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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A consecutive series of 34 severe head-injured patients (DAI) were studied prospectively. Patients were categorized according to a new, simple classification system comprised of four lesion types according to the compression or obliteration of the ventricles or cisterns. Five patients belonged to type II and 19 patients to type IV. Each type was further subdivided into two GCS score ranges (5 to 8 and below 5). The distribution of the posttraumatic infarction was mainly in the frontal and temporal lobes (60% of all cases). Our data demonstrated that the ICP was significantly lower at a 30 degrees head elevation than at 0 degree (18.6 +/- 7.21 mmHg vs 23.0 +/- 10.60 mmHg. t = 4.22 P < 0.001), but head position did not statistically affect CPP (69.4 +/- 19.86 mmHg vs 68.2 +/- 19.87 mmHg. t = -0.54, P < 0.59). The effect of intensive therapy on ICP, CPP and AVDO2 was studied in all cases, employing steroids and diuretics in a modified intensive care scale. In cases where barbiturates were employed, there were statistically significant changes in ICP and AVDO2 (P < 0.001), but CPP was not affected (P < 0.59). Surviving patients were analyzed by using the GOS and the neurological grading score (NGS, Nihon University) of the persistent vegetative state. Our data suggests that head elevation of 30 degrees and barbiturate therapy are more effective on ICP and AVDO2, and NGS more exact than GOS in vegetative patients.
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PMID:Clinical analysis of 34 diffuse axonal injured (DAI) patients below GCS 8. 130 12

ICP control can be achieved removing the surgical masses and manipulating the intracranial compartments; in the intensive care setting that can be attempted using CSF withdrawal or changing the cerebrovascular resistances, the intracranial blood content and the cerebral water content. The reduction of the ICP and the maintenance of a good cerebral perfusion pressure are the main aims of the therapy; when any standard treatment fails to control ICP a further attempt to preserve cerebral perfusion should be done by increasing the mean arterial pressure. In 10 patients with severe brain damage (GCS on admission ranging from 3 to 7, mean 5) from subarachnoid hemorrhage (3 cases) or trauma an infusion of dopamine (25-150 mg/h) and noradrenaline (0.4-2.4 mg/h) was started in case of intractable ICP. The ICP was defined intractable when the pressure was more than 40 mmHg for more than 5 m' after maximum therapy, as evaluated using the Therapy Intensity Level score. The infusion obtained a raise of the MAP of approximately 25% and a variable response on ICP. In 9 cases ICP dropped, in one case, instead, the ICP increased together with the arterial pressure. The reduction of ICP was 20-30%, with a good improvement of the CPP. The patients with a good response survived, the only patient without control of the ICP died. The physiopathologic mechanisms of this treatment are discussed; the most suitable explanation is indicated in an autoregulatory process. The infusion of cathecolamines can be harmful, and the patients eligible for this treatment must be carefully chosen. Notwithstanding this approach deserves further studies for the cases of intractable ICP.
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PMID:[Increasing the pressure of cerebral perfusion to control intracranial pressure]. 162 Apr 43

Barbiturates reduce cerebral activity which again reduce the cerebral metabolic rate probably by activating chloride channels and potentiating GABA's effects on these channels. Protection of the brain against hypoxia might theoretically occur by this mechanism, by vasoconstriction or by inhibiting calcium or glutamate. The barbiturates appear to have a positive effect in head-injury patients with high ICP uncontrollable by conventional therapy (in one study 5% of patients with a GCS < or = 7), and in animal studies of regional ischemia. No effect has been established in complete cerebral ischemia (cardiac arrest). The barbiturates have a depressant effect on the cardiovascular and respiratory systems, and the patients require intensive care. Thus there are some indications in the literature that the barbiturate treatment itself causes complications, and it is possible that this might cancel a potential beneficial effect in some patients. Clinically, the barbiturates are effective anticonvulsants, can be used in an attempt to control an elevated ICP uncontrollable by conventional means, and during transient ischemic episodes in the operating room with adequate monitoring and support systems already in place.
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PMID:Barbiturates in neuroanesthesia and neuro-intensive care. 184 34

Since 1978, decompressive craniotomy was performed according to a standardized protocol. Exclusion criteria were age greater than or equal to 40 years, deleterious primary brain damage, operable space occupying lesions, larger infarctions in CT scan or irreversible brain stem incarceration/ischaemic damage as shown by bulbar syndrome, loss in BAEP or oscillating flow in TCD. Indication was given by progressive intracranial hypertension not controllable by conservative methods, if ICP decompensation was correlated with clinical (GCS, extension spasms, mydriasis) and electrophysiological (EEG, SEP, CCT) deteriorations. 18 patients were decompressed by unilateral. 19 by bilateral craniotomy with large fronto-parieto-temporal bone flap and a dura enlargement by use of temporal muscle/fascia. 37 patients at an age of 18 +/- 7 (4-34) years were operated 5 h-10 d after trauma. Recovery was surprisingly good: only 5 died, 2 due to an ARDS; 3 remained vegetative, all others achieved full social rehabilitation or remained moderately disabled. The best predictor of a favourable outcome was an initial posttraumatic GCS greater than or equal to 7. These in younger patients with delayed posttraumatic decompensation before irreversible ischaemic damage occurs.
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PMID:Traumatic brain swelling and operative decompression: a prospective investigation. 208 28

A method of ICP management is presented based upon maintenance of cerebral perfusion pressure ( CPP = SABP - ICP) at 70-88 mm Hg or in some cases greater. To do this, we have employed volume expansion, nursed patients in the flat position, and actively used catecholamine infusions to maintain the SABP side of the CPP equation at levels necessary to obtain the target CPP. CSF drainage and mannitol have freely been used to maintain the ICP portion of the equation. Thirty-four consecutive patients with GCS less than or equal to 7 were admitted to the Neurosurgical Intensive Care Unit (GCS = 5.1 +/- 1.4) and managed with this protocol. CPP was maintained at 84 +/- 11 mm Hg, ICP was 23 +/- 9.8 mm Hg, and SABP averaged 106 +/- 11 mm Hg. CVP was 8.0 +/- 3.7 mm Hg and average fluid intake was approximately 5.4 +/- 3.9 liters/d. Output averaged 5.0 +/- 4.0 liters/d; additionally, albumin (25%) (33 +/- 44 gm/d) and PRBCs were used for vascular expansion and hemoglobin was maintained (11.5 +/- 1.4 gm/dl). Three patients died of uncontrolled ICP (all protocol errors). Four other patients succumbed, none secondary to ICP and all secondary to potentially avoidable complications. Morbidity (GOS = 4.2 +/- 0.87) appeared to be as good or superior to previous methods of therapy. Overall, mortality was 21% and that from uncontrollable ICP was 8%. This approach to the management of intracranial hypertension proved safe, rational, and greatly enhanced the therapeutic options available. It was also consistent with optimal care of other organ systems. The results bring into question many of the standard tenets of neurosurgical ICP management and suggest new avenues of investigation.
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PMID:Cerebral perfusion pressure management in head injury. 211 69

ICP in 233 patients with severe head injuries was monitored utilizing a subarachnoid catheter technique. The relationships between initial ICP and GCS, between initial ICP and GOS, between maximal ICP and GCS, and between maximal ICP and GOS were examined statistically. The correlation was significant in each case, but particularly so between maximal ICP and GOS. Thus morbidity and mortality may be dependent upon maximal ICP. Catheterization of the subarachnoid space presents little difficulty using a Tuohy needle for epidural anesthesia as an introducer. Though the catheter is very fine (1.0 mm in outer diameter), failure of waveform occurred in only 2.1% of all patients. The procedure can be easily performed at the bedside, is safe, inexpensive, and useful for the management of severe head injuries. Meningitis was recognized in 4.7% of all patients.
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PMID:Useful ICP monitoring with subarachnoid catheter method in severe head injuries. 335 8

The necessity for ICP monitoring together with GCS findings to detect deterioration in head trauma cases and determine the treatment required was studied. There were 18 subjects (14 males, 4 females) aged from 11 to 61. Cases of primary brain stem damage were excluded. Eight cases had GCS of 6-10, and 10 cases scores of 11-15. Initial CTs of these cases indicated the following conditions: thin acute extradural haematoma (A-EDH), thin acute subdural haematoma (A-SDH), brain contusion, and single or multiple intracerebral haematoma (ICH). However, in no case was any mass effect clearly shown. Medical decompression (osmotherapy, barbiturate, steroid and mechanical hyperventilation) was carried out with simultaneous ICP monitoring. Based upon our cases which showed a GCS score of 10 or less, ICP monitoring should accompany medical decompression. Where the ICP cannot be maintained below 20 mm Hg, there is a high risk (about 60%) of haematoma enlargement, delayed haematoma, or increasing brain oedema. ICP monitoring in these cases should be maintained for at least one week. Timely surgical decompression is necessary when the ICP stays above 20 mm Hg, the GCS score drops below 10, and repeat CT scan indicates progress of the mass effect.
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PMID:Necessity for ICP monitoring to supplement GCS in head trauma cases. 338 Feb 37

Four cases of unilateral traumatic cerebral lesion with secondary third nerve palsy are reported. These four cases were observed over the course of one year and represent 5% of all unilateral traumatic cerebral lesion observed in our department during that period. The clinical situation presumptive of tentorial herniation included: partial (2 patients) or total (2 patients) secondary third nerve palsy, homolateral to the cerebral lesion; noncomatose state with initial Glasgow verbal score of 3 or greater; slight or no contralateral deficit. The anatomic lesions are unilateral and included 2 cases of temporal hematoma, one case of hemispheric swelling with acute subdural hematoma, and one case of general brain edema with temporal hematoma; In all 4 cases the clinical course was favorable with medical treatment alone. Based on the clinical information (non comatose state) and CT-scans (basal cisterns present or slight compressed in 3 of 4 cases), the authors believe that there was no tentorial herniation; third nerve palsy occurred without axial compression. The authors analysed several of the accepted criteria for severe head injuries (GCS, CT-scan, and ICP) and referred to the literature in order to determine optimal patient management in such reversible situations that posed a danger of tentorial herniation. Repeated clinical examination and CT-scan for visualization of basal cisterns appeared to be the best criteria for therapeutic decision.
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PMID:[Unilateral traumatic temporal lesions and secondary involvement of the 3d cranial nerve. Role of medical treatment]. 372 45

Barbiturate therapy was performed on 84 head trauma patients which were measured on GCS score of 8 or less, through October 1979 to December 1982. More than 3 g/day of thiamylal or more than 1.5 g/day of pentobarbital were administered for barbiturate therapy. Barbiturate therapy was discontinued in patients whose ICP remained less than 20 mmHg for more than 36 hours. In patients whose ICP sustained higher level, barbiturate was administered continuously until brain death was confirmed or non-filling was recognized. The patients were divided into two groups; Group I in which barbiturate therapy was carried out for 72 hours or less, and Group II in which it was administered for more than 72 hours. The patients in each group were further divided into responder and survivor (a), responder but late death (b), and no-responder or acute brain death (c), As far as age of patients concern, 19 out of 26 patients whose age was less than 20, 22 out of 35 patients whose age was 20-50 and 13 out of 23 patients whose age was more than 50 years responded well to the barbiturate therapy. But one patient died among young age, 4 patients died among middle age and 9 patients died among aged group at later stage. As for Group I (51 patients), Group I a consisted of 22 patients (mean age; 26.2 years, mean GCS score; 6.04, mean initial and maximal ICP; 11.9 and 27.8 mmHg), I b of 8 (52.5 years, 4.75, 17.0 and 27.8 mmHg), and I c of 21 (41.4 years, 4.57, 38.1 and 98.0 mmHg respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Significance of prolonged barbiturate therapy on severe head injuries--ICP regulation and duration of barbiturate administration]. 651 30

A prospective observational study was performed to assess the reliability of fibreoptic oximetric catheters and to identify the incidence and causes of jugular bulb oxygen desaturation in patients with acute closed head injury. There were twenty-five patients (30 +/- 16 years) with GCS < or = 8 in this study. Jugular bulb oximetry, mean arterial pressure, intracranial pressure, end-tidal CO2 and pulse oximetry were monitored continuously. Catheter calibration against a laboratory oximeter was performed post insertion and thereafter eight-hourly. Cerebral venous desaturation was defined as a jugular bulb oxygen saturation < 55% of > 10 minutes duration. There was a poor correlation for the first in vivo calibration (r2 = 0.602, P < 0.001, n = 25). Thereafter a close correlation between jugular bulb catheter and oximetry values was demonstrated (r2 = 0.868, P < 0.001, n = 205). Forty-two episodes of jugular bulb oxygen desaturation of 88 minutes mean duration (range 10 to 555) were observed. 83% occurred within 48 hours following injury. Hypocapnia was associated in 45% of episodes; hypoperfusion in 22%; raised ICP in 9% and a combination of the above in 24%. Validation with a laboratory oximeter is essential prior to continuous jugular bulb oximetry. Sustained episodes of cerebral venous desaturation are frequent within the first 48 hours following acute head injury. Factors such as hypocapnia and cerebral hypoperfusion that primarily reduce cerebral blood flow are predominant.
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PMID:Detection of cerebral venous desaturation by continuous jugular bulb oximetry following acute neurotrauma. 866 39


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