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Query: UMLS:C0268318 (ICP)
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Neurogenic pulmonary edema (NPE) observed in 4 patients admitted in Neurosurgical Intensive Care au SAH by ruptured a vascular malformation. This complication is unusual (1.9%) and has been observed in comatose patients. For 3 patients, NEP resorption was rapid, from 12 to 72 hours with a treatment by CCPV with a P.E.E.P. and with restoring the hemodynamical parameter. The drug must be discussed according to eventual deleterous side effects on cardiac output and systemic resistances. The early hemodynamical study argues for an essentially hemodynamical mechanism due to the brutal symphatic discharge created by cerebral lesions and increasing. ICP, more than a toxic lesionnal edema, as the Weidner's study shows it in ultrastructural analysis of sheep lungs.
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PMID:[Neurogenic pulmonary edema, complication of meningeal hemorrhage: report of 4 cases]. 228 14

Thirty-six patients with SAH were submitted to continuous ICP monitoring: in 33 cases a continuous ventricular fluid pressure recording was performed in acute stage. According to Hunt and Hess, 2 patients were graded I, one II, one III, 13 IV and 16 V. In the remaining 3 cases who developed a normal pressure hydrocephalus 15, 20 and 40 days from bleeding an extradural miniaturized transducer was applied. B and C waves were common findings in acutely recorded patients. Typical A waves accompanied base line recordings in patients with NPH. From analysis of data the authors evidenced that elevated ICP values have been registered not only in patients graded as III, IV and V but also in those graded I and II: as 89% of patients belong to grades IV and V it was impossible to correlate clinical status with ICP. In patients with spasm it was never noted ICP values higher than 20 mmHg during recording time (from 60 hours to 10 days). In order to reduce intracranial hypertension CSF drainage was performed in 33 patients acutely registered. In patients graded I and II this procedure was followed by an ICP reduction and an improvement of the clinical status. In none of the patients graded IV and V in spite of pressure maintained at 10 mmHg, CSF drainage affected clinical evolution.
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PMID:Intracranial pressure in subarachnoid hemorrhage. Preliminary report in 36 cases. 733 18

Treatment of ischemic deficits caused by vasospasm relies on enhancing cardiac output, inducing arterial hypertension, and expanding the intravascular volume in an attempt to improve CBF. Different treatment protocols exist from institution to institution to achieve these goals. The role of calcium-channel blockers now is well established. The newest focus on prevention of vasospasm includes tPA and a variety of anti-inflammatory drugs and potential neuroprotective drugs under research. Endovascular therapy for vasospasm has an increasing role in treating patients who are unable to tolerate induced hypertension or aggressive volume augmentation. We will return to our index case of the 63-year-old woman with SAH caused by an ACoA aneurysm to review some major management issues. After placing a ventriculostomy and slowly lowering ICP, the patient became alert and was fully oriented. She had aneurysm surgery on hospital day 2, with an uncomplicated immediate postoperative course. A Swan-Ganz catheter, placed for intraoperative monitoring, was kept in place and she was hydrated with 125 mL/hour of normal saline, achieving a PAWP of 10 to 16 mm Hg. Her mean arterial blood pressure without pharmacologic intervention was 95 to 110 mm Hg. She had continued clinical improvement with resolution of her left hemiparesis. On hospital day 5, her ventriculostomy was clamped because cerebrospinal fluid drainage was minimal. The following morning, the patient was arousable only to deep pain and her left side was flaccid. An emergent CT scan demonstrated no new hemorrhage, no increase in ventricular size, and no infarct. Vasospasm was considered the most likely cause. Hypertensive therapy was about to be initiated with a phenylephrine drip, but within an hour she was fully alert and moving all extremities equally. A search for other potential causes of neurologic decline was undertaken and revealed a phenytoin level of 5.5. It was thought that the patient most likely had had a seizure and that her clinical deterioration represented a postictal state. She received a bolus infusion of phenytoin. On hospital day 7, the patient became confused, insisting that her nurse was her son and ordering him out of her "apartment." Lower extremity weakness was detected. CT scan was unchanged. Phenylephrine was started but she developed precordial lead ST elevation and elevated cardiac enzymes. Topical nitrate therapy was initiated and phenylephrine was discontinued. The patient underwent emergent cerebral angiography, which demonstrated moderate to severe bilateral ACA spasm and moderate right MCA spasm.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Management of aneurysmal subarachnoid hemorrhage. 747 15

Neurologically critically ill patients, more often than others, are unable to communicate and, for a crucial period of time, have the vital functions of their brains hidden in the "black box" of the cranial vault behind a curtain of ambiguity and immobility. Customarily--and naively--we have relied upon beside clinical observations to pierce these barriers. Recent insights lead us to conclude that these "neurochecks" no longer suffice. This article has surveyed four major monitoring systems relied upon by neurointensivists to evaluate the pathophysiology of their patients. Of these, ICPM has the longest clinical track record. It provides a quantitative measure of the brain's capacity to withstand ICP and helps us monitor interventions to reduce it. To utilize this information intelligently requires an understanding of the principles of ICC, CPP, ICP wave morphology, and the hardware available. NICU-CEEG is a more recent introduction but, in principle, it transfers from the laboratory and operating suite to the ICU bedside, established correlations among electrophysiology, CBF, and CM. Digital EEG has allowed us to overcome significant logistical barriers and made NICU-CEEG a practical ICU tool. Early but impressive data suggest that NICU-CEEG has a significant clinical impact in patients with ACI, uncontrolled seizures, or coma. It also has revealed that NICU patients have a surprisingly high incidence of NCS, which may adversely affect their outcome. TCD has contributed greatly to diagnosis and management of SAH vasospasm. It also can be applied with benefit to patients with increased ICP, and has promising value in patients with ACI. It may prove beneficial in monitoring unstable cerebral embolization. Several bedside methods for monitoring CBF are available, but they require refinement to become true monitoring systems. These methods have revealed clinically important insights in patients with head trauma, SAH vasospasm, and ACI. Methods for directly monitoring CM and CMRo2 are improving our understanding of the brain's responses to injury, and becoming increasingly relevant to bedside management. SjvO2 can detect cerebral ischemia caused by overzealous hyperventilation and accelerated ICP. ICO holds promise as a noninvasive transcranial method for assessing Scvo2. We soon may see a scalp array of such detectors, similar to an EEG "montage," that allows us to assess multiregional Scvo2. To be useful, a clinical method should raise questions for further investigation. If the neurophysiologic monitoring systems described here provide us with some answers and lead us to ask useful new questions, they will prove their benefit to our patients.
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PMID:Neurophysiologic monitoring in the neuroscience intensive care unit. 747 20

The possibility of measuring cerebral blood flow by mobile bedside units with the intravenous 133-Xenon technique increased the interest to monitor haemodynamic changes after head injury and subarachnoid haemorrhage in intensive care. Time course of resting CBF after trauma is variable (reduced CBF, hyperemia) and there is no strong correlation to clinical outcome. Additional studies of CBF/CO2 reactivity show normal and impaired CO2 response in the acute stage after trauma (day 1-8). A permanently impaired CO2 reactivity correlates with severe brain damage and bad outcome (GOS 1,2). A normal or improving CO2 reactivity indicates a favourable outcome (GOS 3-5). There was no significant correlation between CBF and ICP, nor between CBF and CPP. A CPP of more than 70 mmHg did not guarantee a sufficient CBF in every case indicating the variability of the limits of autoregulation. As therapeutic hyperventilation may lead to ischemia, mannitol was preferred to reduce ICP and increased low CBF to normal values. This fact should be considered in the treatment of patients with low CBF and normal CO2 reactivity. Delayed ischemic neurological deficits ("vasospasm") are well-known as significant complications of the clinical course following SAH. Immediately postoperatively performed CBF measurements enable to detect ischemia and allow to start early antiischemic therapy. During "vasospasm" CBF showed a better correlation to the neurological status than blood flow velocity in the basal arteries measured by transcranial doppler sonography. Furthermore hyperemia after SAH could only be verified by CBF measurements.
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PMID:Xenon 133--CBF measurements in severe head injury and subarachnoid haemorrhage. 790 78

Early surgery after SAH is frequently performed. The most important problems for anesthesiologists are the risk of rebleeding, the alteration of autoregulation and CO2 responsiveness, cardiac, respiratory and electrolytic alterations. In this phase the brain may be ischemic-edematous or haemorrhagic-compressive and the choice of anesthetic agent is made on the basis of cerebral conditions. The main goal is to control ICP and maintain adequate CPP. The endovascular treatment with Guglielmi detachable coils is usually performed in patients with poor neurologic and/or medical conditions. General anaesthesia under aggressive monitoring is advisable to control systemic pressure and to avoid movements.
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PMID:[Anesthesia in early surgery and endovascular therapy for aneurysmic subarachnoid hemorrhage]. 977 53

A qualified nursing care is mandatory in patients after SAH. Clinical and instrumental monitoring are basilar to assure the rapid control of dangerous ICP or CPP changes and of epileptic crisis. Prophylaxis of infections is greatly minimized when coherent treatments are applied to any invasive devices, patient body, patient bed and UTI area. Many drugs can be useful to avoid ICP increases by tracheal suctioning and other sensorial stimulations. Having a trained staff, patient outcome can be improved.
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PMID:[Targets and prevention of complications in nursing of subarachnoid hemorrhage]. 977 70

It is suggested that reduced intracranial compliance may be present even when measured ICP is normal and may precede clinical deterioration. Our findings reflect a decompensation of hydrodynamic parameters more pronounced 4-7 postictal days, when compliance is reduced not only in patients with poor clinical condition, but also in patients with Hunt-Hess grade I-III. Increased CSF outflow resistance in the first few days is not surprising; it is thought to be due to the blockage of flow of CSF through the basal subarachnoid cisterns and clogging of the arachnoid villi with erythrocytes and fibrin. Enlargement of ventricles seen on CT scan at the same time suggests the development of acute hydrocephalus. During the first days after SAH, our data reflects evidence of ventricular enlargement in patients presenting with both poor and better clinical condition. We conclude that the monitoring of ICP and dynamic measuring of CSF hydrodynamic parameters is important for longer than the generally accepted few days for selected cases after SAH.
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PMID:The possible role of CSF hydrodynamic parameters following in management of SAH patients. 977 30

It is possible to define thresholds for cerebral swelling or herniation during craniotomy. In 178 patients subjected to craniotomy for space occupying processes subdural ICP was measured before opening of dura. The subdural ICP was correlated to the degree of cerebral swelling or herniation after opening of dura. At subdural ICP < 7 mm Hg cerebral swelling/herniation after opening of dura rarely occurs, while at ICP > or = 10 mm Hg cerebral swelling/herniation occurs with high probability. These ICP thresholds are independent of the pathophysiology (SAH, cerebral tumor), the anaesthetic agent (isoflurane, propofol) and the PaCO2 level (< or = 4.0 kPa, > 4.0 kPa). Generally, a good correlation between the tactile estimation of dural tension and the tendency to cerebral swelling or herniation after opening of dura was found. However, in 8.5% the surgeons were unable to predict swelling/herniation.
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PMID:Subdural monitoring of ICP during craniotomy: thresholds of cerebral swelling/herniation. 977 6

Jugular saturation (SjvO2) monitoring was performed in 26 SAH patients to evaluate the incidence of normal (0.56-0.74) and pathological SjvO2 values in this population and to describe its time course in the first 12 days. We also attempt to quantify the influence of systemic and cerebral hemodynamics on SjvO2 and to assess the relationship between cerebral injury volume measured on CT scan and SjvO2. Mean SjvO2 was 0.66 +/- 0.07 (354 samples, median 0.67, range 0.43-0.89). 73% of the observations (259/354) were in the normal range. On serial measurements, we identified only 37/354 (10%) desaturation episodes (D.E.). ICP was significantly higher during low SjvO2 observation (p = 0.008). No statistical differences were noted regarding the influence of MAP, CPP, PaCO2, PaO2 on SjvO2 but during D.E., lower PaCO2 and CPP were more frequently observed. CT scan lesions > 25 ml were associated initially with lower SjvO2 values and with higher values at second CT.
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PMID:Jugular saturation (SjvO2) monitoring in subarachnoid hemorrhage (SAH). 977 18


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