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PubMed2003

Acute pulmonary edema after cardioversion of cardiac arrhythmias.

OBJECTIVE: To examine the occurrence of acute pulmonary edema after cardioversion of arrhythmias. METHODS: Cases, case series, and related articles on the subject identified through a comprehensive literature search were examined. RESULTS: Thirty cases (23 males) of post cardioversion acute pulmonary edema were identified. The mean age was 53.8 +/- 13 years (range, 18 to 75 years). Underlying arrhythmias were atrial fibrillation (69%), atrial flutter (24%), supraventricular tachycardia (4%), and ventricular tachycardia (4%). The duration of arrhythmia preceding cardioversion varied widely ranging from 1 day to 13 years. Twenty-six (87%) patients had concomitant cardiovascular disease comprising of coronary artery disease (38%), rheumatic heart disease (23%), cardiomyopathy (23%), and hypertension (8%). Direct current electrical cardioversion was used in 28 (93%) patients and pacing in two (7%) patients. Occurrence of pulmonary edema was independent of the amount of energy used for cardioversion (range 20 to 1280 Joules, mean 263 +/- 27 Joules). Short acting general anesthetic drugs were administered in 14 (47%) and sedation in eight (27%) patients. Sinus rhythm was established in 23 (77%) patients. Duration to develop pulmonary edema after cardioversion was available in 23 patients and ranged from immediately to 96 h. Pulmonary edema occurred within 15 min after cardioversion in 22%, within 3 h in 30%, within 24 h in 30%, within 48 h in 17% and within 96 h in remaining 4% of patients. Three patients required mechanical ventilation. CONCLUSION: The rare complication of acute pulmonary edema after cardioversion has been reported mostly in patients with underlying cardiac disease, and is independent of the amount of energy used for cardioversion.

Acute Disease↗
PubMed1998

Prediction of patients with higher order multifetal pregnancy at risk for postpartum pulmonary edema.

OBJECTIVE: This retrospective study aims to verify the factors for the development of maternal pulmonary edema in higher order multifetal pregnancy. STUDY DESIGN: We analyzed medical profiles of a total of 13 triplet, quadruplet and quintuplet pregnancies for the years 1992 through 1997. Some treatments were applied in attempts to promote these multifetal pregnancies. All underwent cesarean section, two of which developed pulmonary edema within a few hours of delivery. There had been no evidence for the development of pulmonary edema antepartum. RESULTS: In the patients affected by pulmonary edema, postoperative values of PaO2/FIO2<250 mmHg showed close association to a value perioperative fluid loading index (FLI)>0; the index consists of an intraoperative fluid balance and preoperative infusion volume within 24 h prior to surgery. Two patients with postoperative pulmonary edema had a perioperative FLI>0, whereas the others had values 0 may have a much higher risk for postoperative pulmonary edema, suggesting the predictive role of the perioperative FLI value.

Adult↗
PubMed2002

Prolonged unilateral vasodilatation and brain edema in fulminant hepatic failure, associated with symptomatic seizure.

We report prolonged unilateral vasodilatation and hemispheric brain edema in a 49-year-old man with fulminant hepatic failure (FHF). The patient presented with a tonic-clonic seizure caused by a hypertensive subcortical hemorrhage in the left parietal lobe. Serial computed tomography (CT) scans showed progressive darkening of the ipsilateral hemisphere, suggesting hemispheric cerebral infarction, but the patient did not show clinical signs of deterioration. Brain magnetic resonance angiography showed dilation of the large arteries of the left hemisphere. Evaluation of cerebral blood flow 7 days postictus with single photon emission CT revealed marked ipsilateral hyperperfusion. The darkening of the hemisphere was brain edema elicited by hyperperfusion. Brain edema was reversible, disappearing 14 days postictus. Hemispheric brain edema was caused by unilateral cerebral vasodilatation and resultant hyperperfusion. Although brain edema is a major complication in FHF patients and cerebral hyperperfusion is responsible for edema formation, CT findings of these patients almost invariably show a bilateral lesion. Unilateral vasodilatation and subsequent hemispheric hyperperfusion may be due to overproduction of vasodilators, already abundant in the brains of patients with severe hepatic failure, by seizure activity.

Brain↗
PubMed1997

Formalin-induced nociceptive behavior and edema: involvement of multiple peripheral 5-hydroxytryptamine receptor subtypes.

The role of 5-hydroxytryptamine and its receptor subtypes in the development of acute inflammation was investigated using the rat paw formalin test as a model for pain (measured by flinching behavior) and edema formation (measured by plethysmometry). The role of endogenously released 5-hydroxytryptamine was assessed using 5-hydroxytryptamine receptor subtype-selective antagonists co-injected with 2.5% formalin, while the receptor subtypes involved in the inflammatory process were further defined by co-injection of 5-hydroxytryptamine or 5-hydroxytryptamine receptor subtype-selective agonists with 0.5% formalin in anticipation of an augmented response. When co-administered with 2.5% formalin, propranolol, tropisetron or GR113808A, but not ketanserin, effectively blocked nociceptive behavior. In the presence of 0.5% formalin, 5-carboxamidotryptamine, 1-(m-chlorophenyl) biguanide or 5-methoxytryptamine, but not (+/-)-1-4-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane, augmented the flinching response. These data suggest involvement of 5-hydroxytryptamine1, 5-hydroxytryptamine3 and 5-hydroxytryptamine4 receptors in peripheral nociception. There may be some dissociation of nociception and edema formation, since no single 5-hydroxytryptamine receptor antagonist inhibited edema formation with 2.5% formalin; however, with 0.5% formalin, edema formation was enhanced by co-administration of 5-hydroxytryptamine, 5-carboxamidotryptamine, (+/-)-1-4-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane or 5-methoxytryptamine, but not 1-(m-chlorophenyl) biguanide. These data suggest involvement of 5-hydroxytryptamine1, 5-hydroxytryptamine2 and possibly 5-hydroxytryptamine4 receptors in edema formation. These results confirm the involvement of 5-hydroxytryptamine1 and 5-hydroxytryptamine3 receptor subtypes in peripheral nociception associated with acute inflammation and further suggest an involvement of the more recently characterized 5-hydroxytryptamine4 receptor in this process. There appears to be a dissociation in 5-hydroxytryptamine receptors involved in peripheral nociception and edema formation.

Animals↗
PubMed2004

A rare complication of generalized edema in juvenile dermatomyositis: a report of one case.

Juvenile dermatomyositis (JDM) is a rare autoimmune disease characterized by inflammation of the muscle, connective tissue, skin, gastrointestinal tract and small nerves. Periorbital and facial edema may also be associated. Although localized edema is a common feature of juvenile dermatomyositis, generalized edema has been reported rarely. In this article, we report a 14-year-old boy with juvenile dermatomyositis presenting with generalized edema. Of the diagnostic criteria of JDM, severe symmetric weakness of the proximal musculature, characteristic cutaneous changes, elevated serum muscle enzymes and myopathic electromyographic abnormalities were observed. Magnetic resonance imaging (MRI) of the lower extremities and pelvis showed marked diffuse edema in the subcutaneous tissue, muscles and myofascia. We suggest that MRI findings, which are not among the diagnostic criteria, may also be included in the diagnostic criteria of JDM. To the best of our knowledge, this is the 19th case of JDM reported for generalized edema in the English literature.

Adolescent↗
PubMed1998

Outcome of children with cerebral edema caused by fulminant hepatic failure.

Mortality is high in patients with fulminant hepatic failure (FHF). Neurologic complications of encephalopathy and cerebral edema are major contributors to mortality. Orthotopic liver transplantation has improved survival in these patients. However, the complexity of medical and surgical problems in this patient population, coupled with a severe shortage of organs, requires careful patient selection. The aim of this study was to describe the neurologic outcome of children with FHF who developed radiologically apparent cerebral edema. The hospital and outpatient records and radiologic studies of 20 children with FHF admitted to Children's Hospital of Pittsburgh from 1981-1995 who developed encephalopathy and computed tomographic evidence of cerebral edema were reviewed. Fourteen patients died (70%), three were left with severe neurologic deficits (15%), and three were left with moderate deficits (15%). Survival was correlated with a lesser degree of coma. Histopathologic examination of eight brains demonstrated cerebral edema and widespread ischemic neuronal necrosis in all eight. The presence of radiographic cerebral edema in children with FHF is an objective measure that indicates a very poor prognosis. Termination of care is a reasonable option. Comprehensive monitoring of cerebral function and intracranial pressure is required in children with FHF. Orthotopic liver transplantation should be performed in children with severe and worsening encephalopathy before the development of radiographically apparent cerebral edema.

Adolescent↗
PubMedDate not supplied

Severe gestational edema.

Lower extremity edema is an almost universal finding in late pregnancy, occurring secondary to increased venous pressure in the legs, obstruction of lymphatic flow, and reduced plasma colloid osmotic pressure.(1) Varney describes gestational edema as the development of an excessive accumulation of fluid in the tissues without coexisting hypertension or proteinuria.(2) Midwives are familiar with this common condition in an otherwise uncomplicated pregnancy and are comfortable reassuring clients that lower extremity edema is non-pathologic. The patient with severe lower extremity edema, however, presents the provider with a clinical challenge. Is the presenting symptom a sign of an underlying disease process, or simply a normal physiologic process with extreme manifestation/expression? Lower extremity edema that rises to include the labia presents an intrapartum challenge of managing tissue integrity during the birth. A case of severe gestational edema is reported. Discussion explores broader considerations in differential diagnosis and management.

Adult↗
PubMed1999

Pars plana vitrectomy in diabetic macular edema.

PURPOSE: To ascertain the association between the improvement of diabetic macular edema and increased visual acuity after pars plana vitrectomy. METHODS: From January 1994 to December 1996 we prospectively studied 18 patients (18 eyes, 7 women and 11 men, mean age 52 years, range 37-68) with type II diabetes and clinically significant macular edema. One group was composed of 9 patients presenting diffuse macular edema (DME); a second group with 9 patients presented cystoid macular edema (CME). All patients underwent pars plana vitrectomy. RESULTS: Preoperative Snellen visual acuity was 20/143 in DME and 20/441 in CME. In both groups vision increased to 20/136 and 20/205, respectively, postoperatively. For the DME this difference was statistically significant (p<0.05) at 1 month after the surgery, but vision decreased again after 10 months reaching preoperative values. CONCLUSIONS: Our results suggest that pars plana vitrectomy for diabetic macular edema may increase visual acuity in diffuse macular edema, although this increase is only short lived.

Adult↗
PubMed2004

[Brain edema].

The most frequent complication of an acute cerebral lesion is brain edema. With increasing size of brain edema an increase in intracranial pressure is observed. This leads to decreased cerebral perfusion and brain death. Cerebral edema can be subdivided into three groups: vasogenic, cytotoxic and interstitial brain edema. This classification is of relative importance because only the extracellular edema can be influenced by drugs. Clinical symptoms of brain edema are related to the increased intracranial pressure, associated with decreased cerebral microperfusion. Symptoms are headache, vomiting, vision disturbances and, with increased intracranial pressure, bradicardy, respiration disturbances and at the end brain death by compression of the cerebrum. Therapy is directed to the underlying disease. Unfortunately, even today specific therapeutical approaches are limited.

Brain↗
PubMed2004

[Edema in pregnancy--trivial?].

In pregnancy total body water increases. At least 25% of the fluid will be distributed to the interstitial space, ultimately clinically imposing as lower leg edema of pregnant women. Next to a cumulative sodium retention, altered local Starling forces and changes in the hydration of extracellular matrix add to the fluid shift. Edema have to be expected in most of the pregnant women and should not be used to diagnose preeclampsia. Atypical edema localization and local, unilateral edema should cast suspicion of other dangerous complications of pregnancy. Diuretics should be restricted to pulmonary edema of preeclampsia, but these drugs are not to be used to manage edema of pregnancy.

Body Weight↗
PubMed1990

Pathophysiological aspects of edema formation in diabetic nephropathy.

The present study was undertaken to evaluate some pathophysiological mechanisms of edema formation in diabetic nephropathy. Sixty-three subjects were investigated: 9 normal subjects (I), 9 normoalbuminuric Type 1 (insulin-dependent) diabetic patients (II), 15 microalbuminuric Type 1 diabetic patients (III), 16 Type 1 diabetic patients with nephropathy without edema (IV), and 14 Type 1 diabetic patients with nephropathy and edema (V). Plasma volume (125I-albumin), glomerular filtration rate and extracellular fluid volume (51Cr-EDTA) were measured. Colloid osmotic pressure and albumin concentration were measured in plasma and in subcutaneous interstitial fluid (suction blister technique). The ratio between plasma volume and interstitial fluid volume was reduced in patients with edema compared with group 1 (P less than 0.05). The interstitial colloid osmotic pressure (mm Hg) was significantly reduced (P less than 0.05) in group V compared with the other groups (V: 4.3 +/- 1.1, I: 7.9 +/- 1.7, II: 7.5 +/- 1.8, III: 6.6 +/- 1.5, IV: 6.6 +/- 1.1), but the transcapillary colloid osmotic gradient in patients with edema was comparable with the remaining subjects. The ratio between interstitial and plasma albumin concentration was significantly reduced in group V compared with groups I and II (V: 0.31 +/- 0.1, I: 0.43 +/- 0.06, II: 0.44 +/- 0.06; P less than 0.01; III: 0.41 +/- 0.07, IV: 0.41 +/- 0.08). This reduction was mainly due to enhanced lymph flow. The wash-down of subcutaneous interstitial protein indicated increased capillary filtration, but at the same time limited the increase in net filtration pressure and thereby prevented progressive edema formation in diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Brain edema induced by in vitro ischemia: causal factors and neuroprotection.

Decreased cerebral blood flow, hence decreased oxygen and glucose, leads to ischemic brain injury via complex pathophysiological events, including excitotoxicity, mitochondrial dysfunction, increased intracellular Ca2+, and reactive oxygen species (ROS) generation. Each of these could also contribute to cerebral edema, which is the primary cause of patient mortality after stroke. In vitro brain slices are widely used to study ischemia. Here we introduce a slice model to investigate ischemia-induced edema. Significant water gain was induced in coronal slices of rat brain by 5 min of oxygen and glucose deprivation (OGD) at 35 degrees C, with progressive edema formation after return to normoxic, normoglycemic medium. Edema increased with increasing injury severity, determined by OGD duration (5-30 min). Underlying factors were assessed using glutamate-receptor antagonists (AP5/CNQX), blockade of mitochondrial permeability transition [cyclosporin A (CsA) versus FK506], inhibition of Na+/Ca2+ exchange (KB-R7943), and ROS scavengers (ascorbate, Trolox, dimethylthiourea, Tempol). All agents except KB-R7943 and FK506 significantly attenuated edema when applied after OGD; KB-R7943 was effective when applied before OGD. Significantly, complete prevention of ischemia-induced edema was achieved with a cocktail of AP5/CNQX, CsA and Tempo applied after OGD, which demonstrates the involvement of multiple, additive mechanisms. The efficacy of this cocktail further shows the potential value of combination therapies for the treatment of cerebral ischemia.

2-Amino-5-phosphonovalerate↗
PubMed2003

Clinically significant facial edema after extensive treatment with purpura-free pulsed-dye laser.

BACKGROUND: Long-pulsed pulsed-dye lasers permit treatment of facial erythema and telangiectasia with purpura-free technique, which may be more comfortable for the patient than purpura-inducing treatment. However, there are anecdotal reports of treatment-associated discomfort even when purpura is not elicited. OBJECTIVE: To determine whether patients experience clinically significant erythema, edema, and pain after purpura-free treatment with pulsed-dye laser. METHODS: In this prospective, controlled study, subjects included 15 patients who were undergoing purpura-free treatment of diffuse erythema and fine telangiectasia of at least half the facial surface area with purpura-free pulsed-dye, and it included 15 age, gender, and skin-type matched control subjects who were undergoing similar treatments but with the induction of trace to mild purpura. Patients were seen in person and were surveyed by phone regarding symptoms and signs during their postoperative courses. RESULTS: Postoperative erythema of a mean 3.3-days duration and 3.4/5.0 intensity was reported by 73% (11 of 15) of the purpura-free patients. Among purpura patients, the duration was 5.6 days. The intensity was 4.0, and again, 73% of patients reported this finding. Postoperative edema occurred among 87% of purpura-free patients, but such edema occurred in all of the purpura patients, in whom it lasted longer and was more intense. Symptomatic eye swelling and uncomfortable/painful edema were seen in 27% and 20%, respectively, of purpura-free patients, but in 40% and 53% of purpura patients. Among purpura-free patients receiving fewer than 250 laser pulses per treatment, erythema and edema lasted less than 1 day and 2.5 days, whereas the mean durations were 3.4 and 5.0 days for purpura-free patients receiving greater than 250 pulses. CONCLUSION: Extensive purpura-free treatment for erythema and telangiectasia of the face with the long-pulsed pulsed-dye laser can lead to clinically significant erythema, edema, and discomfort in patients. The duration, magnitude, and frequency of these undesired effects are markedly less with purpura-free treatment compared with purpura-inducing treatment and are also less for less extensive purpura-free treatments.

Edema↗
PubMed2004

Melatonin suppresses cerebral edema caused by middle cerebral artery occlusion/reperfusion in rats assessed by magnetic resonance imaging.

Melatonin, a pineal secretory product synthesized from tryptophan, has been found to be effective against neurotoxicity. The present study was aimed at demonstrating the effectiveness of melatonin in vivo in reducing ischemia-induced cerebral edema using magnetic resonance imaging (MRI). Rats were subjected to middle cerebral artery (MCA) occlusion/reperfusion surgery. Melatonin was administered twice (6.0 mg/kg, p.o.) just prior to 1 hr of MCA occlusion and 1 day after the surgery. T2-weighted multislice spin-echo images were acquired 1 day after the surgery. In the saline-treated control rats, increases in T2-weighted signals (water content) were clearly observed in the striatum and in the cerebral cortex. In the melatonin-treated group, total volume of edema was reduced by 51.6% compared with control group (P < 0.01). The protective effect of melatonin against edema was more clearly observed in the cerebral cortex (reduced by 59.8%, P < 0.01) than in the striatum (reduced by 34.2%, P < 0.05). Edema volume in a coronal slice was the greatest at the level of the bregma. Suppression of cerebral edema by melatonin was more effective posterior than anterior to the bregma. Melatonin appeared to reduce the volume of the edematous sites rather than to shift the signal intensity distribution. The present MRI study clearly demonstrates the effectiveness of melatonin against cerebral edema formation in ischemic animals in vivo, especially in the cerebral cortex. Melatonin may be highly useful in preventing cortical dysfunctions such as motor, sensory, memory, and psychological impairments associated with ischemic stroke.

Animals↗
PubMed1999

[The significance of morphological changes in the brain-tumor border area for the pathogenesis of brain edema in meningiomas: magnetic resonance tomographic and intraoperative studies].

PURPOSE: The aim of the study was to verify a possible correlation between macroscopic changes of the brain-tumor interface (BTI) and the development of a peritumoral brain edema in meningiomas. METHODS: 27 meningiomas were investigated in this prospective study using an optimized inversion-recovery (IR) sequence. After i.v. administration of 0.2 mmol Gd-DTPA/kg axial and coronary images were acquired (slice thickness = 2 mm). The distances of signal altered cortex and obliterations of the subarachnoid space (SAS) were measured at the BTI and related to the pial tumor circumference (cortical-index and SAS-index). Intraoperatively the BTI was divided into the following categories: 0: SAS not obliterated, 1: SAS partially obliterated, 2: direct contact between tumor and white matter, 3: tumor infiltration into brain. RESULTS: Edema-associated meningiomas showed a significantly (p = 0.0001) increased SAS-index (0.47 vs. 0.07) and cortical index (0.45 vs. 0.0) compared to cases without edema. Intraoperatively 95% of meningiomas with brain edema showed SAS-obliterations, compared to 50% of cases without an edema. CONCLUSIONS: Arachnoid adhesions at the BTI with obliteration of the SAS seem to play an essential role in the induction of brain edema in meningiomas.

Adult↗
PubMed2000

Quantification of rebound edema after steroid treatment.

OBJECTIVE: Return of edema after abrupt discontinuation of steroid treatment has never been studied or quantified. The purpose of this study was to measure the effect of abrupt cessation and tapering doses of steroids on tissue water content (TWC) in a rat skin flap model. DESIGN: A randomized controlled animal trial was designed to study the effects of discontinuation of steroid on skin flap edema. The animals were assigned to a control group (C), a steroid group (S), an abrupt steroid cessation (SC) group, or a tapering steroid (ST) group. MAIN OUTCOME MEASURES: In each group the skin flaps were biopsied at 30 and 36 hours. TWC was determined by a biopsy-drying technique. RESULTS: A significant difference (P = 0.05) was found between the C and S groups and between the SC and S groups at both 30 and 36 hours, with the C group having the highest TWC. No significant difference was noted between the SC and C groups. The ST group had significantly less edema than the C group and similar TWC to that of the S group. CONCLUSION: Edema rebounded in the skin flaps after abrupt cessation of steroids (SC was not different from C), presumably because of destabilization of inflammatory mediators. The rebound effect was not observed in the ST group. The control of rebound edema by a tapering steroid protocol may be important in skin flap survival and may have implications for the management of airway edema.

Animals↗
PubMed2001

Incidence of pulmonary edema after tracheotomy for obstructive sleep apnea.

OBJECTIVE: The phenomenon of postobstructive pulmonary edema (POPE) has been associated with the relief of upper airway obstruction, which itself is fundamental to the pathophysiology of obstructive sleep apnea (OSA). A review of patients with OSA undergoing tracheotomy was performed to characterize this process. STUDY DESIGN: Retrospective chart review of study patients with OSA undergoing tracheotomy and of control patients without OSA undergoing tracheotomy for unrelated problems. Chest radiographs were reviewed in a double-blind fashion to score posttracheotomy changes in pulmonary status. SETTING: Academic tertiary referral center. RESULTS: Thirty (67%) of 45 OSA patients treated by tracheotomy had evidence of POPE, whereas only 5 (20%) of 25 control group patients had increased pulmonary edema. The remaining 15 (33%) of 45 OSA patients and 20 (80%) of 25 control patients had either no change or an improved pulmonary status. Those with OSA that developed POPE were mostly graded as having mild pulmonary edema (22/30, 73%). Far fewer were graded as having moderate pulmonary edema (6/30, 20%), and fewer still with severe pulmonary edema (2/30, 7%). Two (7%) of 45 patients with severe POPE died of complications related to cor pulmonale in the postoperative period. CONCLUSION: Results support maintaining a high index of suspicion for the development of postobstructive pulmonary edema in patients treated for OSA. Treatment options, such as positive pressure ventilation and diuresis, and an increased awareness of this condition may help reduce the morbidity and mortality associated with treatment of this disease.

Humans↗
PubMed1992

Renal revascularization for recurrent pulmonary edema in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients with arteriosclerotic renal artery occlusive disease.

Recurrent pulmonary edema in patients with poorly controlled hypertension and renal insufficiency appears to be a marker of bilateral renal artery occlusive disease. The effectiveness of renal revascularization to prevent recurrent pulmonary edema in this distinct subgroup with renal artery occlusive disease was analyzed in 17 consecutive patients treated at the University of Michigan Hospital between 1984 and 1990. Their mean preoperative blood pressure was 207/110 mm Hg, and mean serum creatinine clearance was 3.8 mg/dl. Pulmonary edema occurred despite evidence of normal ventricular function in 65% of these patients. Bilateral renal artery occlusive disease affected 94% of the patients, and 54% had an occluded renal artery. Renal revascularization was accomplished by iliorenal bypass (41%), aortorenal bypass (29%), endarterectomy (24%), and transluminal angioplasty (6%). Contralateral nephrectomy (41%) and concomitant aortic reconstruction (24%) were also required frequently. No postoperative deaths occurred, and no patient had early postoperative pulmonary edema. Control of hypertension was improved in all patients, two of whom were discharged from the hospital on no antihypertensive medications. Two of the three patients requiring dialysis before operation were able to discontinue dialysis after operation. Late follow-up (mean, 2.4 years) revealed hypertension to be cured in one patient (6%), and improved in 16 patients (94%). Pulmonary edema occurred in one patient during late follow-up. Late follow-up showed renal function (mean creatinine, 1.7 mg/dl) to be improved in 77%, stable in 12%, and worse in two patients; one required dialysis. A single episode of pulmonary edema in a patient with poorly controlled hypertension and renal insufficiency should prompt consideration of this clinical syndrome and early diagnostic angiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗