Unusual complication of peritoneal drainage: migration of a shunt in the subdural space.
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A 65-year-old man scheduled for gastrectomy was anesthetized with nitrous oxide combined with continuous epidural lidocaine. At the end of the operation, morphine 2 mg diluted in 0.25% bupivacaine 5 ml was injected through the epidural catheter. Seventy minutes later, the patient developed life-threatening respiratory depression which was antagonized by naloxone. The patient requested no analgesic during the first 26 postoperative hours. The respiratory depression in this patient was assumed to be caused by epidural morphine. Then subdural catheterization was confirmed radiologically. This was discovered to have resulted from migration of the epidural catheter into the subdural space. Subdural injection of morphine may have resulted in higher cerebrospinal fluid levels than the levels obtained after epidural injection. Subdural catheterization is a complication of epidural anesthesia that probably occurs more frequently than previously recognized. In postoperative patients receiving epidural morphine, their respiratory status should be monitored closely for hours.
Cerebrovascular lesions were seen in 28 of 83 cases (34%) of acquired immune deficiency syndrome (AIDS). Cerebral hemorrhage was noted in 4 cases, cerebral infarct in 23 cases and both in 1 case. Cerebral hemorrhage was in various locations such as intraparenchymal, subarachnoid space, subdural space and epidural space. Large, clinically evident hemorrhage was noted in 2 of 5 cases and bleeding tendency was noted in 2 cases. Most of the 24 cases with cerebral infarcts were not clinically evident; they were multiple, small and mainly involved the striatum, cerebral cortex and brain stem. Mural thickening of occasional small blood vessels was seen in 12 of the cases (50%) with infarcts. Other changes in blood vessels included vasculitis in one case and perivascular lymphocytic infiltration in another. In addition to thrombo-embolism and systemic ischemia/anoxia, these blood vessel changes may have a role in the development of cerebral infarcts in AIDS.
Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.
The clinical application and future prospect of neuroendoscopic surgery are described. In the historical trend, it is emphasized that the neuroendoscopic surgery has become one of the major or leading procedures in "minimally-invasive approaches" to the intracranial lesions. The presently-available instrument include procedures using an endoscope of three different types: rigid-rod, steerable/flexible-fiber-rod and semi-rigid-rod. To use a rigid-rod or fiber-rod scope, it is available to apply forceps, laser, a microballoon and other fine instruments. The indication for neuroendoscopic surgery has been expanded to almost all neurosurgical procedures, as "endoscope-assisted" procedures are applied more to micro neurosurgical procedures (endoscope-assisted microsurgery). The realistic indication for "pure neuroendoscopic surgery" includes reconstruction of cerebrospinal fluid (CSF) pathway such as third ventriculostomy, septostomy, foramen reconstruction, fenestration of septation; removal or biopsy of tumor/cystic lesion, mainly in the intraventricular regions; and removal of hematoma involving the cerebral parenchyma (intracerebral hematoma), ventricles/(intraventricular hematoma) or subdural space (subdural hematoma). The intraparenchymal or deep-seated intracisternal lesions can be the realistic indication for "pure neuroendoscopic surgery" when the instrument are further developed in future. Neuroendoscopic surgery will play a promising and major role in the "minimally-invasive neurological procedure" in the 21st century.
BACKGROUND: Space-occupying subdural hygromas are a late complication of severe traumatic brain injury (TBI) and may delay the patient's recovery. To evaluate the risk factors involved, we performed a semiretrospective, -prospective analysis of three groups of patients, which differed with regard to the techniques used in the management of their cerebral perfusion pressure (CPP) and colloid osmotic pressure (COP) to determine the occurrence of space-occupying subdural hygromas. PATIENTS AND METHODS: Between 1989 and 1997 we examined 696 patients after a severe TBI: Group 1. 1989-1994 mean CPP: 67 (elevated for therapeutic reasons by catecholamines, if necessary), mean COP: 19. Group 2. January 1995-October 1996, mean CPP: 77, mean COP: 20. Group 3. November 1996-December 1997, mean CPP: 79, mean COP: 23 (elevated for therapeutic reasons by infusions of colloids). The groups were comparable for other criteria. RESULTS: Compared to Group 1, Group 2, with a high CPP but lower COP, showed a significantly higher (p < 0.01; chi2-test with correction of Yates) percentage of posttraumatic subdural hygromas with space-occupying aspects, clinical signs of bradycardia, hypertension and impaired consciousness requiring surgery (Group 1: 1.75%; Group 2: 10.46%; Group 3: 0%). In Group 3 we saw no patient with a space-occupying hygroma. CONCLUSION: We conclude that iatrogenic elevated CPP, which has been reported to be helpful in preventing secondary ischemic damage after a severe TBI, may be harmful to a patient if the COP is not maintained within physiological ranges.
The lumbar subdural extraarachnoid space was examined by spinaloscopy in 15 autopsy subjects. Special attention was paid to the ease with which the space opened up and also to the extent of view achieved. In ten cases the space opened up with ease, in four cases with difficulty, and in one case it was not possible to establish the subdural space at all. The bevel of an 18-gauge Tuohy needle introduced into the subdural space could be visualized in eight of 13 cases. An epidural catheter was then passed through the Tuohy needle into the subdural space in eight cases and was visualized in six of them. Although care must be exercised in drawing conclusions for clinical epidural anesthesia from autopsy cases, this study confirms the possibility of placing both the bevel of a Tuohy needle and an epidural catheter in the subdural space. The results reemphasize the need for caution suggested by other reports regarding the possibility of subdural puncture in epidural anesthesia and subsequent injection of anesthetic solution into the subdural space.
Computed tomographic (CT) scans were identified and reviewed for 25 pediatric patients with enlarged heads and extracerebral fluid collections that showed cerebrospinal fluid-like attenuation. Mild to moderate enlargement of the subarachnoid space over the convexity, interhemispheric fissure, and the lateral ventricles was observed in most of the cases. The CT findings are not specific, and it is not always possible to determine the nature of the extracerebral fluid, whether it lies in the subarachnoid space, the subdural space, or both. The differential diagnosis included subdural effusions, hygromas, preclinical or external hydrocephalus, hypodense subdural hematomas, megalocephaly, and possibly a normal variant. CT remains the method of choice for the initial study of these patients and for subsequent follow-up in selected cases.
We describe the inadvertent subdural insertion of a lumbar extradural catheter in a primiparous woman in labour. A small quantity of local anaesthetic resulted in extensive motor and sensory block. Computed tomography performed after contrast injection demonstrated unequivocally that the catheter was in the subdural space. The catheter and injected fluid produced considerable displacement of the arachnoid within the thecal sac. We postulate that this could result in arterial compression or direct damage to the spinal nerve roots. Such a mechanism might explain some of the cases of permanent neurological damage associated with extradural analgesia.
In an effort to duplicate a previous model of neurogenic pulmonary edema (NPE), we maintained intracranial pressure (PIC) at 20 Torr below mean arterial pressure in six closed-chested dogs anesthetized with alpha-chloralose and urethan. This was accomplished by infusing 1) isotonic saline (NS), 2) a gas mixture of 80% helium and 20% oxygen (HeO2), or 3) 100% carbon dioxide (CO2) through a trephined hole into the subdural space. Three more animals were studied with the same protocol after thoracotomy to permit Doppler examination for bubbles in the left pulmonary artery. Significant increases in pulmonary artery pressure, pulmonary vascular resistance, physiological shunt, dead space fraction, and hypoxemia were recorded when Pic was elevated by HeO2 infusion but not during infusion of NS or CO2. Pulmonary gas-bubble embolism was suggested by an increase in the fraction of helium in expired gas during HeO2 infusion and confirmed by Doppler recordings. We conclude that increasing Pic with air produces the physiological changes of air embolism; this is not a satisfactory model for investigating NPE.
Chronic subdural haematoma has not been reported as a complication of transsphenoidal surgery. We present a case of pituitary adenoma which was gross-totally removed by transsphenoidal surgery with the enlarged sellar opening. Postoperative serial imaging showed massive air accumulation in both frontal subdural spaces followed by subdural fluid collection and subsequent chronic subdural haematomas 2 months later. We conclude that close follow up imaging study is required to avoid overlooking chronic subdural haematoma when massive air is introduced into the subdural space by the transsphenoidal surgery.
The rare spinal subdural masses, usually haematomas, are described in 5 patients and the importance of ascending myelography in addition to computed tomography in radiological diagnosis is emphasised.
The etiopathogenesis of traumatic spinal subdural hematoma (SSH) is uncertain. Unlike the supratentorial subdural space, no bridging veins traverse the spinal subdural space. The authors describe a case of subacute SSH that occurred after spontaneous resolution of traumatic intracranial SDH and suggest a causal relationship between the two. A 23-year-old woman suffered an acute intracranial SDH after a snowboarding accident. There was no clinical or radiological evidence of spine injury. Conservative management of the supratentorial SDH resulted in spontaneous radiologically documented resolution with redistribution of blood in the subdural space. Four days after the injury, the patient started noticing new onset of mild low-back pain. The pain progressively worsened. Magnetic resonance imaging of the lumbosacral spine 10 days after the original injury revealed a large L4-S2 SDH. Ten days after the original injury, bilateral L5-S1 laminotomy and drainage of the subacute spinal SDH were performed. The patient experienced immediate pain relief. The authors hypothesize that in some cases spinal SDH may be related to redistribution of blood from the supratentorial subdural space.