroids, immunoglobulin, and fondaparinux. She underwent within 6 h after hospital admission a mechanical thrombectomy in order to allow flow restoration in cerebral venous systems. Neuroendovascular treatment in cerebral venous thrombosis related to VITT has never been described before. It can represent a complementary tool along with the other therapies and a multidisciplinary approach 8).


Two cases of ChAdOx1 nCov-19 (AstraZeneca)-are associated with thrombotic thrombocytopenia syndrome (TTS) and cerebral venous sinus thrombosis (CVST). At the time of emergency room presentation due to persistent headache, blood serum levels revealed reduced platelet counts. Yet, 1 or 4 days after the onset of the symptom, the first MR-angiography provided no evidence of CVST. Follow-up imaging, performed upon headache refractory to nonsteroidal pain medication verified CVST 2-10 days after initial negative MRI. Both the patients received combined treatment with intravenous immunoglobulins and parenteral anticoagulation leading to an increase in platelet concentration in both individuals and resolution of the occluded cerebral sinus in one patient 9).


Rodriguez et al. reported the first described post Ad26.COV2.S (Janssen, Johnson & Johnson) vaccine-induced immune thrombocytopenia (VITT) case outside US. CASE DESCRIPTION: CA young woman without any medical history presented an association of deep vein thrombosis and thrombocytopenia at day 10 after vaccine injection. The patient was treated with low-molecular-weight heparin at a first medical institution. Twelve days post Ad26.COV2.S vaccination, the patient was admitted to the hospital for neurological deterioration and right hemiplegia. Medical imaging using MRI showed thrombosis of the major anterior part of the sagittal superior sinus with bilateral intraparenchymal hemorrhagic complications. Screening tests for antibodies against platelet factor 4 (PF4)-heparin by rapid lateral flow immunoassay and chemiluminescence techniques were negative. Platelet activation test using heparin-induced multiple electrode aggregometry confirmed the initial clinical hypothesis. Despite immediate treatment with intravenous immunoglobulin, dexamethasone, danaparoid, and attempted neurosurgery the patient evolved toward brain death.

Even though it is an extremely rare complication of vaccination physicians should maintain a high index of suspicion of VITT in patients who received an adenovirus-vector-based SARS-CoV-2 vaccine within the last 30 days with persistent complaints compatible with VITT or thromboembolic event associated with thrombocytopenia. The diagnosis should not be excluded if the rapid anti-PF4 immunological or chemiluminescence techniques yield negative results. An adapted functional assay should be performed to confirm the diagnosis. Early treatment with intravenous immunoglobulin and non-heparin anticoagulants is essential as delayed diagnosis and administration of appropriate treatment are associated with poor prognosis 10).


A case of VITT in a young female who presented 11 days after receiving the first dose of the Covishield vaccine, with severe headache and hemiparesis. She was diagnosed with CSVT with a large intraparenchymal bleed, requiring decompressive craniectomy and an extended period of mechanical ventilation.

The patient was successfully treated with intravenous immunoglobulin and discharged after 19 days in ICU. Although she was left with long-term neurological deficits, an early presentation and a multidisciplinary approach to management contributed to a relatively short stay in the hospital and avoided mortality 11).


1)

Franceschi AM, Petrover DR, McMahon TM, Libman RB, Giliberto L, Clouston SAP, Castillo M, Kirsch C. Retrospective review COVID-19 vaccine induced thrombotic thrombocytopenia and cerebral venous thrombosis-what can we learn from the immune response. Clin Imaging. 2022 Jul 15;90:63-70. doi: 10.1016/j.clinimag.2022.06.020. Epub ahead of print. PMID: 35926315; PMCID: PMC9283127.
2)

Eltayeb M, Jayakumar N, Coulter I, Johnson C, Crossman J. Decompressive craniectomy for intracranial hypertension in vaccine-induced immune thrombotic thrombocytopaenia: a case series. Br J Neurosurg. 2022 Aug 25:1-4. doi: 10.1080/02688697.2022.2115007. Epub ahead of print. PMID: 36004613.
3)

Sánchez van Kammen M, Aguiar de Sousa D, Poli S, Cordonnier C, Heldner MR, van de Munckhof A, Krzywicka K, van Haaps T, Ciccone A, Middeldorp S, Levi MM, Kremer Hovinga JA, Silvis S, Hiltunen S, Mansour M, Arauz A, Barboza MA, Field TS, Tsivgoulis G, Nagel S, Lindgren E, Tatlisumak T, Jood K, Putaala J, Ferro JM, Arnold M, Coutinho JM; Cerebral Venous Sinus Thrombosis With Thrombocytopenia Syndrome Study Group, Sharma AR, Elkady A, Negro A, Günther A, Gutschalk A, Schönenberger S, Buture A, Murphy S, Paiva Nunes A, Tiede A, Puthuppallil Philip A, Mengel A, Medina A, Hellström Vogel Å, Tawa A, Aujayeb A, Casolla B, Buck B, Zanferrari C, Garcia-Esperon C, Vayne C, Legault C, Pfrepper C, Tracol C, Soriano C, Guisado-Alonso D, Bougon D, Zimatore DS, Michalski D, Blacquiere D, Johansson E, Cuadrado-Godia E, De Maistre E, Carrera E, Vuillier F, Bonneville F, Giammello F, Bode FJ, Zimmerman J, d’Onofrio F, Grillo F, Cotton F, Caparros F, Puy L, Maier F, Gulli G, Frisullo G, Polkinghorne G, Franchineau G, Cangür H, Katzberg H, Sibon I, Baharoglu I, Brar J, Payen JF, Burrow J, Fernandes J, Schouten J, Althaus K, Garambois K, Derex L, Humbertjean L, Lebrato Hernandez L, Kellermair L, Morin Martin M, Petruzzellis M, Cotelli M, Dubois MC, Carvalho M, Wittstock M, Miranda M, Skjelland M, Bandettini di Poggio M, Scholz MJ, Raposo N, Kahnis R, Kruyt N, Huet O, Sharma P, Candelaresi P, Reiner P, Vieira R, Acampora R, Kern R, Leker R, Coutts S, Bal S, Sharma SS, Susen S, Cox T, Geeraerts T, Gattringer T, Bartsch T, Kleinig TJ, Dizonno V, Arslan Y. Characteristics and Outcomes of Patients With Cerebral Venous Sinus Thrombosis in SARS-CoV-2 Vaccine-Induced Immune Thrombotic Thrombocytopenia. JAMA Neurol. 2021 Nov 1;78(11):1314-1323. doi: 10.1001/jamaneurol.2021.3619. PMID: 34581763; PMCID: PMC8479648.
4)

Perry RJ, Tamborska A, Singh B, Craven B, Marigold R, Arthur-Farraj P, Yeo JM, Zhang L, Hassan-Smith G, Jones M, Hutchcroft C, Hobson E, Warcel D, White D, Ferdinand P, Webb A, Solomon T, Scully M, Werring DJ, Roffe C; CVT After Immunisation Against COVID-19 (CAIAC) collaborators. Cerebral venous thrombosis after vaccination against COVID-19 in the UK: a multicentre cohort study. Lancet. 2021 Sep 25;398(10306):1147-1156. doi: 10.1016/S0140-6736(21)01608-1. Epub 2021 Aug 6. PMID: 34370972; PMCID: PMC8346241.
5)

Waqar U, Ahmed S, Gardezi SMHA, Tahir MS, Abidin ZU, Hussain A, Ali N, Mahmood SF. Thrombosis with Thrombocytopenia Syndrome After Administration of AZD1222 or Ad26.COV2.S Vaccine for COVID-19: A Systematic Review. Clin Appl Thromb Hemost. 2021 Jan-Dec;27:10760296211068487. doi: 10.1177/10760296211068487. PMID: 34907794; PMCID: PMC8689609.
6)

Scutelnic A, Krzywicka K, Mbroh J, van de Munckhof A, Sánchez van Kammen M, Aguiar de Sousa D, Lindgren E, Jood K, Günther A, Hiltunen S, Putaala J, Tiede A, Maier F, Kern R, Bartsch T, Althaus K, Ciccone A, Wiedmann M, Skjelland M, Medina A, Cuadrado-Godia E, Cox T, Aujayeb A, Raposo N, Garambois K, Payen JF, Vuillier F, Franchineau G, Timsit S, Bougon D, Dubois MC, Tawa A, Tracol C, De Maistre E, Bonneville F, Vayne C, Mengel A, Michalski D, Pelz J, Wittstock M, Bode F, Zimmermann J, Schouten J, Buture A, Murphy S, Palma V, Negro A, Gutschalk A, Nagel S, Schoenenberger S, Frisullo G, Zanferrari C, Grillo F, Giammello F, Martin MM, Cervera A, Burrow J, Garcia Esperon C, Chew BLA, Kleinig TJ, Soriano C, Zimatore DS, Petruzzellis M, Elkady A, Miranda MS, Fernandes J, Hellström Vogel Å, Johansson E, Philip AP, Coutts SB, Bal S, Buck B, Legault C, Blacquiere D, Katzberg HD, Field TS, Dizonno V, Gattringer T, Jacobi C, Devroye A, Lemmens R, Kristoffersen ES, Bandettini di Poggio M, Ghiasian M, Karapanayiotides T, Chatterton S, Wronski M, Ng K, Kahnis R, Geeraerts T, Reiner P, Cordonnier C, Middeldorp S, Levi M, van Gorp ECM, van de Beek D, Brodard J, Kremer Hovinga JA, Kruip MJHA, Tatlisumak T, Ferro JM, Coutinho JM, Arnold M, Poli S, Heldner MR. Management of cerebral venous thrombosis due to adenoviral COVID-19 vaccination. Ann Neurol. 2022 Jun 10. doi: 10.1002/ana.26431. Epub ahead of print. PMID: 35689346.
7)

Wiedmann M, Skattør T, Stray-Pedersen A, Romundstad L, Antal EA, Marthinsen PB, Sørvoll IH, Leiknes Ernstsen S, Lund CG, Holme PA, Johansen TO, Brunborg C, Aamodt AH, Schultz NH, Skagen K, Skjelland M. Vaccine Induced Immune Thrombotic Thrombocytopenia Causing a Severe Form of Cerebral Venous Thrombosis With High Fatality Rate: A Case Series. Front Neurol. 2021 Jul 30;12:721146. doi: 10.3389/fneur.2021.721146. PMID: 34393988; PMCID: PMC8363077.
8)

Mirandola L, Arena G, Pagliaro M, Boghi A, Naldi A, Castellano D, Vaccarino A, Silengo D, Aprà F, Cavallo R, Livigni S. Massive cerebral venous sinus thrombosis in vaccine-induced immune thrombotic thrombocytopenia after ChAdOx1 nCoV-19 serum: case report of a successful multidisciplinary approach. Neurol Sci. 2022 Mar;43(3):1499-1502. doi: 10.1007/s10072-021-05805-y. Epub 2022 Jan 10. PMID: 35001190; PMCID: PMC8743093.
9)

Braun T, Viard M, Juenemann M, Struffert T, Schwarm F, Huttner HB, Roessler FC. Case Report: Take a Second Look: Covid-19 Vaccination-Related Cerebral Venous Thrombosis and Thrombotic Thrombocytopenia Syndrome. Front Neurol. 2021 Nov 22;12:763049. doi: 10.3389/fneur.2021.763049. PMID: 34880826; PMCID: PMC8645635.
10)

Rodriguez EVC, Bouazza FZ, Dauby N, Mullier F, d’Otreppe S, Jissendi Tchofo P, Bartiaux M, Sirjacques C, Roman A, Hermans C, Cliquennois M. Fatal vaccine-induced immune thrombotic thrombocytopenia (VITT) post Ad26.COV2.S: first documented case outside US. Infection. 2022 Apr;50(2):531-536. doi: 10.1007/s15010-021-01712-8. Epub 2021 Oct 9. PMID: 34626338; PMCID: PMC8501343.
11)

Kotal R, Jacob I, Rangappa P, Rao K, Hosurkar G, Anumula SK, Kuberappa AM. A rare case of vaccine-induced immune thrombosis and thrombocytopenia and approach to management. Surg Neurol Int. 2021 Aug 16;12:408. doi: 10.25259/SNI_689_2021. PMID: 34513173; PMCID: PMC8422498.
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