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.

Neurogenic pulmonary edema associated with a colloid cyst in the third ventricle

1980 ◽  
Vol 52 (3) ◽  
pp. 395-398 ◽  
Author(s):  
Gideon Findler ◽  
Shamay Cotev
Keyword(s):  
Pulmonary Edema ◽  
Third Ventricle ◽  
Colloid Cyst ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Acute Hydrocephalus ◽  
The Third ◽  
Hypothalamic Nuclei ◽  
Fine Print

✓ Neurogenic pulmonary edema (NPE) is usually the result of head trauma. The authors describe the case of a 13-year-old girl, in whom NPE was associated with a colloid cyst of the third ventricle causing acute hydrocephalus. The mechanisms involved in the development of NPE are briefly discussed. The possible role of the colloid cyst in the distortion of the anatomical relationships in the vicinity of the hypothalamic nuclei is considered.

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.

Experimental neurogenic pulmonary edema in cats

1978 ◽  
Vol 48 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Julian T. Hoff ◽  
Merry Nishimura
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
Quantitative Measurement ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Microscopic Appearance ◽  
Content Type ◽  
Intraventricular Infusion ◽  
Normal Lungs ◽  
Fine Print

✓ Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p < 0.05) and lung blood (p < 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

Experimental neurogenic pulmonary edema

1981 ◽  
Vol 54 (5) ◽  
pp. 632-636 ◽  
Author(s):  
Jose Garcia-Uria ◽  
Julian T. Hoff ◽  
Sandra Miranda ◽  
Merry Nishimura
Keyword(s):  
Arterial Hypertension ◽  
Pulmonary Edema ◽  
Main Pulmonary Artery ◽  
Neurogenic Pulmonary Edema ◽  
Increased Intracranial Pressure ◽  
Content Type ◽  
Systemic Arterial Hypertension ◽  
Pulmonary Arterial ◽  
Pressure Changes ◽  
Fine Print

✓ Pressure changes in the aorta, left atrium, and main pulmonary artery were measured before, during, and after inducing increased intracranial pressure in cats. By selectively controlling each of the three pressures, it was concluded that pulmonary arterial hypertension is the single most important precursor of experimental neurogenic pulmonary edema. An earlier observation that neurogenic pulmonary edema may develop in the absence of systemic arterial hypertension was confirmed.

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.

The use of intraarterial papaverine in the management of vasospasm complicating arteriovenous malformation resection

1995 ◽  
Vol 82 (2) ◽  
pp. 296-299 ◽  
Author(s):  
Michael K. Morgan ◽  
Maurice J. Day ◽  
Nicholas Little ◽  
Verity Grinnell ◽  
William Sorby
Keyword(s):  
Arteriovenous Malformation ◽  
Perfusion Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Venous Occlusion ◽  
Neurological Deterioration ◽  
Unusual Complication ◽  
Content Type ◽  
First Case ◽  
Normal Perfusion Pressure Breakthrough ◽  
Fine Print

✓ The authors report two cases of treatment by intraarterial papaverine of cerebral vasospasm complicating the resection of an arteriovenous malformation (AVM). Both cases had successful reversal of vasospasm documented on angiography. In the first case sustained neurological improvement occurred, resulting in a normal outcome by the time of discharge. In the second case, neurological deterioration occurred with the development of cerebral edema. This complication was thought to be due to normal perfusion pressure breakthrough, on the basis of angiographic arterial vasodilation and increased cerebral blood flow. These two cases illustrate an unusual complication of surgery for AVMs and demonstrate that vasospasm (along with intracranial hemorrhage, venous occlusion, and normal perfusion pressure breakthrough) should be considered in the differential diagnosis of delayed neurological deterioration following resection of these lesions. Although intraarterial papaverine may be successful in dilating spastic arteries, it may also result in pathologically high flows following AVM resection. However, this complication has not been seen in our experience of treating aneurysmal subarachnoid hemorrhage by this technique.

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.

Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign

2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intraventricular Hemorrhage ◽  
Pneumococcal Meningitis ◽  
Clinical Importance ◽  
Neurological Deterioration ◽  
Content Type ◽  
Transient Nature ◽  
Fine Print

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.

Surgical experiences with giant intracranial aneurysms

1984 ◽  
Vol 61 (6) ◽  
pp. 1009-1028 ◽  
Author(s):  
Lindsay Symon ◽  
Janos Vajda
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Intracranial Aneurysms ◽  
Visual Loss ◽  
Considerable Improvement ◽  
Brain Circulation ◽  
Content Type ◽  
Space Occupying Lesion ◽  
Fine Print

✓ A series of 35 patients with 36 giant aneurysms is presented. Thirteen patients presented following subarachnoid hemorrhage (SAH) and 22 with evidence of a space-occupying lesion without recent SAH. The preferred technique of temporary trapping of the aneurysm, evacuation of the contained thrombus, and occlusion of the neck by a suitable clip is described. The danger of attempted ligation in atheromatous vessels is stressed. Intraoperatively, blood pressure was adjusted to keep the general brain circulation within autoregulatory limits. Direct occlusion of the aneurysm was possible in over 80% of the cases. The mortality rate was 8% in 36 operations. Six percent of patients had a poor result. Considerable improvement in visual loss was evident in six of seven patients in whom this was a presenting feature, and in four of seven with disturbed eye movements.

Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms

1993 ◽  
Vol 79 (2) ◽  
pp. 161-173 ◽  
Author(s):  
Gary K. Steinberg ◽  
Charles G. Drake ◽  
Sydney J. Peerless
Keyword(s):  
Clinical Outcome ◽  
Vertebral Artery ◽  
Brain Stem ◽  
Intracranial Aneurysms ◽  
Artery Occlusion ◽  
Neurological Deterioration ◽  
Content Type ◽  
Vertebrobasilar Junction ◽  
Aneurysm Thrombosis ◽  
Fine Print

✓ Deliberate occlusion of the basilar or vertebral arteries was performed in 201 patients with intracranial aneurysms, where the aneurysmal neck could not be clipped directly. The aneurysms arose from the basilar apex in 83 cases, the basilar trunk in 46, the vertebrobasilar junction in 35, and the vertebral artery in 37; 87% of the aneurysms were classified as giant lesions (> 2.5 cm). There were 85 upper basilar occlusions, 41 lower basilar occlusions, 29 bilateral vertebral occlusions, and 48 unilateral vertebral artery occlusions. The clinical follow-up period varied from 1 to 23 years, with a mean of 9.5 years. Overall long-term results were excellent in 68% of the patients, good in 5%, and poor in 3%; 24% died. Clinical outcome varied according to aneurysm site; excellent or good results were achieved in 64% of the patients with basilar apex, 76% with basilar trunk, 74% with vertebrobasilar junction, and 87% with vertebral artery aneurysms. Clinical outcome also varied depending on preoperative grade: 86% of the patients with an excellent presenting grade achieved excellent results. The size of the posterior communicating arteries was a good predictor of tolerance to basilar artery occlusion (p < 0.05). Successful aneurysm thrombosis was achieved in 78% of the patients. The neurological status in 26 patients (13%) deteriorated due to vertebrobasilar ischemia occurring within the 1st postoperative week, and thrombosis or embolism was implicated much more frequently than hemodynamic insufficiency. Subarachnoid hemorrhage (SAH) in 14 patients, vasospasm in five patients, and surgical trauma in seven patients accounted for additional morbidity in the 1st month following operation; however, many of these patients ultimately made an excellent recovery. Late vertebrobasilar ischemic complications or neurological deterioration from persistent mass effect occurred in 4% of patients with successful aneurysm thrombosis 6 weeks to 18 months after arterial ligation. Among the 43 patients with incompletely thrombosed aneurysms, 67% developed early or late neurological deterioration from SAH, progressive brain-stem compression, or brain-stem stroke, with 86% of the complications proving fatal.

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