scholarly journals Cerebral oedema and dural sinus thrombosis in an adolescent with diabetic ketoacidosis

2021 ◽  
Vol 14 (4) ◽  
pp. e241690
Author(s):  
Julia L Bassell ◽  
David W Swenson ◽  
Monica Serrano-Gonzalez ◽  
Lisa Swartz Topor
Neurosurgery ◽  
2003 ◽  
Vol 52 (3) ◽  
pp. 534-544 ◽  
Author(s):  
Scott W. Soleau ◽  
Richard Schmidt ◽  
Steve Stevens ◽  
Anne Osborn ◽  
Joel D. MacDonald

Abstract OBJECTIVE Dural sinus thrombosis (DST) is an uncommon cause of stroke. The safest and most effective therapy for DST has not been conclusively identified. METHODS A retrospective chart review of data for 31 patients who were treated for DST at our institution between 1992 and 2001 was performed. Four treatment strategies were identified, i.e., 1) medical observation only, 2) systemic anticoagulation (AC) therapy with heparin, 3) endovascular chemical thrombolysis with urokinase or tissue plasminogen activator and concurrent systemic AC therapy, and 4) mechanical endovascular clot thrombolysis with concurrent systemic AC therapy. Complications and clinical outcomes were assessed for each group. RESULTS Patients treated solely with medical observation fared the worst; four of five patients experienced intracranial hemorrhagic complications, and only two of five exhibited clinical improvement. Patients who received systemic AC therapy experienced no hemorrhagic complications, even when pretreatment hemorrhage was present; 75% (six of eight patients) exhibited improvement with AC therapy alone. Chemical thrombolysis was very effective in restoring sinus patency (90% of patients); however, 30% of patients (3 of 10 patients) experienced hemorrhagic complications. Sixty percent of patients (6 of 10 patients) who underwent chemical thrombolysis exhibited clinical improvement. Patients who underwent mechanical thrombectomies demonstrated a low hemorrhagic complication rate, and most (88%) made good recoveries. CONCLUSION Therapy directed at the underlying clot in DST must begin without delay. Our results suggest that supportive medical management of DST, without therapy directed at the clot or clotting process, is not effective. Systemic AC therapy, even in the presence of intracerebral hemorrhage, seems to be safe. Heparin can be safely titrated to yield partial thromboplastin times of 60 to 70 seconds. Chemical clot thrombolysis is efficacious in opening occluded sinuses but may cause intracranial hemorrhage. We currently recommend either systemic AC therapy or systemic AC therapy in conjunction with mechanical clot thrombectomy as a safe effective treatment for DST.


Seizure ◽  
2014 ◽  
Vol 23 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Vahid Davoudi ◽  
Kiandokht keyhanian ◽  
Mohammad Saadatnia

1993 ◽  
Vol 29 (1) ◽  
pp. 51
Author(s):  
Si Kyung Lee ◽  
Chun Hwan Han ◽  
Moon Ok Lee ◽  
Kyung Joo Park ◽  
Joo Hyuk Lee

1937 ◽  
Vol 11 (6) ◽  
pp. 755-771 ◽  
Author(s):  
Orville T. Bailey ◽  
George M. Hass

2009 ◽  
Vol 29 (8) ◽  
pp. 808-813 ◽  
Author(s):  
G. Legendre ◽  
O. Picone ◽  
J. M. Levaillant ◽  
J. Delavaucoupet ◽  
A. Ozanne ◽  
...  

2003 ◽  
Vol 127 (10) ◽  
pp. 1359-1361 ◽  
Author(s):  
Christina L. Stephan ◽  
Karen SantaCruz ◽  
Corrie May ◽  
Steve B. Wilkinson ◽  
Mark T. Cunningham

Abstract Inherited thrombophilia is a risk factor for dural sinus thrombosis (DST). To our knowledge, this is the first description with autopsy findings of a patient with DST associated with heterozygous factor V Leiden and a short activated partial thromboplastin time (aPTT). A 51-year-old woman presented with a 3-day history of headache, nausea, right-sided weakness, and focal motor seizure; she died 3 days after admission. At autopsy, a gross examination showed hemorrhage of bilateral parietal lobes and left primary motor cortex, uncal and tonsillar herniation, and pulmonary embolus of the right upper lobe. A microscopic examination of the brain showed an organizing thrombus in the superior sagittal sinus, diffuse cerebral edema, and extensive venous congestion. Laboratory studies showed heterozygous factor V Leiden by polymerase chain reaction and a very short aPTT of 17 seconds (reference range, 22–30 seconds). The combination of a heterozygous factor V Leiden mutation and a short aPTT may have contributed to the fatal DST in this patient.


Author(s):  
Neil M. D’Souza ◽  
Sumayya J. Almarzouqi ◽  
Michael L. Morgan ◽  
Andrew G. Lee

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