Pulmonary edema following fatal aneurysm rupture

1978 ◽  
Vol 49 (4) ◽  
pp. 502-507 ◽  
Author(s):  
Bryce K. Weir
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Pulmonary Edema ◽  
Clinical Diagnosis ◽  
Aneurysm Rupture ◽  
Pathological Diagnosis ◽  
Therapeutic Approaches ◽  
Content Type ◽  
Pathological Analysis ◽  
Fine Print

✓ A retrospective clinico-pathological analysis of 78 cases of fatal subarachnoid hemorrhage (SAH) was carried out: 71% had a pathological diagnosis of pulmonary edema (PE), and of these 31% had a clinical diagnosis of PE. Patients with pathological PE were younger and died sooner after their SAH than those without. The incidence of PE fell with the passage of time following SAH, while the occurrence of pneumonia and embolism increased. There were hypoxemia and hypocapnia in both groups, more severe in the group that had pathological PE. The pathophysiology of neurogenic PE is discussed and possible therapeutic approaches indicated.

Early management of aneurysmal subarachnoid hemorrhage

1981 ◽  
Vol 54 (2) ◽  
pp. 141-145 ◽  
Author(s):  
Harold P. Adams ◽  
Neal F. Kassell ◽  
James C. Torner ◽  
Donald W. Nibbelink ◽  
Adolph L. Sahs
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Medical Management ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Aneurysm Rupture ◽  
Early Management ◽  
Neurological Sequelae ◽  
Content Type ◽  
Antifibrinolytic Therapy ◽  
Effective Reduction ◽  
Fine Print

✓ The overall results are presented of early medical management and delayed operation among 249 patients studied during the period 1974 to 1977, treated within 3 days of subarachnoid hemorrhage (SAH) and evaluated 90 days after aneurysm rupture. The results included 36.2% mortality, 17.9% survival with serious neurological sequelae, and 46% with a favorable outcome. Of the patients admitted in good neurological condition, 28.7% had died and only 55.7% had a favorable recovery at 90 days after SAH. These figures represent the results despite effective reduction in early rebleeding by antifibrinolytic therapy and successful surgery in those patients reaching operation. Further therapeutic advances are needed for patients hospitalized within a few days after SAH.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage

2000 ◽  
Vol 93 (6) ◽  
pp. 1014-1018 ◽  
Author(s):  
Toshiaki Hayashi ◽  
Akifumi Suzuki ◽  
Jun Hatazawa ◽  
Iwao Kanno ◽  
Reizo Shirane ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Circulation ◽  
Cerebral Blood Volume ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Metabolism ◽  
Aneurysm Rupture ◽  
Acute Stage ◽  
Content Type ◽  
Positron Emission ◽  
Fine Print

Object. The mechanism of reduction of cerebral circulation and metabolism in patients in the acute stage of aneurysmal subarachnoid hemorrhage (SAH) has not yet been fully clarified. The goal of this study was to elucidate this mechanism further.Methods. The authors estimated cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), O2 extraction fraction (OEF), and cerebral blood volume (CBV) preoperatively in eight patients with aneurysmal SAH (one man and seven women, mean age 63.5 years) within 40 hours of onset by using positron emission tomography (PET). The patients' CBF, CMRO2, and CBF/CBV were significantly lower than those in normal control volunteers. However, OEF and CBV did not differ significantly from those in control volunteers. The significant decrease in CBF/CBV, which indicates reduced cerebral perfusion pressure, was believed to be caused by impaired cerebral circulation due to elevated intracranial pressure (ICP) after rupture of the aneurysm. In two of the eight patients, uncoupling between CBF and CMRO2 was shown, strongly suggesting the presence of cerebral ischemia.Conclusions. The initial reduction in CBF due to elevated ICP, followed by reduction in CMRO2 at the time of aneurysm rupture may play a role in the disturbance of CBF and cerebral metabolism in the acute stage of aneurysmal SAH.

Cost—benefit value of microscopic examination of intervertebral discs

1998 ◽  
Vol 89 (3) ◽  
pp. 378-381 ◽  
Author(s):  
Dana M. Grzybicki ◽  
Edward J. Callaghan ◽  
Stephen S. Raab
Keyword(s):  
Intervertebral Disc ◽  
Histological Examination ◽  
Clinical Diagnosis ◽  
Cost Benefit ◽  
Intervertebral Discs ◽  
Pathological Diagnosis ◽  
Histopathological Diagnosis ◽  
Content Type ◽  
Virtual Absence ◽  
Fine Print

Object. Given the virtual absence of histologically detected, clinically unsuspected disease in intervertebral disc specimens, some authors have advocated that histological examination be discontinued. However, the examination of intervertebral disc specimens remains common practice in most pathology laboratories. No cost—benefit analysis of this practice has been made; therefore, the authors' goal in this study was perform such an analysis. Methods. Using the University of Iowa surgical pathology database, 1109 patients who had undergone a laminectomy were identified retrospectively. These cases were classified into four categories based on the patients' preoperative clinical diagnosis and final histopathological diagnosis: insignificant clinical diagnosis/insignificant pathological diagnosis (ICIP), significant clinical diagnosis/insignificant pathological diagnosis (SCIP), significant clinical diagnosis/significant pathological diagnosis (SCSP), and insignificant clinical diagnosis/significant pathological diagnosis (ICSP). A significant clinical diagnosis was defined as one other than a benign, noninfectious indication for laminectomy. A significant pathological diagnosis was a diagnosis other than degenerative changes. The cost—benefit value of performing a histological examination in cases with significant or insignificant clinical diagnoses was examined. The cases were classified as: 1068 ICIP, 17 SCIP, 21 SCSP, and three ICSP. On chart review, in all three cases of ICSP an epidural abscess was identified perioperatively and the subsequent histological diagnosis did not affect patient care. The costs per case of identifying a significant pathological diagnosis with a significant and an insignificant clinical diagnosis were $44.79 and $8811, respectively. Conclusions. Histological examination of intervertebral disc specimens is cost beneficial only if there is a significant preoperative clinical diagnosis.

Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study

2002 ◽  
Vol 97 (4) ◽  
pp. 771-778 ◽  
Author(s):  
Jan Hillman ◽  
Steen Fridriksson ◽  
Ola Nilsson ◽  
Zhengquan Yu ◽  
Hans Säveland ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Tranexamic Acid ◽  
Hospital Admission ◽  
Acid Treatment ◽  
Aneurysm Rupture ◽  
Clinical Findings ◽  
Ct Scans ◽  
Content Type ◽  
Fisher Grade ◽  
Fine Print

Object. By pursuing a policy of very early aneurysm treatment in neurosurgical centers, in-hospital rebleeds can be virtually eliminated. Nonetheless, as many as 15% of patients with aneurysm rupture suffer ultraearly rebleeding with high mortality rates, and these individuals are beyond the reach of even the most ambitious protocol for diagnosis and referral. Only drugs given immediately after the diagnosis of subarachnoid hemorrhage (SAH) has been established at the local hospital level can, in theory, contribute to the minimization of such ultraearly rebleeding. The object of this randomized, prospective, multicenter study was to assess the efficacy of short-term antifibrinolytic treatment with tranexamic acid in preventing rebleeding. Methods. Only patients suffering SAH verified on computerized tomography (CT) scans within 48 hours prior to the first hospital admission were included. A 1-g dose of tranexamic acid was given intravenously as soon as diagnosis of SAH had been verified in the local hospitals (before the patients were transported), followed by doses of 1 g every 6 hours until the aneurysm was occluded; this treatment did not exceed 72 hours. In this study, 254 patients received tranexamic acid and 251 patients were randomized as controls. Age, sex, Hunt and Hess and Fisher grade distributions, as well as aneurysm locations, were congruent between the groups. Outcome was assessed at 6 months post-SAH by using the Glasgow Outcome Scale (GOS). Vasospasm and delayed ischemic neurological deficits were classified according to clinical findings as well as by transcranial Doppler (TCD) studies. All events classified as rebleeding were verified on CT scans or during surgery. Conclusions. More than 90% of patients reached the neurosurgical center within 12 hours of their first hospital admission after SAH; 70% of all aneurysms were clipped or coils were inserted within 24 hours of the first hospital admission. Given the protocol, only one rebleed occurred later than 24 hours after the first hospital admission. Despite this strong emphasis on early intervention, however, a cluster of 27 very early rebleeds still occurred in the control group within hours of randomization into the study, and 13 of these patients died. In the tranexamic acid group, six patients rebled and two died. A reduction in the rebleeding rate from 10.8 to 2.4% and an 80% reduction in the mortality rate from early rebleeding with tranexamic acid treatment can therefore be inferred. Favorable outcome according to the GOS increased from 70.5 to 74.8%. According to TCD measurements and clinical findings, there were no indications of increased risk of either ischemic clinical manifestations or vasospasm that could be linked to tranexamic acid treatment. Neurosurgical guidelines for aneurysm rupture should extend also into the preneurosurgical phase to guarantee protection from ultraearly rebleeds. Currently available antifibrinolytic drugs can provide such protection, and at low cost. The number of potentially saved lives exceeds those lost to vasospasm.

Delayed nonfatal pulmonary edema following subarachnoid hemorrhage

1979 ◽  
Vol 51 (6) ◽  
pp. 856-859 ◽  
Author(s):  
Anthony Fisher ◽  
Hesham Tawfik Aboul-Nasr
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Pulmonary Edema ◽  
Response To Therapy ◽  
Neurological Deterioration ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Fine Print

✓ A case of neurogenic pulmonary edema (NPE) is reported which is unusual in that it was delayed 4 days after the initial subarachnoid hemorrhage, and occurred at a time when the patient was improving clinically. After a favorable response to therapy, it recurred 48 hours later, again without neurological deterioration. The possible mechanisms in the production of NPE are discussed.

The role of hemoglobin in the etiology of cerebral vasospasm

1983 ◽  
Vol 59 (2) ◽  
pp. 231-236 ◽  
Author(s):  
David J. Boullin ◽  
Philip Tagari ◽  
George du Boulay ◽  
Victoria Aitken ◽  
J. Trevor Hughes
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Angiography ◽  
Aneurysm Rupture ◽  
Neurological Deficits ◽  
Arterial Spasm ◽  
Content Type ◽  
Experimental Animals ◽  
Fine Print

✓ Oxyhemoglobin was injected intracisternally into three baboons, and methemoglobin into one baboon, in an attempt to mimic the prolonged cerebral arterial spasm sometimes seen after subarachnoid hemorrhage due to aneurysm rupture. Cerebral angiography was performed for up to 7 days after injection of hemoglobin, and the degree of vasospasm was estimated from the angiograms. Oxyhemoglobin caused slight arterial narrowing, which lasted for 3 days. Methemoglobin had no significant effects. Motor neurological deficits and histopathological signs, characteristic of prolonged cerebral vasospasm, were not observed. It was concluded that hemoglobin alone is not capable of causing the cerebral vasospasm syndrome in these experimental animals.

Significance of “ultra-early” rebleeding in subarachnoid hemorrhage

1988 ◽  
Vol 68 (6) ◽  
pp. 901-907 ◽  
Author(s):  
Jan Hillman ◽  
Claes von Essen ◽  
Waclaw Leszniewski ◽  
Ingegerd Johansson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Aneurysm Rupture ◽  
Unfavorable Outcome ◽  
Content Type ◽  
Mortality And Morbidity ◽  
Print Knowledge ◽  
Fine Print ◽  
Late Operation

✓ Knowledge of the local incidence of aneurysm rupture permits the conclusion that almost every patient in the population of 933,800 persons served by the authors' institution who was stricken by this catastrophe and survived long enough to be transported was treated at this center (121 patients during 34 months). Of these, 9.1% were admitted late (> 72 hours after subarachnoid hemorrhage (SAH)); of the remaining cases, 94.5% were seen within 24 hours and 50% within 6 hours post-SAH. Of the 121 patients, 10% were neurologically devastated on arrival, a late operation was planned for 19%, and the earliest possible surgery and nimodipine administration was selected for 71%. In this latter group, 50% of the operations were begun within 24 hours and 76% within 48 hours post-SAH. Sixty percent of all mortality and morbidity could be linked to the initial aneurysm bleed. The remaining 40% could be ascribed to potentially avoidable causes of unfavorable outcome. No less than 9.6% of all patients admitted within 24 hours after SAH suffered from “ultra-early” rebleeding during transportation or preparation for operation. The mortality rate from such rebleeding was 7.4%, compared with the 9.1% combined mortality rate from complications and late ischemia.

Aneurysm-induced third nerve palsy

1972 ◽  
Vol 36 (5) ◽  
pp. 548-551 ◽  
Author(s):  
Iftikhar A. Raja
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Recovery ◽  
Poor Prognosis ◽  
Nerve Palsy ◽  
Nerve Function ◽  
Content Type ◽  
Third Nerve Palsy ◽  
Carotid Ligation ◽  
Third Nerve ◽  
Fine Print

✓ Forty-two patients with aneurysm-induced third nerve palsy are described. After carotid ligation, 58% showed satisfactory and 42% unsatisfactory functional recovery. In some patients the deficit continued to increase even after carotid ligation. Early ligation provided a better chance of recovery of third nerve function. Patients in whom third nerve palsy began after subarachnoid hemorrhage had a poor prognosis. No relationship was noted between the size of the aneurysm and the recovery of third nerve function.

Arteriovenous malformation of choroid plexus

1975 ◽  
Vol 42 (4) ◽  
pp. 457-461 ◽  
Author(s):  
Charles J. Hodge ◽  
Robert B. King
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Arteriovenous Malformation ◽  
Choroid Plexus ◽  
Content Type ◽  
Fine Print

✓ The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports.

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