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Intracerebral hemorrhage following epinephrine application for anaphylactic reaction
... 3,4 However, previous published reports have rarely shown the incidence of intracranial hemorrhage following anaphylactic shock treated with adrenaline injection. 5,6 Furthermore, intracerebral hemorrhage can occur after adrenaline administration via any route, including in patients undergoing therapeutic upper-gastrointestinal endoscopy and those with asthma. 7,8 Although a definitive pathogenesis of these adverse events has not been elucidated, these serious adverse events can be fatal and require further intervention. ...
... Leukopenia, non-occlusive mesenteric ischemia, ischemic stroke, and intracerebral hemorrhage are adverse events after anaphylactic shock that have previously been reported in the medical literature. 5,[10][11][12][13] Although other etiologies cannot be excluded, we assume that acute hypertensive attack induced by adrenaline and dialysis with a high risk of hemorrhage may be associated with the pathogenesis of intracerebral hemorrhage, in our case at least partially. Indeed, during anaphylactic shock, our patient's cerebral blood flow decreased more than what could be anticipated based on the blood pressure observed in animal experiments. ...
... Similar to our case, previous reports have hypothesized that intracerebral hemorrhage after anaphylactic shock can result from elevated blood pressure induced by adrenaline administration when there is no evidence of vascular abnormality or intracerebral tumor. 5,6 Adrenaline is one of the most commonly used medications to manage conditions such as cardiac arrest, asthma, septic shock, and anaphylactic shock, but serious adverse events can occur, including arrhythmias, lactic acidosis, pulmonary edema, and cerebrovascular disease. 6,[15][16][17] Intracerebral hemorrhage after administration of adrenaline via different routes, including intravenous and intramuscular administration and inhalation, has previously been described. ...
Intracerebral hemorrhage should be considered as a possible adverse event in patients with anaphylactic shock who are treated with adrenaline administration, especially in those at high risk of serious bleeding events. Although prompt intramuscular injection of adrenaline is the first‐line treatment for anaphylactic shock, physicians should recognize that adrenaline injection can lead to intracerebral hemorrhage, especially in high bleeding risk patients.
... Leukopenia, non-occlusive mesenteric ischemia, ischemic stroke, and intracerebral hemorrhage are adverse events after anaphylactic shock that have previously been reported in the medical literature [5][10] [11][12] [13]. ...
... Therefore, the pathogenesis of intracerebral hemorrhage may have etiologies other than anaphylaxis. Similar to our case, previous reports have hypothesized that intracerebral hemorrhage after anaphylactic shock can result from elevated blood pressure induced by adrenaline administration when there is no evidence of vascular abnormality or intracerebral tumor [5] [6]. ...
... Adrenaline is one of the most commonly used medications to manage conditions such as cardiac arrest, asthma, septic shock, and anaphylactic shock, but serious adverse events can occur, including arrhythmias, lactic acidosis, pulmonary edema, and cerebrovascular disease [6] [15][16] [17]. Intracerebral hemorrhage after administration of adrenaline via different routes, including intravenous and intramuscular administration and inhalation, has previously been described [5][8] [18]. Adrenaline can lead to stimulation of all α and β adrenergic receptors, eliciting short-term systolic hypertension, and suppress inflammatory mediators released from mast cells and basophils [19]. ...
Intracerebral hemorrhage should be considered as a possible adverse event in patients with anaphylactic shock who are treated with adrenaline administration, especially those on dialysis.
... Common adverse effects from epinephrine administration include anxiety, palpitations, and headaches with more severe adverse effects being ventricular arrhythmias, angina, or even myocardial infarction; however, these are typically only seen in epinephrine overdose [4]. Although not commonly listed, there are a number of reports of adverse neurologic events associated with the use of IM epinephrine including ischemic stroke and intracranial hemorrhage [5][6][7][8]. We present a case of transient neurologic deficits following intramuscular epinephrine administration for the treatment of anaphylaxis. ...
... These include intracerebral hemorrhage, ischemic stroke, and TIA. In these cases, given the temporal association with IM epinephrine administration and subsequent neurologic deficits, the proposed etiology is acute severe hypertension from the alphaadrenergic mediated vasoconstrictive effect of epinephrine [5][6][7]. In our patient, small vessel cerebral vasospasm from the same mechanism is postulated to have caused his predominately unilateral and transient neurologic deficits, which is also supported by the temporal association between IM epinephrine administration and symptom onset. ...
Anaphylaxis is an acute, potentially life-threatening severe allergic reaction commonly caused by foods, insect stings, and medications. Intramuscular epinephrine is the cornerstone of treatment for anaphylaxis in order to reverse immediate symptoms and prevent progression to life-threatening hemodynamic or respiratory collapse. By nature of its mechanism of action, epinephrine may induce a number of neurovascular-related adverse effects; even at usual therapeutic doses. Rarely described adverse events include transient ischemic attacks, ischemic stroke, intracerebral hemorrhage, and myocardial infarction. These events may be observed more frequently in patients with cardiovascular risk factors including hypertension, hyperlipidemia, and diabetes mellitus. We present a case of transient neurologic deficits in a patient with underlying cardiovascular disease related to intramuscular epinephrine use for the treatment of anaphylaxis. This case serves to further highlight serious adverse neurologic events that may result from intramuscular epinephrine administration.
... We assume that in minority of patients, early compensatory vasopressor response may be dominant, which can cause anaphylactic reactions manifesting with hypertensive attacks. Especially, in young patients, the possibility of a hypertensive attack in anaphylactic reactions should be kept in mind, and the arterial blood pressure should be measured prior to the epinephrine injection to avoid a potential dangerous side effect of epinephrine (Wendt et al. 2011). There is no information in the literature regarding rates of hypertensive anaphylactic reactions. ...
Background
Although a few case reports about hypertensive anaphylaxis (HA) are available in the present literature, there is no study about the prevalence of HA. In this study, we review our cases with anaphylaxis presenting with hypertension and ascertain its prevalence. The documents of the patients who had anaphylactic reactions after the procedures performed for the diagnosis and treatment of allergic diseases in GATA Haydarpasa Clinic of Allergy and Immunology between January 2010 and December 2014 were retrospectively reviewed. Within the study period, 324 patients had undergone 4332 procedures in which 62 of them had developed anaphylaxis.
Results
During the procedures, the rate of anaphylaxis was found to be 1.43 %. The rate of HA among the anaphylaxis patients was 12.9 % (8 of 62 patients). During treatments, 2 patients received adrenaline injections without any adverse reaction.
Conclusions
HA may be seen at a considerable rate during an anaphylactic reaction. Anaphylaxis and hypertension can be recovered by adrenaline injection when required. According to the best of our knowledge, this study is the first original study about the prevalence of HA in English-language medical literature.
... Main side effects A detailed discussion of epinephrine can be found in other reviews. Epinephrine has a narrow therapeutic window and can cause severe side effects, including arrhythmias, pulmonary edema, hypertension [31], and cerebral hemorrhage [32]. More commonly, epinephrine leads to side effects of pallor, tremor, and anxiety [29]. ...
Characterization of mediators and mechanisms of anaphylaxis will allow for more specific and effective treatment with fewer side effects. Recent studies have shown that platelet-activating factor (PAF) is a pivotal mediator of the life-threatening manifestations of anaphylaxis. The putative role of PAF in human anaphylaxis is based on a large body of evidence in experimental and human anaphylaxis. In animal models of anaphylaxis, intravenous administration of PAF reproduces the severe physiologic derangements of anaphylaxis. PAF receptor knock-out mice are resistant to experimental anaphylaxis. Data from human anaphylaxis show that levels of PAF increase proportionately with the severity of anaphylaxis, whereas a deficiency in the enzyme that inactivates PAF predisposes to severe or fatal anaphylaxis. Many of the biologic effects of PAF appear to be transduced by nitric oxide production. PAF receptor antagonists protect against the lethal effects of exogenous PAF, but, importantly, also protect against experimental anaphylaxis following allergen challenge. Mice treated with an enzyme that inactivates PAF are similarly resistant to anaphylaxis. Some clinically available medications for anaphylaxis act at different points of the PAF pathway. Epinephrine, the first-line treatment for anaphylaxis, appears to act in part by phosphorylation and inactivation of the PAF receptor, whereas methylene blue, which reduces the actions of nitric oxide, can reverse severe anaphylaxis that is refractory to conventional treatment. Taken together, these studies have shown that therapies targeting the PAF pathway might hold the potential for more specific and effective treatments for this potentially life-threatening condition.
Oxidative stress and matrix metalloproteinases (MMPs) contribute to hemorrhagic transformation after ischemic stroke and brain injury after intracerebral hemorrhage (ICH). The goal of this study was to develop a new model of spontaneous ICH, based on the hypothesis that acute, superimposed on chronic, hypertension produces ICH. We hypothesized that increases in angiotensin II (AngII)-mediated oxidative stress and activation of MMPs are associated with, and may precede, spontaneous ICH during hypertension. In C57BL/6 mice, chronic hypertension was produced with AngII infusion and an inhibitor of nitric oxide synthase. During chronic hypertension, mice with acute hypertension from injections of AngII developed ICH. Oxidative stress and MMP levels increased in the brain even before developing ICH. Active MMPs colocalized with a marker of oxidative stress, especially on cerebral vessels that appeared to lead toward regions with ICH. Incidence of ICH and levels of oxidative stress and MMP-9 were greater in mice with acute hypertension produced by AngII than by norepinephrine. In summary, we have developed an experimental model of ICH during hypertension that may facilitate studies in genetically altered mice. We speculate that acute hypertension, especially when induced by AngII, may be critical in spontaneous ICH during chronic hypertension, possibly through oxidative stress and MMP-9.
We report a case of intracerebral hemorrhage (ICH) in a young man following intravenous self-administration of epinephrine. Arteriography evidenced normal intracranial vessels, and namely excluded the presence of vascular malformations which could have been implicated in the pathogenesis of ICH. We believe that the main pathogenetic agent in this case was the sudden rise in arterial blood pressure. This report aims at underlying the severe implications of non-medical use of sympathomimetic drugs.
To better define the etiologic importance of hypertension for spontaneous intracerebral hemorrhage, hospital records were studied for all patients sustaining intracerebral hemorrhage during 1982 in the Cincinnati metropolitan area. Hypertension pre-dating the hemorrhage was present in 45% (69 of 154), as determined by history. A more inclusive definition of hypertension, combining those with a positive history with those found to have left ventricular hypertrophy by electrocardiogram or cardiomegaly by chest radiography, applied in 56% (87 of 154). The cases were compared to controls with and without hypertension derived from the NHANES II study of blood pressure (n = 16,204) to determine relative risk. For the presence of hypertension by history, the relative risk of intracerebral hemorrhage was 3.9 (95% confidence interval, 2.7 to 5.7). For the inclusive definition of hypertension, the relative risk was 5.4 (3.7 to 7.9). Relative risk was also determined for hypertension in blacks (= 4.4), age greater than 70 (= 7), prior cerebral infarction (= 22), and diabetes (= 3). We conclude that the term "hypertensive hemorrhage" should be used very selectively, particularly in whites, and propose that hypertension be viewed as one of several important risk factors for spontaneous intracerebral hemorrhage.
An unusual case in which pulmonary edema and intracranial hemorrhage occurred during adenotonsillectomy is presented. The possible causes of this intracranial hemorrhage are discussed, especially in relationship to local epinephrine infiltration.
Nontraumatic intracerebral hemorrhage is bleeding into the parenchyma of the brain that may extend into the ventricles and, in rare cases, the subarachnoid space. Each year, approximately 37,000 to 52,400 people in the United States have an intracerebral hemorrhage.1,2 This rate is expected to double during the next 50 years as a result of the increasing age of the population and changes in racial demographics. Intracerebral hemorrhage accounts for 10 to 15 percent of all cases of stroke and is associated with the highest mortality rate, with only 38 percent of affected patients surviving the first year.3 Depending on . . .
Phenylpropanolamine (PPA) and pseudoephedrine are sympathomimetics contained in over-the-counter cold preparations. A case-control study linked PPA use with hemorrhagic stroke in women. Twenty-two patients with stroke associated with use of these drugs are described.
In a consecutive stroke registry since 1988, 22 patients had stroke associated with over-the-counter sympathomimetics. Sympathomimetic dosage and type, time interval until stroke onset, and neuroimaging findings are described.
Ten male and 12 female patients were included. Intracerebral hemorrhage occurred in 17 patients, subarachnoid hemorrhage in 4, and ischemic stroke in 1. Stroke was associated with PPA use in 16 patients (dose 75 to 675 mg), with pseudoephedrine in 4 (dose 60 to 300 mg), and with others administered by the nasal route in 2 (oxymetazoline and phenylephrine). Stroke occurred after a single dose in 17 patients and after daily use during several days in 5. The interval between drug exposure and clinical onset varied from 30 minutes to 24 hours. Stroke occurred after recommended doses of PPA (50 to 75 mg) in 32% and pseudoephedrine (60 mg) in 50% of patients. Eight patients had acute hypertension at stroke onset. Cerebral angiography was normal in 8 cases and showed diffuse vasospasm or beading in 10 patients.
Stroke related to over-the-counter sympathomimetics was associated with acute hypertension and/or vasospasm or angiitis mechanisms, most related to the use of PPA; however, stroke also occurred with the use of other sympathomimetics, particularly pseudoephedrine. Although stroke complications occurred when doses were used that were higher than recommended doses, apparently there is also a stroke risk when these agents are taken properly.
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There is continuing controversy over whether the pattern of circadian blood pressure (BP) variation that includes a nocturnal decline in BP and a morning pressor surge has prognostic significance for stroke risk. In this study, we followed the incidence of stroke in 1430 subjects aged > or =40 years in Ohasama, Japan, for an average of 10.4 years. The association between stroke risk and the pattern of circadian BP variation was analyzed with a Cox proportional hazards model after adjustment for possible confounding factors. There was no significant association between total stroke risk and the nocturnal decline in BP (percentage decline from diurnal level) or between total stroke risk and the morning pressor surge. The cerebral infarction risk was significantly higher in subjects with a <10% nocturnal decline in BP as compared with subjects who had a > or =10% nocturnal decline in BP (P=0.04). The morning pressor surge was not associated with a risk of cerebral infarction. On the other hand, an increased risk of cerebral hemorrhage was observed in subjects with a large morning pressor surge (> or =25 mm Hg; P=0.04). Intracerebral hemorrhage was also observed more frequently in extreme dippers (those with a > or =20% nocturnal decline in BP) than dippers (those with a 10% to 19% decline; P=0.02). A disturbed nocturnal decline in BP is associated with cerebral infarction, whereas a large morning pressor surge and a large nocturnal decline in BP, which are analogous to a large diurnal increase in BP, are both associated with cerebral hemorrhage.