Therapeutic anticoagulation is an important treatment of thromboembolic complications, such as DVT, PE, and blunt cerebrovascular injury. Traumatic intracranial hemorrhage has traditionally been considered to be a contraindication to anticoagulation.
Therapeutic anticoagulation can be safely accomplished in select patients with traumatic intracranial hemorrhage.
Patients who developed thromboembolic complications of DVT, PE, or blunt cerebrovascular injury were stratified according to mode of treatment. Patients who underwent therapeutic anticoagulation with a heparin infusion or enoxaparin (1 mg/kg BID) were evaluated for neurologic deterioration or hemorrhage extension by CT scan.
There were 42 patients with a traumatic intracranial hemorrhage that subsequently developed a thrombotic complication. Thirty-five patients developed a DVT or PE. Blunt cerebrovascular injury was diagnosed in four patients. 26 patients received therapeutic anticoagulation, which was initiated an average of 13 days after injury. 96% of patients had no extension of the hemorrhage after anticoagulation was started. The degree of hemorrhagic extension in the remaining patient was minimal and was not felt to affect the clinical course.
Therapeutic anticoagulation can be accomplished in select patients with intracranial hemorrhage, although close monitoring with serial CT scans is necessary to demonstrate stability of the hemorrhagic focus.
To analyze the risk factors, presentation, etiologies, and outcomes of adult cancer patients with intracranial hemorrhage (IH).
We analyzed 208 patients retrospectively with the diagnosis of IH from the Memorial Sloan-Kettering neurology database from January 2000 through December 2007. Charts were examined for clinical and radiographic data. Survival was calculated using the Kaplan-Meier method. Survival between groups was compared via the log-rank test. Logistic regression models were used to assess for prognostic indicators of 30- and 90-day mortality.
There were 181 intracerebral and 46 subarachnoid hemorrhages. Sixty-eight percent of patients had solid tumors, 16% had primary brain tumors, and 16% had hematopoietic tumors. Hemiparesis and headache were the most common symptoms. Intratumoral hemorrhage (61%) and coagulopathy (46%) accounted for the majority of hemorrhages, whereas hypertension (5%) was rare. Median survival was 3 months (95% confidence interval [CI] 2-4), and 30-day mortality was 31%. However, nearly one-half of patients were completely or partially independent at the time of discharge. Patients with primary brain tumors had the longest median survival (5.9 months, 95% CI 2.9-11.8, p = 0.05). Independent predictors of 30-day mortality were not having a primary brain tumor, impaired consciousness, multiple foci of hemorrhage, hydrocephalus, no ventriculostomy, and treatment of increased intracranial pressure.
Intracranial hemorrhage in patients with cancer is often due to unique mechanisms. Prognosis is poor, but comparable to intracranial hemorrhage in the general population. Aggressive care is recommended despite high mortality, because many patients have good functional outcomes.
= confidence interval;
= disseminated intravascular coagulation;
= intracerebral hemorrhage;
= intracranial pressure;
= intracranial hemorrhage;
= international normalized ratio;
= intratumoral hemorrhage;
= intraventricular hemorrhage;
= Memorial Sloan-Kettering Cancer Center;
= partial thromboplastin time;
= subarachnoid hemorrhage.
Intracranial hemorrhage was the most serious hemorrhage as measured by death and disability, occurring during long-term anticoagulant drug therapy of 1,626 patients. Among 95 hemorrhagic episodes considered life-threatening or potentially crippling, 30 were intracranial and 56 were gastrointestinal. Over two-thirds of the patients with intracranial hemorrhage died, as against one-tenth of those with gastrointestinal hemorrhage.
The incidence of intracranial hemorrhage is increased among hypertensive patients, but the results of a controlled study indicate that the incidence of intracranial hemorrhage is not affected by whether or not the hypertensive patient is receiving anticoagulant therapy. Hypertension is the important precipitating factor, not the prothrombin level. Even at excessively low prothrombin levels only one intracranial hemorrhage occurred in 337 instances.
In this series, reducing coagulability to a desirable range did not increase the probability of intracranial hemorrhage. Once bleeding occurred, however, it increased the risk of death and disability.
Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant genetic disease with a wide spectrum of vascular malformations involving multiple organs. Nine-16% of patients with HHT harbor brain arteriovenous malformations (AVMs), which can cause intracranial hemorrhage. Our objective was to study clinical manifestations of brain AVM in patients with HHT and correlate these with the specific gene mutated. We reviewed records of 171 patients with HHT and brain AVMs. A history of intracranial hemorrhage was found in 27% (41/152) patients, with a mean (range) age of 26 +/− 18 (0–68) years. All patients with intracranial hemorrhage were neurologically asymptomatic prior to intracranial hemorrhage. Multiple brain AVMs were found in 23% (170/39) of patients on initial examination. Genetic test results were available in 109 (64%) patients. Mutations in ENG, ACVRL1, and SMAD4 were present in 75 (69%), 18 (17%) and 2 (2%), respectively. A history of intracranial hemorrhage was reported in 24% of patients with an ENG mutation and 27% of patients with an ACVRL1 mutation, with a mean (range) age of 26 +/− 16 (2–50) and 18 +/− 21 (0–48) years, respectively. No statistically significant differences in age at first brain AVM diagnosis, prevalence of intracranial hemorrhage history, age at intracranial hemorrhage, or other manifestations of brain AVMs were observed among gene groups. In conclusion, no evidence for differences in brain AVM characteristics was observed among HHT gene groups, although we cannot exclude clinically important differences. Larger studies are needed to further guide brain AVM screening decisions in patients with HHT.
Hereditary Hemorrhagic Telangiectasia; Brain Arteriovenous Malformation; Genotype; Intracranial Hemorrhage
Treatment of acute ischemic stroke with intravenous tissue-type plasminogen activator is underutilized partly due to the risk of life-threatening hemorrhage. In response to the clinical need for safer stroke therapy, we explored using an aptamer-based therapeutic strategy to promote cerebral reperfusion in a murine model of ischemic stroke. Aptamers are nucleic acid ligands that bind to their targets with high affinity and specificity, and can be rapidly reversed with an antidote. Here we show that a Factor IXa aptamer administered intravenously after 60 minutes of cerebral ischemia and reperfusion improved neurological function and was associated with reduced thrombin generation and decreased inflammation. Moreover, when the aptamer was administered in the setting of intracranial hemorrhage, treatment with its specific antidote reduced hematoma volume and improved survival. The ability to rapidly reverse a pharmacologic agent that improves neurological function after ischemic stroke should intracranial hemorrhage arise indicates that aptamer–antidote pairs may represent a novel, safer approach to treatment of stroke.
Bevacizumab in combination with chemotherapy is now being studied for the treatment of malignant gliomas. However, the risk of intracranial hemorrhage has limited its use in patients requiring full anticoagulation for venous thrombosis. To assess the safety of using anticoagulation with bevacizumab, we conducted a retrospective review of our patients who were treated with bevacizumab while receiving anticoagulation. We reviewed their medical records and imaging for signs of hemorrhage. In total, we had 21 patients who received anticoagulation and bevacizumab concurrently for a median time of 72 days. Eighteen patients had adequate anticoagulation for venous thrombosis. There were no frank lobar hemorrhages in any patient. Three patients had small, intraparenchymal hemorrhages on MRI, but only one patient actually developed symptoms due to the hemorrhage. None of these patients had residual neurological deficits from the hemorrhages. Two more patients had evidence of a minor increase in signal on noncontrast T1-weighted sequence, presumed to be petechial hemorrhages, without any clinical sequelae or progression. In contrast, seven patients who had symptomatic hemorrhages from bevacizumab were not on any anticoagulation. In this retrospective review, anticoagulation did not lead to any major hemorrhages and does not appear to be a contraindication for starting bevacizumab therapy.
anticoagulation; bevacizumab; glioma; hemorrhage
This study investigated and summarized endovascular therapeutic strategies for intracranial ruptured aneurysms associated with arteriovenous malformations (AVMs). Between June 2005 and June 2009, we identified 16 aneurysms in 14 hemorrhagic cases of intracranial AVM using digital subtraction angiography (DSA). Of the 16 aneurysms, 14 were ruptured and two were unruptured. Aneurysms were classified as types I to IV, and were treated. Aneurysm treatment was followed by AVM treatment via various therapies, including embolization, gamma knife radiotherapy, or follow-up and observation to reduce the risk of aneurysm rupture or intracranial hemorrhage. Over a follow-up period ranging from six months to one year, none of the patients had aneurysm ruptures or intracranial hemorrhage. Most (13/14) patients had a Glasgow Outcome Scale (GOS) score of 5, and one patient had a score of 4. Sixteen aneurysms were treated successfully, as confirmed by DSA examination, and no AVMs re-grew. Clinical therapeutic strategies for intracranial ruptured aneurysms associated with AVMs should include aneurysm treatment first to reduce the risk of rupture and intracranial hemorrhage, eventually leading to a better prognosis.
aneurysm, arteriovenous malformation, endovascular treatment
Intracranial pressure monitoring is commonly implemented in patients with neurologic injury and at high risk of developing intracranial hypertension, to detect changes in intracranial pressure in a timely manner. This enables early and potentially life-saving treatment of intracranial hypertension.
An intraparenchymal pressure probe was placed in the hemisphere contralateral to a large basal ganglia hemorrhage in a 75-year-old Caucasian man who was mechanically ventilated and sedated because of depressed consciousness. Intracranial pressures were continuously recorded and never exceeded 17 mmHg. After sedation had been stopped, our patient showed clinical signs of transtentorial brain herniation, despite apparently normal intracranial pressures (less than 10 mmHg). Computed tomography revealed that the size of the intracerebral hematoma had increased together with significant unilateral brain edema and transtentorial herniation. The contralateral hemisphere where the intraparenchymal pressure probe was placed appeared normal. Our patient underwent emergency decompressive craniotomy and was tracheotomized early, but did not completely recover.
Intraparenchymal pressure probes placed in the hemisphere contralateral to an intracerebral hematoma may dramatically underestimate intracranial pressure despite apparently normal values, even in the case of transtentorial brain herniation.
Cavernous malformations (CMs) are the second most common intracranial vascular lesions. They typically present after hemorrhage or as incidental findings. Several risk factors have been identified for hemorrhage, however, electrocution as a cause has not been described. We performed a literature review of electrocution associated with CM hemorrhage and of the mechanisms of pathological injury in the central nervous system (CNS) secondary to electrocution. We found no cases of hemorrhage of CMs associated with electrocution.
A 19-year-old male electrician was accidentally electrocuted with 277 V of alternating current (AC) at a job site. He suffered no trauma or physical injuries and reported no immediate abnormal findings. He then experienced progressive nausea, emesis, and lethargy until he presented to the emergency department (ED) where it was discovered that he had a left thalamic/midbrain hemorrhage with hydrocephalus. His hydrocephalus was treated and he began to improve. Subsequent magnetic resonance imaging (MRI) of his head demonstrated characteristic features of a CM.
There are several proposed mechanisms in the literature by which electrocution may cause CNS damage. It is conceivable that given the pathology of CMs and the proposed mechanisms of electrical injury, these lesions may have an increased risk of hemorrhage as result of electrocution and we are reporting the first case of such an association.
Cavernoma; cavernous malformation; electrocution; hemorrhage
Patients with intracranial hemorrhage due to traumatic brain injury are at high risk of developing venous thromboembolism including deep vein thrombosis (DVT) and pulmonary embolism (PE). Thus, there is a trade-off between the risks of progression of intracranial hemorrhage (ICH) versus reduction of DVT/PE with the use of prophylactic anticoagulation. Using decision analysis modeling techniques, we developed a model for examining this trade-off for trauma patients with documented ICH.
The decision node involved the choice to administer or to withhold low molecular weight heparin (LMWH) anticoagulation prophylaxis at 24 hours. Advantages of withholding therapy were decreased risk of ICH progression (death, disabling neurologic deficit, non-disabling neurologic deficit), and decreased risk of systemic bleeding complications (death, massive bleed). The associated disadvantage was greater risk of developing DVT/PE or death. Probabilities for each outcome were derived from natural history studies and randomized controlled trials when available. Utilities were obtained from accepted databases and previous studies.
The expected value associated with withholding anticoagulation prophylaxis was similar (0.90) to that associated with the LMWH strategy (0.89). Only two threshold values were encountered in one-way sensitivity analyses. If the effectiveness of LMWH at preventing DVT exceeded 80% (range from literature 33% to 82%) our model favoured this therapy. Similarly, our model favoured use of LMWH if this therapy increased the risk of ICH progression by no more than 5% above the baseline risk.
Our model showed no clear advantage to providing or withholding anticoagulant prophylaxis for DVT/PE prevention at 24 hours after traumatic brain injury associated with ICH. Therefore randomized controlled trials are justifiable and needed to guide clinicians.
Acute aneurysmal subarachnoid hemorrhage (SAH) is a complex multifaceted disorder that plays out over days to weeks. Many SAH patients are seriously ill and require a prolonged ICU stay. Cardiopulmonary complications are common. The management of SAH patients focuses on the anticipation, prevention and management of these secondary complications.
Source data were obtained from a PubMed search of the medical literature.
Data Synthesis and Conclusion
The rupture of an intracranial aneurysm is a sudden devastating event with immediate neurologic and cardiac consequences that require stabilization to allow for early diagnostic angiography. Early complications include rebleeding, hydrocephalus, and seizures. Early repair of the aneurysm (within 1-3 days) should take place by surgical or endovascular means.
Over the first 1-2 weeks after hemorrhage, patients are at risk for delayed ischemic deficits due to vasospasm, autoregulatory failure and intravascular volume contraction. Delayed ischemia is treated with combinations of volume expansion, induced hypertension, augmentation of cardiac output, angioplasty and intra-arterial vasodilators. Subarachnoid hemorrhage is a complex disease with a prolonged course that can be particularly challenging and rewarding to the intensivist.
aneurysm; subarachnoid hemorrhage; vasospasm; hypertension; treatment; endovascular
Prostacyclin analogs therapy has been associated with development of thrombocytopenia. Little is known whether this treatment increases the risk of intracranial hemorrhage in pulmonary artery hypertension (PAH) patients. We queried the Cleveland Clinic billing database to identify cases of nontraumatic sudural hematoma (SDH) in patients with PAH. We identified those individuals who were receiving prostacyclin analogs therapy at the time of the neurological event and assessed whether these patients were also taking antiplatelet or anticoagulation therapies. We identified three cases of nontraumatic SDH in 856-patient-year of prostacylin analog treatment. All patients were women, had low normal platelet counts or thrombocytopenia, and were concomitantly receiving anticoagulation therapy in the appropriate therapeutic anticoagulation range. All three patients were managed conservatively and had no neurologic sequelae. Nontraumatic acute subdural hematoma is a rare event in patients with PAH treated with prostacyclin analogs. All affected patients were concomitantly receiving anticoagulation therapy.
anticoagulation; prostacyclin analogs; pulmonary hypertension; subdural hematoma
Hereditary hemorrhagic telangiectasia is a genetic disease characterized by teleangiectasias involving virtually every organ. There are limited data in the literature regarding the natural history of liver vascular malformations in hemorrhagic telangiectasia and their associated morbidity and mortality.
This prospective cohort study sought to assess the outcome of liver involvement in hereditary hemorrhagic telangiectasia patients.
We analyzed 16 years of surveillance data from a tertiary hereditary hemorrhagic telangiectasia referral center in Italy. We considered for inclusion in this study 502 consecutive Italian patients at risk of hereditary hemorrhagic telangiectasia who presented at the hereditary hemorrhagic telangiectasia referral center and underwent a multidisciplinary screening protocol for the diagnosis of hereditary hemorrhagic telangiectasia. Of the 502 individuals assessed in the center, 154 had hepatic vascular malformations and were the subject of the study; 198 patients with hereditary hemorrhagic telangiectasia and without hepatic vascular malformations were the controls. Additionally, we report the response to treatment of patients with complicated hepatic vascular malformations.
The 154 patients were included and followed for a median period of 44 months (range 12–181); of these, eight (5.2%) died from VM-related complications and 39 (25.3%) experienced complications. The average incidence rates of death and complications were 1.1 and 3.6 per 100 person-years, respectively. The median overall survival and event-free survival after diagnosis were 175 and 90 months, respectively. The rate of complete response to therapy was 63%.
This study shows that substantial morbidity and mortality are associated with liver vascular malformations in hereditary hemorrhagic telangiectasia patients.
Hereditary hemorrhagic telangiectasia; Liver vascular malformations; Heart failure; Portal hypertension; Gastrointestinal bleeding; Liver transplantation
Contributions from the neurosciences to Critical Care in 2011 covered an array of topics. We learned about potential biomarkers for, and the effect of cerebral oxygen metabolism on, delirium, in addition to treatment of the latter. A group of investigators studied surface cooling in healthy awake volunteers, and incidence of infection associated with therapeutic hypothermia. The effects of statin and erythropoietin on stroke were revisited, and the role of adhesion molecule in the inflammatory reaction accompanying intracerebral hemorrhage was scrutinized. Biomarkers in subarachnoid hemorrhage and their relationship to vasospasm and outcome, and effect of daylight on outcome in this patient population, as well as a new meta-analysis of statin therapy were among the research in subarachnoid hemorrhage. Moreover, 2011 witnessed the publication of a multidisciplinary consensus conference's recommendations on the critical care management of subarachnoid hemorrhage. Results of studies regarding the diagnosis and vascular complications of meningitis were reported. Traumatic brain injury received its share of articles addressing therapy with hypertonic saline and surgical decompression, the development of coagulopathy, and biomarkers to help with prognostication. Finally, research on the treatment of Guillain-Barre syndrome in children, prediction of long-term need of ventilatory support, and pathophysiology of critical illness polyneuropathy and myopathy were reported.
AIM: To evaluate the clinical characteristics of nonvariceal upper gastrointestinal hemorrhage (NGIH) in patients with chronic kidney disease (CKD).
METHODS: From 2003 to 2010, a total of 72 CKD patients (male n = 52, 72.2%; female n = 20, 27.8%) who had undergone endoscopic treatments for NGIH were retrospectively identified. Clinical findings, endoscopic features, prognosis, rebleeding risk factors, and mortality-related factors were evaluated. The characteristics of the patients and rebleeding-related data were recorded for the following variables: gender, age, alcohol use and smoking history, past hemorrhage history, endoscopic findings (the cause, location, and size of the hemorrhage and the hemorrhagic state), therapeutic options for endoscopy, endoscopist experience, clinical outcomes, and mortality.
RESULTS: The average size of the hemorrhagic site was 13.7 ± 10.2 mm, and the most common hemorrhagic site in the stomach was the antrum (n = 21, 43.8%). The most frequent method of hemostasis was combination therapy (n = 32, 44.4%). The incidence of rebleeding was 37.5% (n = 27), and 16.7% (n = 12) of patients expired due to hemorrhage. In a multivariate analysis of the risk factors for rebleeding, alcoholism (OR = 11.19, P = 0.02), the experience of endoscopists (OR = 0.56, P = 0.03), and combination endoscopic therapy (OR = 0.06, P = 0.01) compared with monotherapy were significantly related to rebleeding after endoscopic therapy. In a risk analysis of mortality after endoscopic therapy, only rebleeding was related to mortality (OR = 7.1, P = 0.02).
CONCLUSION: Intensive combined endoscopic treatments by experienced endoscopists are necessary for the treatment of NGIH in patients with CKD, especially when a patient is an alcoholic.
Chronic kidney diseases; Gastrointestinal hemorrhage; Endoscopy; Peptic ulcer; Alcoholics
Hemorrhagic coagulopathy (without neurological injuries) constitutes 40% of injury-related death in civilian hospitals and on the battlefield, and the underlying contributing mechanisms remain unclear. The purpose of this study is to investigate the effects of fibrinogen availability on coagulation function after hemorrhage in pigs. Sixteen crossbred commercial Yorkshire swine were randomized into the control group (group C) (n = 8) and hemorrhage group (group H) (n = 8). Hemorrhage was induced in group H by bleeding 35% of the estimated total blood volume, followed by resuscitation with lactated Ringer solution at three times the bled volume. Pigs in group C were not hemorrhaged or resuscitated. Blood samples were withdrawn at baseline, 15 min, 3 h, 6 h, and 24 h after hemorrhage and lactated Ringer (LR) resuscitation (H–LR). Coagulation was assessed by using thrombelastography. All baseline measurements were similar between groups C and H. Hemorrhage caused a decrease in mean arterial pressure and an increase in heart rate in group H, but LR resuscitation corrected these changes within 1 h. Compared to baseline values, fibrinogen concentrations in group H decreased at 15 min, 3 h and 6 h after H–LR, but increased to double that of the baseline value at 24 h; platelet counts decreased throughout the study; clot strength was decreased at 15 min, 3 h and 6 h, but returned to baseline value at 24 h after H–LR. Hemorrhage caused decreases in fibrinogen and platelets, and compromised clot strength. The rebound of fibrinogen at 24 h restored clot strength despite platelet deficit. These data suggest the potential compensatory role of fibrinogen in restoring coagulation function in vivo after hemorrhagic shock.
Traumatic intracranial aneurysms in children are rare and mostly related to skull fracture or rapid decelerating closed head injury. We report the case of an infant who developed intracranial aneurysm after minor head trauma and managed by endovascular treatment.
A seven-month-old infant presented with delayed intracranial hemorrhage following minor head trauma. Cerebral angiography disclosed a multilobulated fusiform aneurysm involving the right anterior cerebral artery (ACA) distal to the anterior communicating artery. Endovascular treatment of the aneurysm was performed and the infant made an excellent recovery during six months clinical and radiological follow-up.
Delayed presentation of intracranial hemorrhage with acute deterioration in the infant after head trauma warrants angiography for proper diagnosis and management of the traumatic aneurysm, which has a high mortality rate after rupture and rebleeding. Endovascular treatment of traumatic aneurysm is feasible in infants, and occlusion of distal intracranial arterial aneurysms can be safely and precisely achieved using current coil technology.
brain aneurysms, endovascular treatment, trauma
In recent years, intracranial hemorrhage (ICH) with parenchymal involvement has been diagnosed more often in full-term neonates due to improved neuroimaging techniques. The aim of this study is to describe clinical and neuroimaging data in the neonatal period and relate imaging findings to outcome in a hospital-based population admitted to a level 3 neonatal intensive care unit (NICU).
From our neuroimaging database, we retrospectively retrieved records and images of 53 term infants (1991–2008) in whom an imaging diagnosis of ICH with parenchymal involvement was made. Clinical data, including mode of delivery, clinical manifestations, neurological symptoms, extent and site of hemorrhage, neurosurgical intervention, and neurodevelopmental outcomes, were recorded.
Seventeen of the 53 term infants had infratentorial ICH, 20 had supratentorial ICH, and 16 had a combination of the two. Seizures were the most common presenting symptom (71.7%), another ten infants (18.9%) presented with apneic seizures, and five infants had no clinical signs but were admitted to our NICU because of perinatal asphyxia (n = 2), respiratory distress (n = 2), and development of posthemorrhagic ventricular dilatation (n = 1). Continuous amplitude-integrated electroencephalography recordings were performed in all infants. Clinical or subclinical seizures were seen in 48/53 (90.6%) infants; all received anti-epileptic drugs. Thirteen of all 53 (24.5%) infants died. The lowest mortality rate was seen in infants with supratentorial ICH (10%). Three infants with a midline shift required craniotomy, six infants needed a subcutaneous reservoir due to outflow obstruction, and three subsequently required a ventriculoperitoneal shunt. The group with poor outcome (death or developmental quotient (DQ) <85) had a significantly lower 5-min Apgar score (p = .006). Follow-up data were available for 37/40 survivors aged at least 15 months. Patients were assessed with the Griffiths Mental Developmental Scales, and the mean DQ of all survivors was 97 (SD = 12). Six infants (17%) had a DQ below 85 [two of them had cerebral palsy (CP)]. Three infants developed CP (8.6%); one had cerebellar ataxia, and two had hemiplegia.
ICH with parenchymal involvement carries a risk of adverse neurological sequelae with a mortality of 24.5% and development of CP in 8.6%. The high mortality rate could partly be explained by associated perinatal asphyxia. Infants with supratentorial ICH had a lower, although not significant, mortality rate compared with infants with infratentorial ICH and infants with a combination of supratentorial ICH and infratentorial ICH. In spite of often large intraparenchymal lesions, 30 of the 34 survivors without CP (88.2%) had normal neurodevelopmental outcome at 15 months.
Intracranial hemorrhage; Intraparenchymal hemorrhage; Subdural hemorrhage; Full-term newborns
Objective. To assess prevalence, clinical characteristics, trends in treatment pattern, and outcome in patients with intracranial vascular malformations (IVMs). Methods. Nationwide inpatient sample. Patients with the diagnosis of an IVM admitted to US hospitals from 2000 to 2007. Results. In 58,051 IVM-related admissions (detection rate 2.4/100,000 person-years; mean age 49 ± 17 years; 52% women) major diagnoses were intracranial hemorrhage (ICrH) in 15%, seizure 32%, ischemia 5%, and headache 9%. Procedures included surgery (13%), embolization (13%), radiation therapy (2%), aneurysm clipping (1%), and mechanical ventilation (6%). Ventilation and ICrH were associated with death (2%), whereas ventilation, ICrH, surgery, seizure, and ischemia were associated with unfavorable outcome (20%). IVM detection rate and hospital outcome remained stable over time, whereas mean age and comorbid diagnosis of cerebral ischemia increased (ICrH and seizure decreased). Conclusion. IVMs are infrequent and present in 1/6 patients with some form of ICrH. Overall, seizure is the dominant comorbid diagnosis (1/3 patients). IVMs are equally prevalent among race-ethnic groups and are increasingly detected later in life. The inpatient care of IVM patients results in death or discharge into specialized care in 1/5 patients.
There was no abundance of data on the use of anticoagulant in patients with previous high risk of thromboembolic conditions under a newly developed intracranial hemorrhage in Korean society. The purpose of this study was to evaluate the safety of discontinuance and suggest the proper time period for discontinuance of anticoagulant among these patients.
We reviewed the medical records of 19 patients who took anticoagulant because of thromboembolic problems and were admitted to our department with newly developed anticoagulation associated intracranial hemorrhage (AAICH), and stopped taking medicine due to concern of rebleeding from January 2008 to December 2012. Analysis of the incidence of thromboembolic complications and proper withdrawal time of anticoagulant was performed using the Kaplan-Meier method.
Our patients showed high risk for thromboembolic complication. The CHA2DS2-VASc score ranged from two to five. Thromboembolic complication occurred in eight (42.1%) out of 19 patients without restarting anticoagulant since the initial hemorrhage. Among them, three patients (37.5%) died from direct thromboembolic complications. Mean time to outbreak of thromboembolic complication was 21.38±14.89 days (range, 8-56 days). The probability of thromboembolic complications at 7, 14, and 30 days since cessation of anticoagulation was 0.00, 10.53, and 38.49%, respectively.
Short term discontinuance of anticoagulant within seven days in patients with AAICH who are at high embolic risk (CHA2DS2-VASc score >2) appears to be relatively safe in Korean people. However, prolonged cessation (more than seven days) may result in increased incidence of catastrophic thromboembolic complications.
Anticoagulation; Intracerebral hemorrhage; Thromboembolic complication
Oral anticoagulant therapy (OAT) is used to prevent/treat thromboembolism. Major bleeding is common in patients on OAT; eg, warfarin increases intracranial hemorrhage (ICH) risk.
A 71-year-old male on warfarin (to reduce stroke risk) presented at Accident and Emergency Minor Injuries Unit with headache after reportedly sounding ‘drunk’. On triage, the patient appeared lucid and well. However, International Normalized Ratio (INR) was 4.1. Head computed tomography (CT) indicated a large right-sided subdural hematoma. Prothrombin complex concentrate (PCC; Beriplex® P/N, CSL Behring) with vitamin K normalized the INR within minutes of administration. The patient underwent neurosurgery without complications, and was discharged after 5 days, with no residual neurological symptoms.
ICH patients can present with no neurological signs. In OAT patients with headache, INR must be established; if ≥3.0, normalization of INR and head CT are essential. PCC is the best option to rapidly reverse anticoagulation and correct INR pre-surgery.
anticoagulation reversal; Beriplex® P/N; computed tomography; International Normalized Ratio; intracranial hemorrhage; prothrombin complex concentrate
Intracerebral hemorrhage is by far the most destructive form of stroke. The clinical presentation is characterized by a rapidly deteriorating neurological exam coupled with signs and symptoms of elevated intracranial pressure. The diagnosis is easily established by the use of computed tomography or magnetic resonance imaging. Ventilatory support, blood pressure control, reversal of any preexisting coagulopathy, intracranial pressure monitoring, osmotherapy, fever control, seizure prophylaxis, treatment of hyerglycemia, and nutritional supplementation are the cornerstones of supportive care in the intensive care unit. Dexamethasone and other glucocorticoids should be avoided. Ventricular drainage should be performed urgently in all stuporous or comatose patients with intraventricular blood and acute hydrocephalus. Emergent surgical evacuation or hemicraniectomy should be considered for patients with large (>3 cm) cerebellar hemorrhages, and in those with large lobar hemorrhages, significant mass effect, and a deteriorating neurological exam. Apart from management in a specialized stroke or neurological intensive care unit, no specific medical therapies have been shown to consistently improve outcome after intracerebral hemorrhage.
Most serious hemorrhages that occur during long-term anticoagulant drug therapy are due either to poor patient selection or to poor management of the patient, or both.
In each patient being considered for treatment, the risk of bleeding must be evaluated and classified as high, moderate or low.
The clinician must especially assess the risk of intracranial hemorrhage in hypertensive patients, and must screen all patients for potential sources of gastrointestinal bleeding. There is ample time for such investigations, since initiating long-term anticoagulant therapy is not an emergency procedure.
The desired level of prothrombin activity must be adjusted to the risks determined for each individual patient. There is no single “therapeutic range” applicable to all patients with their varying hemorrhagenic risks.
Proper management includes sufficient laboratory testing to maintain the desired prothrombin level, and continued vigilance to detect signs of early bleeding.
Preventable hemorrhage cannot be cited as evidence against the value of anticoagulant drug therapy.
Nonmissile penetrating intracranial injuries are uncommon events in modern times. Most reported cases describe trajectories through the orbit, skull base foramina, or areas of thin bone such as the temporal squama. Patients who survive such injuries and come to medical attention often require foreign body removal. Critical neurovascular structures are often damaged or at risk of additional injury resulting in further neurological deterioration, life-threatening hemorrhage, or death. Delayed complications can also be significant and include traumatic pseudoaneurysms, arteriovenous fistulas, vasospasm, cerebrospinal fluid leak, and infection. Despite this, given the rarity of these lesions, there is a paucity of literature describing the management of neurovascular injury and skull base repair in this setting. The authors describe three cases of nonmissile penetrating brain injury and review the pertinent literature to describe the management strategies from a contemporary cerebrovascular and skull base surgery perspective.
Penetrating trauma; brain; skull base; pseudoaneurysm
Severe complications that develop in the early stages in patients with acute leukemia have a mortal course. Bleeding, leukostasis, and less frequently, infections are responsible for early mortality. Hemorrhage is most common in acute leukemia and usually leads to death. Hemorrhage may occur due to chemotherapy or bone marrow transplantation in patients with acute leukemia. Leukocytosis, thrombocytopenia, sepsis, and coagulopathy increase the risk of bleeding. There may be multiple etiologic factors. Subdural or subarachnoid hemorrhage is less common than an intra-axial hemorrhage. The incidence of spontaneous subdural hematoma is higher in patients with leukemia. Although advances in the treatment of platelet transfusion and disseminated intravascular coagulation have decreased the incidence of hemorrhagic complications in patients receiving chemotherapy for acute leukemia, intracranial hemorrhage-related deaths are a significant problem. We discussed the etiology and management of chronic subdural hematoma detected in a two-year-old male patient with Acute Myeloid Leukemia and hyperleukocytosis.
Acute myeloid leukemia; child; leukocytosis; subdural hematoma