Bloody Spinal Fluid Research Articles

Cerebrospinal Fluid Drain-Related Complications in Patients Undergoing Open and Endovascular Repairs of Thoracic and Thoracoabdominal Aortic Pathologies: A Systematic Review and Meta-Analysis

Search of electronic databases of PubMed and Scopus for randomized controlled trials, prospective studies, and retrospective studies in all languages from 1990 to 2017. Thirty-four studies including 4714 patients were analyzed examining the results of cerebrospinal drainage (CSF) drainage performed as an adjunct for endovascular or open repair of thoracic or thoracoabdominal aneurysm repair. The pooled event rate of CSF drainage was 6.5% overall: 2% for minor complications (puncture-site bleeding, bloody spinal fluid, CSF leak not requiring intervention, hypotension, drain fracture left in place, occluded/dislodged catheters), 3.7% for moderate complications (spinal headache, CSF leak requiring intervention, drain fracture), and 2.5% for severe complications (epidural hematoma, intracranial hemorrhage, subarachnoid hemorrhage, meningitis, catheter/drainage-related neurological deficit). The drainage-related mortality-pooled event rate was 0.9%. There was no difference in complication rates between open and endovascular approaches or between different CSF drainage protocols. The complication rate for CSF drainage is approximately 6% with severe complications occurring in 2.5% of patients. These results help define a more accurate risk-benefit ratio

Patched Closure of Dural Outlet of External Ventricular Drainage Catheter: Better Way to Prevent Cerebrospinal Fluid Leakage.

Postoperative continuous bloody cerebral spinal fluid drainage with external ventricular drainage catheter could decrease the incidence of inflammation. But the drainage catheter left in place will interrupt the watertight dura matter closure. To prevent the related cerebrospinal fluid leakage and subgaleal pseudomeningocele after the catheter removal, we developed a patched closure method to seal the dural outlet of the drainage catheter with a favorable clinical outcome.

Early Experience With Automatic Pressure-Controlled Cerebrospinal Fluid Drainage During Thoracic Endovascular Aortic Repair

Purpose: To report initial experience with automatic pressure-controlled cerebrospinal fluid drainage (CSFD) during thoracic endovascular aortic repair (TEVAR). Methods: A prospective nonrandomized study enrolled 30 consecutive patients (median age 68 years, range 42–89; 18 men) who underwent TEVAR between March 2012 and July 2013 and were considered to be at high risk for postoperative spinal cord ischemia (SCI), fulfilling 2 of the following criteria: stent-graft length >20 cm, left subclavian artery coverage, and previous infrarenal aortic repair. All patients received perioperative CSFD via the LiquoGuard system. The protocol aimed for a CSF pressure of 10 mm Hg and duration of CSFD of 3 or 7 days in asymptomatic or symptomatic patients, respectively. Muscle strength of the lower extremities was assessed with the Oxford muscle strength grading scale. Results: Completion of the CSFD protocol was achieved in 26 (87%) of 30 patients. CSFD was prematurely stopped due to catheter dislocation in 1 patient and bloody spinal fluid in 3 patients. CSFD was performed for a median of 3 days (range 1–7). Median total CSFD volume was 714 mL (range 13–2369), with a median 192 mL drained per 24 hours. The SCI rate was 3% (1/30). CSFD-related complications were observed in 33% of the patients: 1 fatal intracranial hemorrhage, 3 bloody spinal fluid episodes, 3 persistent CSF leaks requiring epidural blood patch, and 3 post lumbar puncture headaches. Mortality during a median follow-up of 16 months (range 10–25) was 3% (1/30). Conclusion: Prophylactic CSFD was associated with a low SCI rate in a high-risk patient collective undergoing TEVAR. Monitoring and drainage by an automatic modus was feasible, reproducible, and reliable but associated with relevant drainage-associated complications.

Complications of spinal fluid drainage in thoracic and thoracoabdominal aortic aneurysm surgery in 724 patients treated from 1987 to 2013.

To study complications from spinal fluid drainage in open thoracic/thoracoabdominal and thoracic endovascular aortic aneurysm repairs to define risks of spinal fluid drainage. Retrospective, prospectively maintained, institutionally approved database. Single institution university center. 724 patients treated from 1987 to 2013 INTERVENTIONS: The authors drained spinal fluid to a pressure≤6 mmHg during thoracic aortic occlusion/reperfusion in open and ≤8 mmHg after stent deployment in endovascular procedures. Low pressure was maintained until leg strength was documented. If bloody fluid appeared, drainage was stopped. Head computed tomography (CT) and, if indicated, spine CT and magnetic resonance imaging (MRI) were performed for bloody spinal fluid or neurologic deficit. Spinal fluid drainage was studied for bloody fluid, CT/MRI-identified intracranial and spinal bleeding, neurologic deficit, and death. Seventy-three patients (10.1%) had bloody fluid; 38 (5.2%) had intracranial blood on CT. One patient had spinal epidural hematoma. Higher volume of fluid drained and higher central venous pressure during proximal clamping were associated with intracranial blood. Most patients with intracranial blood were asymptomatic. Six patients had neurologic deficits: of the 6, 3 died (0.4%), 1 (0.1%) had permanent hemiparesis, and 2 recovered. Three of the six deficits were delayed, associated with heparin anticoagulation. 10% of patients had bloody spinal fluid; half of these had intracranial bleeding, which was almost always asymptomatic. In these patients, immediately stopping drainage and correcting coagulopathy may decrease the risk of serious complications. Neurologic deficit from spinal fluid drainage is uncommon (0.8%), but has high morbidity and mortality.

Stroke Classification

Because all history is to some extent personal, and because I have been active throughout attempts at classification, I was asked to provide a personal account of stroke subtyping and stroke registries bringing the topic up to date. ### Early Studies Clinicopathological studies during the first half of the 20th century focused on clinical signs in patients who died after stroke. Brain hemorrhages and infarcts were recognized at necropsy, but could they be separated during life? In 1935, Aring and Merritt1 analyzed 245 stroke patients studied clinically and at necropsy at the Boston City Hospital. They reported demographic, epidemiological, historical, and clinical data to determine which features differentiated thrombosis from hemorrhage. Hemorrhages (intracerebral or subarachnoid) were found in 15% of patients and 82% had ischemic infarcts called “thrombotic;” however, only 3% were considered to have cardiogenic embolic brain infarcts. The main features favoring hemorrhage were headache, vomiting, impaired consciousness, progression of the clinical neurological deficit, bloody spinal fluid, and increased spinal fluid pressure.1 This series was biased toward patients with large fatal hemorrhages and infarcts. Later, Dalsgaard-Nielsen2 in Scandinavia compiled a series of 1 000 stroke patients, and clinicians at the Mayo Clinic analyzed series of patients seen during 1945 through 19543 and from 1955 through 1969.4 These studies were based on retrospective chart reviews and all preceded CT. Infarcts were >4-times more common than hemorrhages. Infarcts were classified as embolic only if the patients had rheumatic heart disease or recent myocardial infarction. Rates of brain embolism using these criteria ranged from 3% to 8%. Nonembolic brain infarcts were assumed to be “thrombotic” and related to occlusion of brain supplying large arteries. Carotid and vertebral artery disease in the neck and lacunar infarction were not diagnoses included in any of these early studies. ### The Harvard Stroke Registry5,–,8 In 1971, Howard Bleich, a …

Spinal Cord Protection with a Cerebrospinal Fluid Drain in a Patient Undergoing Thoracic Endovascular Aortic Repair

Paralysis and paraparesis are dreaded complications of thoracic endovascular aortic repair (TEVAR) that occur with an incidence of 2%-6%. Risks factors include the type of thoracic aortic pathology treated, coverage of the left subclavian artery origin without revascularization, concomitant infrarenal abdominal aortic aneurysm repair, extent of stent graft coverage of the thoracic aorta, and renal failure. Cerebral spinal fluid (CSF) drains have been advocated as one of several protective strategies to prevent spinal cord ischemia. This case discussion briefly addresses the evidence supporting the use of CSF drains in patients undergoing TEVAR and offers an algorithm for managing CSF drains.

Complications of spinal fluid drainage in thoracoabdominal aortic aneurysm repair: A report of 486 patients treated from 1987 to 2008

Spinal fluid drainage reduces paraplegia risk in thoracic (TAA) and thoracoabdominal (TAAA) aortic aneurysm repair. There has not been a comprehensive study of the risks of spinal fluid drainage and how these risks can be reduced. Here we report complications of spinal fluid drainage in patients undergoing TAA/TAAA repair. The study comprised 648 patients who had TAA or TAAA repair from 1987 to 2008. Spinal drains were used in 486 patients. Spinal fluid pressure was measured continuously, except when draining fluid, and was reduced to <6 mm Hg during thoracic aortic occlusion and reperfusion. After surgery, spinal fluid pressure was kept <10 mm Hg until patients were awake with normal leg lift. Drains were removed 48 hours after surgery. Spinal and head computed tomography (CT) scans were performed in patients with bloody spinal fluid or neurologic deficit. We studied the incidence of headache treated with epidural blood patch, infection, bloody spinal fluid, intracranial and spinal bleeding on CT, as well as the clinical consequences. Twenty-four patients (5%) had bloody spinal fluid. CT exams showed seven had no evidence of intracranial hemorrhage, 14 (2.9%) had intracranial blood without neurologic deficit, and three with intracranial bleeding and cerebral atrophy had neurologic deficits (1 died, 1 had permanent hemiparesis, and 1 with transient ataxia recovered fully). Two patients without bloody spinal fluid or neurologic deficit after surgery presented with neurologic deficits 5 days postoperatively and died from acute on chronic subdural hematoma. Neurologic deficits occurred after spinal fluid drainage in 5 of 482 patients (1%), and 3 died. The mortality from spinal fluid drainage complications was 0.6% (3 of 482). By univariate and multivariate analysis, larger volume of spinal fluid drainage (mean, 178 mL vs 124 mL, P < .0001) and higher central venous pressure before thoracic aortic occlusion (mean, 16 mm Hg vs 13 mm Hg, P < .0012) correlated with bloody spinal fluid. Strategies that reduce the volume of spinal fluid drainage but still control spinal fluid pressure are helpful in reducing serious complications. Patients with cerebral atrophy are at increased risk for complications of spinal fluid drainage.

Recognition of subarachnoid hemorrhage.

The medical records of 109 patients who presented to the emergency department during a five-year period with proven nontraumatic, spontaneous subarachnoid hemorrhage (SAH) were retrospectively reviewed. The clinical presentation, diagnostic modalities used, and accuracy of diagnosis by emergency physicians were analyzed. The most common historical features were headache (81 patients, or 74%), nausea or vomiting (85 patients, or 77%), and loss of consciousness (58 patients, or 53%). Nonexertional activities preceding SAH were more frequent than exertional events (57% vs 21%). Neurologic findings were present in 70 patients (64%) and consisted primarily of altered levels of consciousness. Thirty-eight patients (35%) had nuchal rigidity. Ninety-six emergency cranial computed tomography scans were performed, of which 91 were diagnostic for SAH (sensitivity, 95%). Lumbar puncture was performed on two patients with normal computed tomography scans and revealed bloody spinal fluid. The overall diagnostic accuracy by emergency physicians was 85%. The correct diagnosis was delayed in 16 patients (15%), the majority of whom had headaches and normal neurologic examinations. Atypical symptoms, the warning leak syndrome, and the need for prompt diagnosis and therapy are reviewed.

Determination of leukocytosis in traumatic spinal tap specimens

White and red blood cell counts from peripheral blood and from the cerebrospinal fluid of all patients who had traumatic lumbar punctures over a five-year period were studied to determine the diagnostic value of using the ratio of white blood cell to red blood cells in peripheral blood to adjust the white blood cell count found in the bloody cerebrospinal fluid. In patients without meningitis, 55 percent of the cerebrospinal fluid specimens had more white blood cells than could be attributed to trauma. However, in only 10 percent was the actual white blood cell count more than 10 times greater than the number referable to trauma. In 38 percent, there were fewer white blood cells in the cerebrospinal fluid than the ratio predicted. Such underestimation was uncommon among patients with culture-positive meningitis: the ratio failed to detect leukocytosis in only 10 percent, and all but one of these patients had clinical reasons for the low cerebrospinal fluid count. It is concluded that true leukocytosis is rarely masked in blood-contaminated cerebrospinal fluid, and that the presence of more than 10 times the number of white blood cells than allowed by the adjustment is a sensitive and specific indicator of meningitis. However, a simple mechanical use of the formula is not justified, and all available clinical and laboratory data should be used when deciding whether to institute treatment in a patient with possible meningitis and bloody spinal fluid.

Neonatal Seizures, Intracerebral Hematoma, and Subarachnoid Hemorrhage in Full-Term Infants

During the first days of life intracranial hemorrhage is a frequent cause of convulsions in the full-term infant.1,2 If spinal fluid is bloody and there is no evidence of asphyxia, infection, or acute metabolic disease, then a presumptive diagnosis of primary subarachnoid hemorrhage is often made.1-3 These infants appear remarkably well in the interictal period, and their outcome is usually good.1,2 Since pathologic confirmation is not available, it has been assumed that bleeding occurs directly into the subarachnoid space and not as an extension of a subdural, intraventricular, or intracerebellar hemorrhage.1,3-5 During a 13-month period at our institution, only four full-term infants had seizures and bloody spinal fluid.

Analysis of Relations Between Head Injury and Acoustic Lesion (Bradyacusia, Tinnitus)

Relation between head injury and acoustic lesion was analyzed systematically in 1, 447 head injury cases which were examined by extensive hearing and tinnitus tests.In this report, the relation between the existence and extent of bleeding from the ear, bleeding from the nose, a bloody spinal fluid, unconsciousness, abnormal tympanic membrane and the nature and range of tinnitus was studied. And the following results were obtained.In general, the continuous and high pitched tinnitus existed in whom the extent of head injury was thought to be slight showing no bleeding from the ear, no bleeding from the nose, no bloody spinal fluid, no unconsciousness and no abnormal tympanic membrane. Therefore the results opposed to a medical common sense.

Fetal Hemoglobin in the Diagnosis of Neonatal Subarachnoid Hemorrhage

Intracranial hemorrhage is a leading cause of mortality and morbidity in newborn infants, particularly those born prematurely.1-8 Major intracranial hemorrhage in the preterm infant is usually intraventricular.3-6 Although intraventricular hemorrhage is a common autopsy finding, it may be difficult to diagnose before death because its early signs are also often associated with cardiopulmonary disease.3-7 Thus, particularly in prematurely born infants with severe hyaline membrane disease, there may be no pathognomonic sign of intracranial bleeding and often only a presumptive clinical diagnosis can be made. Laboratory diagnosis based on bloody spinal fluid may also be misleading, since the blood in the spinal fluid could be the result of either a traumatic lumbar puncture or preexisting subarachnoid blood.

Chromate 51 labeling of red blood cells in the study of subarachnoid hemorrhage

Spontaneous subarachnoid hemorrhage usually occurs in such a catastrophic and clearcut way that there is little doubt as to the moment it happens. As a rule, if the patient survives, serial lumbar punctures in the next few days or weeks show a bloody spinal fluid with an elevated pressure which gradually returns to normal. There is also a gradual decrease in the concentration of red blood cells until the fluid becomes xanthochromic and finally colorless. Occasionally, however, the cerebrospinal fluid (CSF) in certain patients remains intensely bloody for as long as seven to ten days without a clinical episode indicating recurrent hemorrhage. These findings suggest that such patients may have an abnormally slow clearance of red blood cells (RBC’s) from the cerebrospinal fluid or that red blood cells are entering the subarachnoid space slowly at a rate closely corresponding to their rate of clearance from the spinal fluid. We have investigated subarachnoid hemorrhage in a small series of patients by labeling the peripheral blood with radioactive chromate ion (Crsl)

Cerebral spinal fluid studies in eclampsia

During the 5 year period 1966–1970, 94 eclamptic patients were delivered of infants at the City of Memphis Hospitals. The cerebrospinal fluid of the last 21 patients was studied in an attempt to clarify the various neurological manifestations of this syndrome. The results were compared with cerebral spinal fluid obtained at delivery from 25 patients with severe pre-eclampsia, 10 with chronic hypertensive vascular disease, 9 with documented seizure disorders, and 35 patients with normal term pregnancies. Nineteen of the 21 eclamptic patients had bloody spinal fluid (hematorrhachis), and this finding, in addition to others, is correlated with neurological deficits and prognosis.

Normal Concentrations of Lactate, Glucose, and Protein in Cerebrospinal Fluid, and the Diagnostic Implications of Abnormal Concentrations

Abstract Normal values for glucose, lactate, and protein in cerebrospinal fluid have been established and the relationships among them studied. Normal protein concentration is related to age. Glucose and lactate values are correlated with each other and with sex and age. By the technique of pattern appreciation, these estimations provide a useful confirmatory test for cerebrovascular accidents and for differentiating intracranial hemorrhage from other types of accident and from bloody spinal fluid taps, and they have considerable prognostic value in assessing the milder cases. They also have a restricted value in certain other conditions.

The angiographic evaluation of anterior polar brain injury.

CEREBRAL angiography provides the most accurate means for study of the intracranial status after severe closed-head trauma. Surgical intervention is clearly indicated if well defined intra- or extra-axial masses are demonstrated. If balancing, bilateral, intra-axial masses are not appreciated, however, patients may be denied proper surgical treatment. Diffuse, bilateral brain injury resulting in contusion or “pulping” of two or more of the anterior poles of the brain is such a condition. “Pulping” is defined as hemorrhage, edema, and necrosis of brain tissue (1, 3). The symmetry of mass effect may minimize any midline vessel shift, so that the severity and volume of tissue injury may be grossly underestimated. Prompt removal of hematoma and contused brain in this situation may be life-saving or improve the chances for more normal recovery of brain function. Three representative cases of bilateral anterior brain injury follow. Case Reports CASE 1. A. II., a 5l-year-cld man with a history of previous myocardial infarction, was admitted about four hours after a 15-foot fall down a chute containing waste glass. He was unconscious at first but slowly improved to a restless, irrational, partially cooperative state. Radiographs showed a left occipital linear fracture, clouding of the sphenoid sinus, and compression of L1 vertebra. While his multiple lacerations were being repaired, the patient was noted to move his legs less well than before. Laminectomy was considered but deferred because of the head injury. Lumbar puncture showed an opening pressure of 600 mm of cerebrospinal fluid and bloody spinal fluid. The echoencephalogram disclosed a normal midline position. For twenty-four hours the patient improved slightly, then became more obtunded, prompting right brachial angiography. This showed bilateral frontal lobe swelling (Fig. 1). The same day he underwent bifrontal craniotomy for removal of intracerebral dot and contused, necrotic brain from both frontal lobes. Postoperatively the patient improved greatly, was alert, talking, recognized members of his family, but at times was mildly disoriented. However, on the eighth postoperative day he died suddenly, following another myocardial infarction. CASE II: R. W., a 19-year-old boy, was comatose and immobile for forty-five minutes after an auto accident, then became increasingly restless and combative by the time of admission six hours later. He was completely disoriented, without lateralizing findings, and had normal pupillary responses. Bilateral carotid arteriograms showed evidence of bifrontal and bitemporal intra-axial masses (Fig. 2). During the following day his condition fluctuated, showing occasional pupillary inequality, bradycardia, and slight right hemiparesis. He improved with intravenous 20 per cent Mannitol until the next day when he became decerebrate, with dilated and fixed pupils.

Localized Dissecting Hemorrhage and Arteritis

PERIARTERITIS NODOSA has been gradually redefined over the past hundred years so as to become but a phase in a broad spectrum of vascular disease in which the individual members tend to lose their identity. To most people, however, it represents a widely disseminated panarteritis with ischemic rather than primarily hemorrhagic manifestations which are characteristically not isolated. This case is presented primarily (1) because it proves distinctive and variant in its histological pattern, (2) for the isolated localization of its principal lesions, and (3) for its totally deceptive manifestations mimicking a ruptured aneurysm of a cerebral artery. Report of a Case The patient, a 26-year-old white woman, had been known to have hypertension for the last ten years and migraine headaches for many more. This last illness began suddenly with severe headache followed by unresponsiveness, nuchal rigidity, and grossly bloody spinal fluid. Her temperature was 103 F (39.4 C) on

Multiple Considerations in Studying the CVA

To the Editor:— The study by Eisenberg et al on Cerebrovascular Accidents ( JAMA 189 :883 [Sept 21] 1964) is timely and informative. However, I question whether their diagnosis of embolism, hemorrhage, and is exact, unless they obtained supportive information which was not published. I would like to know the percentage of patients with embolism who had had auricular fibrillation; the percentage of those with the diagnosis of hemorrhage who had proven bloody spinal fluid; and, finally, in what percentage of all the classifications was the diagnosis proven by cerebro-angiography, operation, or autopsy. The term cerebral thrombosis is used too loosely, since this diagnosis can only be made by gross and microscopic examination of the vessels. Perhaps a better designation would be cerebrovascular occlusive disease of undetermined etiology or cerebrovascular insufficiency of undetermined etiology. The above comments do not detract from the general excellence of the survey and the information

CAROTID ARTERITIS: A CAUSE OF HEMIPLEGIA IN CHILDHOOD.

c EREBROVASCULAR accidents are less common in children than in adults but the results may be just as devastating. Until recently, diagnosis of the mechanism of the s t roke has been made either on the basis of clinical estimation, without arteriographic confirmation, or else by pathological findings. Specific therapy ordinarily has been directed only to those patients in whom bloody spinal fluid or some other evidence of spontaneous hemorrhage has been present. Children suffering sudden strokes with no evidence of intracranial hemorrhage have been less well studied, understood and treated. The etiology of the neurological deficit in many such patients is never determined accurately and a purely clinical diagnosis of arterial thrombosis, embolism or spasm, or of cortical venous thrombosis is made. Until recently there has been little antemortem documentation of cerebral arterial occlusion in childhood, and the number of reported cases is still quite small. A review of the literature made in 1960 by Wisoff and Rothballer 36 yielded 27 cases, to which they added 2 of their own. In 1962 Byers and McLean 6 in their discussion of childhood hemiplcgia and aphasia reported cerebral arterial occlusion in 4 children. Three of these are included in this report. A review of all symptomatic cercbrovascular accidents on file at the Children's Hospital Medical Center has been made for a 14year period, 1948-1962, in an effort to clarify the frequency of cerebral arterial occlusions in the pediatric age group, and to analyze their clinical course. With the interest and

Roentgenologic signs of resolving subdural hematomas.

Subdural hematoma has been a recognized entity since the eighteenth century and possibly earlier (1). In spite of its long history, many questions concerning this condition remain unanswered. Among these is: Does a subdural hematoma ever undergo spontaneous resolution? Occasional reports (2–4) have appeared in the literature concerning subdural collections diagnosed by cerebral angiography or pneumography which subsequently cleared. The nature of these collections, however, whether cerebrospinal fluid or blood, has remained unknown. Cerebral atrophy may give the angiographic appearance of an acute subdural collection (5). Occlusion of several small branches of the middle cerebral artery may also simulate an acute subdural collection on the anteroposterior view. The purpose of the investigation to be reported here was to determine whether subdural hematomas ever regress spontaneously. It was not meant to offer a new mode of therapy for this condition. The patients were selected because of their good clinical condition. They were observed constantly and if, at any time, this had worsened, they would have been subjected immediately to surgery—burr holes and/or craniotomy. The clinical aspects of these cases will be included in another report. Case I: A 29-year-old man was well until two weeks prior to admission, when he first experienced frontal headaches and low back pain. He was drowsy upon entering the hospital and exhibited a left central facial palsy and slight nuchal rigidity. The left upper extremity was a little weak, the deep tendon reflexes were increased on the left, and the superficial abdominal reflexes were absent on that side. Lumbar puncture revealed xanthochromic fluid. On the seventh hospital day a left carotid angiogram (Fig. 1) demonstrated an acute subdural collection. The following day a left parietal burr hole was made. A 20-gauge needle was inserted through the dura, 0.4 c.c, of brownish-red material resembling old blood was aspirated, and the wound closed. The benzidine test of this fluid was positive. The patient was then followed with serial angiograms. He became alert, coherent, and oriented, and his neurological deficit disappeared. After eight weeks all angiographic signs of subdural hematoma had vanished. Case II: A middle-aged man was confused, disoriented, and drowsy upon admission to the hospital. No history could be obtained. Physical and neurological examinations were negative. After a bout of delirium tremens he was alert and oriented by the fourth hospital day. A lumbar puncture at that time revealed grossly bloody spinal fluid with a xanthochromic supernatant. During the following days the patient remained alert and exhibited only a “glove and stocking” sensory impairment of the limbs. Ten weeks after admission a right carotid angiogram (Fig. 2) revealed a chronic subdural fluid collection. Six days later a right parietal burr hole was made and a 20-gauge needle was inserted through the dura.