Professor, New York University Long Island School of Medicine
Firstly hypertension at 60 discount 0.1mg clonidine with amex, different ischemia-mediated cellular death pathways are intimately related or at least arrhythmia heart beats clonidine 0.1 mg line, necrosis and apoptosis are blood pressure medication impotence order clonidine 0.1mg with amex. Secondly blood pressure chart with age and height purchase 0.1 mg clonidine amex, strategies that seemed effective blocking necrotic cellular death may not be relevant in the long term with regards to patient outcome, since apoptotic mechanisms induce late cellular death (this is probably the case of anesthetics-mediated neuroprotection). Finally, it is difficult to imagine a single protective measure capable of slowing down all these events, or altering early features induced by ischemic cascade, owing to the fact that many patients arrive at the emergency area several hours after the onset of the ischemic injury. Thus, many processes which result harmful at one point in time can be beneficial at another. The final purpose is to minimize cerebral damage and maximize neurological recovery. Furthermore, secondary injury will decisively contribute to final neurological outcome unless effective neuroprotective measures are implemented. Finally, secondary injury consequences have probably been underestimated in the past. There is evidence supporting the hypothesis that cognitive dysfunction associated with mild cerebral injuries may be due to this secondary injury. As well as precociousness, other factors seem to be of crucial importance for protective measures to be effective: intensity with which a treatment is applied (drugs given at different doses, levels of hypothermia, etc. Moreover, neurons represent only 5% of cells in cortical grey matter, with glia and astrocytes being much more numerous. This goal can be achieved by increasing tissular oxygen delivery and decreasing metabolic demands. Nevertheless, this pathway is neither the only, nor the most relevant in order to establish neuroprotection. It is an innate protective mechanism which reduces damage induced by ischemia-reperfusion. Basically, it consists of inducing cellular tolerance by provoking ischemic situations previous to a severe injury that otherwise would be lethal. It has been observed that patients who had suffered from transient ischemic events prior to a serious stroke showed better recovery than those who had not. Two different preconditioning types can be distinguished: early and late preconditioning. The former is developed within minutes to hours after the initial insult, and it is independent of protein synthesis, whilst the latter takes place between 12 and 24 hours after the preconditioning stimulus, lasts for 2 or 3 days, and depends on genetic regulation and protein synthesis. Neuroprotection can be elicited by certain drugs such as inhaled anesthetics, opioids, adenosine, statins, etc. On the one hand, remote preconditioning can be elicited by applying brief periods of ischemia to tissues with ischemic tolerance, thus protecting vital organs more susceptible to ischemic damage. For instance, skeletal muscle ischemia is a potent preconditioning stimulus for heart and probably, for brain too [8]. It can be performed quickly and inexpensively, requiring only a blood pressure cuff applied in an arm or a lower limb. On the other hand, postconditioning entails brief ischemia periods (10 seconds approximately) applied during reperfusion and separated by 30-second intervals. It appears to be a promising strategy after myocardial ischemia, and its role in cerebral protection is being studied, since cellular injury mechanisms are similar. However, results in neuroprotection are less satisfactory than in the heart, so postconditioning might only be applicable to mild or moderate injuries. Nevertheless, from a practical point of view, it is more useful for physicians to know the potential and applications of measures at their disposal. However, there is less clear evidence that ideal values of these parameters should be generalized for all patients. Hypoxemia and Hypotension Hypoxemia and hypotension during the acute phase of cerebral injury are associated with poor prognosis and should be treated aggressively [12]. Hyperoxia has also been shown to reduce lactate levels in cerebral microdialysis, but not the lactate/piruvate rate, which is a more reliable indicator of the energetic state. In addition, lactate may be used as an energetic substrate in case of severe metabolic depletion in the brain. Furthermore, arterial hypertension may contribute to vasogenic cerebral swelling in the case of cerebral autoregulation abnormalities, which are frequently established following severe acute injuries. Control of arterial blood pressure may reduce cerebral swelling and the risk of hemorrhagic transformation following stroke. Nevertheless, this effect must be balanced against the risk of decreasing perfusion in the penumbra areas. Antihypertensive treatment is discouraged for patients who are non-candidate for thrombolytic therapy, unless diastolic blood pressure is above 120 mmHg or systolic above 220 mmHg. Anti-hypertensive drugs are recommended for patients following thrombolytic treatment, within the first 24 hours, if diastolic or systolic blood pressure are above 110 or 185 mmHg respectively [14]. Despite the lack of clear evidence in spontaneous cerebral hemorrhage, recent studies suggest that maintaining systolic blood pressure below 140 mmHg may reduce hematoma growth [15]. Fluid Management and Transfusion As a rule, normovolemia is the therapeutic target and, in any case, hypovolemia and hypo-osmolarity should be avoided. Since the brain is very sensitive to secondary injury induced by ischemia, anemia should also be avoided. In those cases, the risk-benefit ratio of blood transfusion versus anemia should be assessed [16]. Monitoring can help in taking individualized decisions for these patients regarding transfusion therapy. Some coexisting diseases (such as coronary disease) may also affect the transfusion threshold.
In most instances arteria auricular posterior buy clonidine 0.1mg overnight delivery, vancomycin combined with a cephalosporin with antipseudomonal activity (ceftazidime or cefepime) or meropenem is indicated until culture results are available blood pressure goals chart 0.1mg clonidine mastercard. In selected cases where there are no risk factors for nosocomial drug-resis1012 the Diagnosis and Management of Central Nervous System Infections in the Neurocritical Care Unit tant organisms blood pressure 6 year old discount clonidine 0.1mg mastercard, empiric therapy with nafcillin (or oxacillin) blood pressure medication voltaren order generic clonidine online, combined with a third-generation cephalosporin (ceftriaxone or cefotaxime) may be appropriate. Antibiotic coverage should be narrowed once culture data are available, and treatment should continue for 3 to 4 weeks. In the case of vertebral osteomyelitis or discitis, treatment for 4 to 6 weeks is indicated [72]. Subdural Empyema Early surgical evacuation in addition to appropriate antibiotic therapy is usually required for successful management. Empiric antibiotic selection for subdural empyema is the same as that for intracranial epidural abscess, as the bacteriology of these infections is identical [75]. Adequate hydration should be maintained during treatment, because acyclovir can cause a crystal nephropathy that is usually reversible. Prolonged high dose oral valacyclovir for 3 months after 3 weeks of treatment is also being studied. Corticosteroids and mannitol are usually reserved for patients with cerebral edema and intracranial hypertension. Ganciclovir and foscarnet are associated with severe adverse effects, including renal insufficiency, bone marrow suppression, encephalopathy, and seizures. Both ganciclovir and foscarnet require careful monitoring and dose adjustment in the setting of renal dysfunction [166]. Patients with life-threatening enterovirus infections have been treated successfully with pleconaril on a compassionate-use basis, and it is deserving of further study [167,168]. Causative organisms include Cryptococcus neoformans, Coccidioides immitis, Histoplasma capsulatum, Candida albicans, Sporothrix schenkii, Blastomyces dermatidis, Zygomycetes species, and Aspergillus species, with the latter two more commonly causing brain abscess [169]. The incidence of invasive fungal infections is rising despite the emergence of newer antifungal agents, and outcomes in general are poor [170]. Most treatment regimens consist of an initial induction phase with an amphotericin-based regimen that lasts 2 to 6 weeks, depending on clinical response. This is followed by a chronic suppressive phase with a triazole antifungal with activity against the pathogen being treated (usually fluconazole or voriconazole) that can last from 6 weeks to lifelong suppression. Optimal treatment also should include management of risk factors for fungal disease, such as hyperglycemia, and minimizing immunosuppressant drugs where appropriate. The dose of amphotericin B deoxycholate (AmB) is 1 mg/kg intravenously daily, combined with flucytosine 25 mg/kg orally every 6 hours. Flucytosine requires dose adjustment in the setting of renal insufficiency, and serum levels should be monitored. Levels greater than 100 mg/ml are associated with an increased risk of bone marrow depression, which can be irreversible and result in death [172,173]. The goal peak flucytosine level is 70 mg/ml to 80 mg/ml (drawn 4 hours after a dose at steady state), and the goal trough level is 30 mg/ml to 40 mg/ml. In patients with renal insufficiency, a lipid-based amphotericin product is recommended. Thirty-one percent of subjects survived for a median of 390 days and 38% had neurosurgical intervention for the infection, which was associated with improved survival, making it difficult to clearly discern the impact of voriconazole on outcomes. Initial dosing of voriconazole is 6 mg/kg intravenously every 12 hours for two doses, followed by 4 mg/kg intravenously every 12 hours. Posaconazole is an extended spectrum triazole antifungal with in vitro activity against Candida, Aspergillus, Zygomycosis, and Fusarium species. Successful outcomes were observed in 14 of 29 (48%) of patients with cryptococcal disease, and 5 of 10 (50%) patients with other fungal infections [182]. Based on this report, and animal studies suggesting efficacy [183,184], posaconazole may be considered as salvage therapy in cryptococcal meningitis where other therapies have failed. Currently, posaconazole is only available as an oral medication (200 mg every 6 hours for 7 days, followed by 400 mg twice daily). It is highly lipophilic, with a very large volume of distribution (1,774 l), and is highly protein bound (>98%). It is an inhibitor of cytochrome P450 3A4, and is therefore subject to numerous clinically significant drug interactions. Caspofungin and micafungin are the first of a new class of antifungals (echinocandins) that target the fungal cell wall through inhibition of -1,3 glucan synthesis. Hsue and colleagues [186] reported a case of treatment failure associated with the use of caspofungin for meningeal coccidiomycosis. It can be administered through a reservoir device or as an intraventricular injection, and is typically given in conjunction with systemic amphotericin and flucytosine. Adverse effects associated with intrathecal AmB include arachnoiditis, paraplegia, paresthesias, nausea, vomiting, headache, and back pain. Hydrocortisone (15 mg to 25 mg) can be added to the intraventricular mixture to reduce toxicity. Prophylactic administration of antipyretics and antiemetics may also help alleviate some adverse effects. A Cochrane collaboration review including 18 clinical trials and 2750 people concluded that adjunctive steroid treatment is associated with a reduction in mortality and hearing loss in all patients (adults and children) with bacterial meningitis without major adverse events [193], a finding that concurs with the recommendations of the Infectious Diseases Society of America [92]. Subgroup analysis for causative organisms showed mortality benefit in patients with S.
The most severe complication of this entity is recurrent ischemic stroke which occurs in 831 Intensive Care in Neurology and Neurosurgery Figure 46 blood pressure medication young age buy clonidine 0.1mg otc. At higher magnification blood pressure over 200 in elderly generic 0.1 mg clonidine free shipping, these granular osmeophilic deposits are irregularly shaped hypertension education buy clonidine visa, 0 heart attack and vine cheap clonidine 0.1mg line. Other typical clinical manifestations are psychiatric disorders and subcortical dementia. Magnetic resonance imaging of brain shows ischemic lesions in the periventricular white matter and around the basal ganglia, with particular focus on the anterior pole of the temporal lobe and external capsule. Electron microscopy of skin biopsy shows the presence of granular osmiophilic deposits adjacent to the basement membrane of smooth muscle cells of the arteriolar wall (Figure 46. Finally, this disease can also be diagnosed by identifying the mutation in the Notch3 gene in a sample of peripheral blood. In the absence of specific treatment for this disease, efforts should focus on identifying and correcting cardiovascular risk factors. This enzyme is a lysosomal hydrolase involved in the metabolism of glycosphingolipids. Its deficiency causes the intralisosomal accumulation of sphingolipids with -galactosyl residues, particularly globotriaosylceramide (Gb3). The gene coding for the -gal is located on the X chromosome and more than 400 mutations have been described. However, there are numerous reports indicating that, due to non-random tissue-specific X chromosome inactivation, women may have atypical presentations. Due to the small number of patients studied, it is unclear whether enzyme replacement can reduce the recurrence of cerebral ischemia. In heterozygous individuals with ischemic stroke the use of antiplatelet agents or anticoagulants (depending on the case) and the correction of vascular risk factors are recommended. In the nervous system, mitochondrial dysfunction and consequent energy deficit present with stroke-like episodes. Clinically the patient presents with neurological deficits that correlate with parenchymal brain lesions. On magnetic resonance imaging, these are typically hyperintense hyperintense on diffusion-weighed image sequences and apparent diffusion coefficient, suggesting the presence of vasogenic edema. These lesions are not located in a defined vascular area, have a predilection for the posterior regions of the brain and may progressively extend to other areas. It has been postulated that mitochondrial failure of intracerebral small vessels causes vascular dysfunction affecting the perfusion of the brain parenchyma (the "mitochondrial angiopathy" theory). Coenzyme Q10 is usually used alone or in combination with creatine and lipoic acid. The latter is related to the occurrence of stroke-like events and recurrent seizures. Several of these entities have therapeutic peculiarities that can considerably change the prognosis and natural history. It should be emphasized that the evaluation of these cases can be complex, extensive and expensive. Diagnosis and individualized plans for each patient are in the hands of the treating specialist who, according to personal experience, will select diagnostic studies at a reasonable cost. Nevertheless, these data should be analyzed carefully since the size of the samples is usually small. Studies based on administrative data show a lower mortality at discharge in young patients with stroke. Note: this table simply summarizes the most frequent complementary studies in the etiological diagnosis of stroke in young people. The goal is to simply provide a guide, not an exhaustive reference for the reader. The order of the studies should be individualized depending on the past medical history, family history, and physical exam findings. These data confirm that age is one of the two most important prognostic factors in patients with ischemic stroke (after stroke severity).
Serum sodium disorders are very common: hypernatremia is especially frequent usually multifactorial in origin blood pressure recommendations buy 0.1mg clonidine fast delivery. In cas1727 Intensive Care in Neurology and Neurosurgery es it is a result of diabetes insipidus with concomitant contraction of blood volume blood pressure chart what is too low generic 0.1mg clonidine overnight delivery. This alteration is especially harmful for liver function and may compromise subsequent graft take pulse pressure below 20 purchase clonidine amex. The treatment is with hypotonic infusions such as dextrose or hyposaline solutions blood pressure during heart attack generic clonidine 0.1mg line. Hyponatremia is less frequent but can ensue from inadequate intake, inappropriate correction of hormonal disorders, gastrointestinal losses or kidney failure. Treatment is based on fluid restriction and isotonic saline administration with serial laboratory monitoring. Less frequent are alterations in magnesium, which often occur with refractory hypokalemia, both preventable with the administration of magnesium in conjunction with phosphate to preserve cell membrane integrity. Temperature Control the progressive destruction of the hypothalamus leads to a loss of body temperature in relationship to the external environment, with the patient becoming a poikilotherm donor. We must therefore prevent the dispersion of heat by mean of heating systems and fluid replacement. Hypothermia can generate hemodynamic instability, cardiac arrhythmias, renal and coagulation alterations and deviation of the dissociation curve of hemoglobin to the left. Hyperpyrexia should be avoided; in patients who had infections we must ensure negative cultures, negative screening for emboligenic foci from the heart and other locations, and adequate antibiotic treatment before authorizing organ donation. Hematological Control the origin of hematological disturbances is multifactorial: it may be due to severe blood loss in multiple trauma, previous transfusions with citrated blood, hypothermia and the continued release of large amounts of tissue fibrinolytic factors, as well as severe skull base trauma, multiple fractures internal organ (liver) injuries, major pelvic fractures or severe leg damage. Furthermore, ischemic-necrotic tissues can release great amounts of thromboplastin. There may also be non-specific abnormalities due to disseminated intravascular coagulopathy. Treatment is based on the administration of plasma and platelets and packed red cells if the hematocrit is <30% for kidney donors or 35% for multiorgan donors. Renal Function It is necessary to maintain an hourly urine output of 1 ml/kg in adult patients and 2 ml/ kg in children. Polyuria, (urine output >3-4 ml/kg) can perpetuate a situation of hypovolemia due to diabetes insipidus or hyperglycemia. The most frequently used include furosemide at doses of 20-60 mg and intravenous mannitol at doses of 0. Specific Corneal Care Exclusion criteria for cornea donation are the same as general criteria. Periodically, lubricants, artificial tear solutions, antibiotic drops of tobramycin or gentamicin should be administrated. Occasionally, corneal epithelial alterations should be minimized with the administration of local cold. Diagnostic Determinations in Intensive Care General diagnostic tests are performed to monitor potential donors; however, to evaluate different viscera we must follow a series of requirements as described below. A general test is the determination of blood count and blood group with Rh factor and investigation of isogroups, which have been obtained by previous requirements. In addition, immunological compatibility between donor and recipient is necessary for heart, liver and lung transplants, as is determining serology. Monitoring and Special Tests for Lung Donation Previous care is essential to avoiding volutrauma and barotrauma in mechanically ventilated patients. Assessment will include previous infections, history of smoking, drugs, chemotherapy or radiotherapy, and evaluation of previous occupational risks. Before a patient can be considered as a potential lung donor, it is imperative to measure PaO2 >300 mmHg after the administration of 100% oxygen for 15 min- Figure 95. Chest radiography is important for lung as- axis (B and C) and the largest thoracic diameter sessment. Anthropometric assessment will include measurement of body weight, height, waist circumference and chest circumference. Lung transplantation also requires measurement of the diaphragmatic dome-lung apex axis (B and C) and the largest thoracic diameter measured between both costophrenic sinuses (A) (Figure 95. Monitoring and Special Tests for Heart Donation It is essential to anticipate an adrenergic storm, which is not dangerous for the heart and will not provoke heart failure. Just as in the lung donor, we must search for salient events in the medical history and risk factors. Alterations in these enzymes may indicate chronic liver disease, hepatic necrosis secondary to tissue hypoperfusion due to complications arising from maintenance of hemodynamic status. Also important is the search for tumour markers such as alpha-fetoprotein associated with hepatocellular carcinomas and germ cell tumours. Monitoring and Special Tests for Kidney Donation Detailed clinical history and risk behaviours. Renal profile by laboratory determinations should include: complete urinalysis, proteinuria, blood urea and creatinine. Monitoring and Special Tests for Pancreatic Activity Clinical history and risk behaviours are a common step to other organs, focusing on smoking habits, history of gallstones, and alcohol consumption. The specific pancreatic profile for the laboratory includes: blood glucose and serum amylase and lipase, especially for assessing the viability of the pancreas for transplantation. Lipase levels are not usually affected by brain death, but blood glucose and amylase >10 mg/l are.
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