Search

We report the case of a 52-year-old hyperglycemic woman with type 2 diabetes and severe coronavirus disease 2019 (COVID-19)-associated pneumonia, possibly involving the subcutaneous insulin resistance (SIR) syndrome. After admission for pneumonia, her average daily blood glucose (BG) levels remained at 300–400 mg/dL, although the required dosage of subcutaneous insulin markedly increased (~ 150 units/day; ~ 2.63 units/kg/day). Furthermore, the patient had generalized edema along with hypoalbuminemia, developed extensive abdominal purpuras, and had increased plasma D-dimer levels during treatment, suggestive of coagulation abnormalities. Therefore, intravenous infusion of regular insulin was initiated. The BG level subsequently decreased to

In patients with diuretic resistance due to heart failure, higher doses or continuous furosemide infusion and adding hypertonic saline solution (HSS) to diuretics could be effective. The goal of this study was to assess the effectiveness of hypertonic saline solution administration in weight loss of hospitalized patients with diuretic-resistant edema due to heart failure. In a randomized double-blinded clinical trial, adult patients with diffuse peripheral edema due to heart failure who were unresponsive to 80 mg of oral furosemide were enrolled. The patients were randomized into two groups. In the intervention and control groups, patients received 150 mL of HSS and normal saline, respectively. Subjects in both groups received 250 mg IV furosemide every 12 h for 48 h. The change in body weight, urine output, blood pressure, uric acid, urine osmolality, blood biochemistry, and urinary cystatin C levels were assessed. Based on defined inclusion and exclusion criteria, 28 patients, 14 in each group, were recruited. The groups were similar in demographic and baseline laboratory characteristics. A significant decrease in body weight was observed in the intervention group (P = 0.002). The change in other measured parameters, including urine output and urinary cystatin C levels, was not reached statistical significance. Our findings suggest that the administration of HSS as an adjunct to loop diuretics could provide a safe and effective treatment for increasing urine output and decreasing weight in patients with heart failure.

We present a female in her sixties with mixed connective tissue disease who underwent (99m)Tc-human serum albumin diethylenetriaminepentaacetic acid ((99m)Tc-HSA-DTPA) scintigraphy to clarify the cause of generalized edema. Scintigraphy findings directed the diagnosis to protein-losing gastroenteropathy. Various disorders are known to be associated with protein-losing gastroenteropathy; however, mixed connective tissue disease is a rare cause. (99m)Tc-HSA-DTPA scintigraphy is helpful in the diagnosis and following the response to therapy of protein-losing gastroenteropathy.

A 30-year-old female with postpartum cardiomyopathy, chronic hepatitis C infection, and ongoing substance use disorder presented to an outside community hospital with generalized edema and dyspnea after having a week of myalgias, cough, and nasal congestion. Her social history was notable for

Le syndrome miroir ou syndrome de Ballantyne est une entité pathologique rare, définit par l´association d´une anasarque fœtale et d´un œdème maternel généralisé pouvant se compliquer d´une prééclampsie. L´objectif de ce travail est de mettre en exergue les particularités diagnostic et thérapeutique de cette entité clinique grave, qui, en dépit de sa rareté, ne doit pas être méconnu. Et ceux à travers la description d´un cas clinique d´une parturiente de 35 ans qui s´est présentée aux urgences, à 26 semaines d´aménorrhée, dans un tableau de syndrome miroir idiopathique dont l´évolution fut rapidement marquée par la survenue d´un décès in utéro puis régression de la symptomatologie clinico-biologique maternelle une fois la vacuité utérine obtenue. En effet, un traitement spécifique in utéro est vivement souhaitable. Quoique dans certains cas graves idiopathiques, seule l´obtention de la vacuité utérine permet l´amélioration du pronostic maternel voire fœtale.

Renal involvement in Waldenström’s macroglobulinemia is a rare manifestation. Although most renal involvement is due to monoclonal immune deposits, pathology can also be unrelated to it. Here, we describe a 68-year-old female with a history of Waldenström’s macroglobulinemia who presented with generalized edema and nephrotic range proteinuria. A renal biopsy showed findings consistent with focal segmental glomerulosclerosis. Treatment with oral prednisone leads to the resolution of proteinuria. This case highlights the importance of identifying pathology that might not be directly related to monoclonal gammopathy, which could have implications on the management.

Insulin edema is a rare complication of insulin therapy that can occur after the initiation of insulin. Various timelines to the initiation of insulin have been reported after insulin therapy. Here, we report the occurrence of generalized edema in a 40-year-old woman early after the initiation of insulin. Significant differentials were excluded and resolution achieved after two weeks with diuretics. We reviewed the current literature and the possible mechanisms behind this phenomenon.

Coupled plasma filtration adsorption (CPFA) is an extracorporeal supportive therapy based on nonspecific adsorption of pro- and anti-inflammatory mediators combined with continuous renal replacement therapy. The main field of CPFA application is septic shock, and there are limited data about its efficacy in the treatment of other acute conditions characterized by a dysregulation in immune homeostasis. Capillary leak syndrome (CLS) defines a life-threatening condition sustained by hypercytokinemia and characterized by abrupt onset of increased capillary permeability leading to severe generalized edema and hypovolemic shock refractory to fluid administration. Therapy for CLS is not specific and, at present time, it consists in the use of steroids or intravenous immunoglobulins. We present the case of a 34-year-old woman who developed CLS superimposed to acute generalized exanthematous pustulosis after initiating therapy with hydroxychloroquine for undifferentiated connective tissue disease. CLS did not respond to steroids and intravenous immunoglobulins, while it was successfully treated with CPFA. This observation supports the possible role of CPFA in restoring a proper immunologic homeostasis not only in sepsis but also in other devastating conditions sustained by hypercytokinemia.

Background Idiopathic systemic capillary leak syndrome (ISCLS), is a rare disorder characterized by recurrent attacks of varying severity of hypovolemic shock and generalized edema in association with hemoconcentration and hypoalbuminemia in the absence of albuminuria. The chronic form of ISCLS is extremely rare with only a few cases reported in the literature. Case presentation Here we report the case of a young woman who developed chronic ISCLS characterized by massive, generalized and persistent edema. The work up confirmed the presence of monoclonal gammopathy. She was treated with several agents with no response. Conclusion Chronic ISCLS is a very rare disease of unknown etiology and results in devastating complications. The medical community should be aware of this disease with the hope that targeted therapy will become available in the future.

Albiglutide is a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist administered by weekly injection. Albiglutide-treated patients experience incidences of adverse effects, including cardiovascular, renal, and gastrointestinal symptoms and injection-site reactions. We report the first case of generalized edema induced by albiglutide. We present a 35-year-old female with type-2 diabetes. She developed generalized edema after the start of albiglutide. Her physical examination and all the laboratory tests, including thyroid function tests, albumin level test, and renal function test were unremarkable, and did not explain her generalized edema. Later on, her albiglutide was discontinued, which lead to the resolution of her edema. We conclude that her generalized edema could be due to a possible side effect of albiglutide.

Objectives and Study: Protein losing enteropathy (PLE) is a rare complication following paediatric liver transplantation (LTx), mostly related to venous outflow obstruction of the liver. Here, we discuss diagnosing a thus far unknown cause of PLE following paediatric LTx and its surgical treatment. Method: Case-study Results: A boy received an LTx (segments 2 and 3, postmortal heart-beating donor, Roux-en-Y hepaticojejunostomy) at the age of 7 months because of ornithine transcarbamylase deficiency. At the age of 18 months, he developed generalized edema and ascites. PLE was diagnosed, as faecal alpha-1 antitrypsin levels were markedly increased. Clinically, he required suppletion of albumin intravenously every two weeks, for which a venous access port was implanted. Routine diagnostic work-up for PLE was negative. No infectious cause of PLE was found. Endoscopy (gastroduodeno-/ colonoscopy, capsule endoscopy) showed no mucosal injuries and no signs of lymphangiectasia. PET/CT scan showed no signs of post-transplant lymphoproliferative disorder. Vascular origin, most notably venous outflow obstruction, is a known cause of PLE following LTx. Therefore catheterisation was performed, which showed no signs of venous outflow obstruction (normal central venous pressure of 9 mm Hg in the inferior vena cava and normal pressure in the hepatic vein of 9 mmHg), and only a slightly increased wedge pressure in the hepatic vein (19 mmHg). A liver biopsy taken during the same procedure showed no relevant pathology. To find the localization of protein loss, an albumin scan (technetium-99m labeled albumin) was performed, which confirmed intestinal albumin loss. Of note, early recordings (dynamic 0-30 min and early static SPECT-CT recordings at 30, 60, 90 minutes after tracer injection instead of after 120 minutes) were done, to detect where albumin entered the intestine. The affected area on the albumin scan was where the Roux loop was expected. With regard to the albumin loss in the Roux loop, local bacterial overgrowth or local lymphangiectasia, possibly due to (venous) congestion, were considered. Treatment with Metronidazole did not improve albumin loss, rendering local bacterial overgrowth an unlikely cause of the PLE. Therefore a surgical revision of the Roux loop was performed. During the procedure, no torsion of the Roux loop was observed. The explanted loop macroscopically showed a small abnormal area with a thin hyperaemic mucosa (Figure 1A). Histological analysis showed focal lymphangiectasia (Figure 1B), which was considered the site of protein loss. Following surgical revision, PLE disappeared and serum albumin levels remained stable, up to now (6 months post-revision, Figure 1C). We suspect that the local PLE in the Roux loop arose from local congestion of lymphatic outflow. Conclusion: Here, we report diagnosing a thus far unknown cause of PLE following LTx in a child. The Roux loop was found to be the site of albumin loss using early SPECT-CT recordings during an albumin scan. Notably, this was in the absence of relevant portal hypertension. Surgical revision of the Roux loop has stopped the PLE up to now, 6 months post-revision (Figure presented).

Objectives and Study: Protein losing enteropathy (PLE) is a rare complication following paediatric liver transplantation (LTx), mostly related to venous outflow obstruction of the liver. Here, we discuss diagnosing a thus far unknown cause of PLE following paediatric LTx and its surgical treatment. Method: Case-study Results: A boy received an LTx (segments 2 and 3, postmortal heart-beating donor, Roux-en-Y hepaticojejunostomy) at the age of 7 months because of ornithine transcarbamylase deficiency. At the age of 18 months, he developed generalized edema and ascites. PLE was diagnosed, as faecal alpha-1 antitrypsin levels were markedly increased. Clinically, he required suppletion of albumin intravenously every two weeks, for which a venous access port was implanted. Routine diagnostic work-up for PLE was negative. No infectious cause of PLE was found. Endoscopy (gastroduodeno-/ colonoscopy, capsule endoscopy) showed no mucosal injuries and no signs of lymphangiectasia. PET/CT scan showed no signs of post-transplant lymphoproliferative disorder. Vascular origin, most notably venous outflow obstruction, is a known cause of PLE following LTx. Therefore catheterisation was performed, which showed no signs of venous outflow obstruction (normal central venous pressure of 9 mm Hg in the inferior vena cava and normal pressure in the hepatic vein of 9 mmHg), and only a slightly increased wedge pressure in the hepatic vein (19 mmHg). A liver biopsy taken during the same procedure showed no relevant pathology. To find the localization of protein loss, an albumin scan (technetium-99m labeled albumin) was performed, which confirmed intestinal albumin loss. Of note, early recordings (dynamic 0-30 min and early static SPECT-CT recordings at 30, 60, 90 minutes after tracer injection instead of after 120 minutes) were done, to detect where albumin entered the intestine. The affected area on the albumin scan was where the Roux loop was expected. With regard to the albumin loss in the Roux loop, local bacterial overgrowth or local lymphangiectasia, possibly due to (venous) congestion, were considered. Treatment with Metronidazole did not improve albumin loss, rendering local bacterial overgrowth an unlikely cause of the PLE. Therefore a surgical revision of the Roux loop was performed. During the procedure, no torsion of the Roux loop was observed. The explanted loop macroscopically showed a small abnormal area with a thin hyperaemic mucosa (Figure 1A). Histological analysis showed focal lymphangiectasia (Figure 1B), which was considered the site of protein loss. Following surgical revision, PLE disappeared and serum albumin levels remained stable, up to now (6 months post-revision, Figure 1C). We suspect that the local PLE in the Roux loop arose from local congestion of lymphatic outflow. Conclusion: Here, we report diagnosing a thus far unknown cause of PLE following LTx in a child. The Roux loop was found to be the site of albumin loss using early SPECT-CT recordings during an albumin scan. Notably, this was in the absence of relevant portal hypertension. Surgical revision of the Roux loop has stopped the PLE up to now, 6 months post-revision (Figure presented).

Objectives and Study: Protein losing enteropathy (PLE) is a rare complication following paediatric liver transplantation (LTx), mostly related to venous outflow obstruction of the liver. Here, we discuss diagnosing a thus far unknown cause of PLE following paediatric LTx and its surgical treatment. Method: Case-study Results: A boy received an LTx (segments 2 and 3, postmortal heart-beating donor, Roux-en-Y hepaticojejunostomy) at the age of 7 months because of ornithine transcarbamylase deficiency. At the age of 18 months, he developed generalized edema and ascites. PLE was diagnosed, as faecal alpha-1 antitrypsin levels were markedly increased. Clinically, he required suppletion of albumin intravenously every two weeks, for which a venous access port was implanted. Routine diagnostic work-up for PLE was negative. No infectious cause of PLE was found. Endoscopy (gastroduodeno-/ colonoscopy, capsule endoscopy) showed no mucosal injuries and no signs of lymphangiectasia. PET/CT scan showed no signs of post-transplant lymphoproliferative disorder. Vascular origin, most notably venous outflow obstruction, is a known cause of PLE following LTx. Therefore catheterisation was performed, which showed no signs of venous outflow obstruction (normal central venous pressure of 9 mm Hg in the inferior vena cava and normal pressure in the hepatic vein of 9 mmHg), and only a slightly increased wedge pressure in the hepatic vein (19 mmHg). A liver biopsy taken during the same procedure showed no relevant pathology. To find the localization of protein loss, an albumin scan (technetium-99m labeled albumin) was performed, which confirmed intestinal albumin loss. Of note, early recordings (dynamic 0-30 min and early static SPECT-CT recordings at 30, 60, 90 minutes after tracer injection instead of after 120 minutes) were done, to detect where albumin entered the intestine. The affected area on the albumin scan was where the Roux loop was expected. With regard to the albumin loss in the Roux loop, local bacterial overgrowth or local lymphangiectasia, possibly due to (venous) congestion, were considered. Treatment with Metronidazole did not improve albumin loss, rendering local bacterial overgrowth an unlikely cause of the PLE. Therefore a surgical revision of the Roux loop was performed. During the procedure, no torsion of the Roux loop was observed. The explanted loop macroscopically showed a small abnormal area with a thin hyperaemic mucosa (Figure 1A). Histological analysis showed focal lymphangiectasia (Figure 1B), which was considered the site of protein loss. Following surgical revision, PLE disappeared and serum albumin levels remained stable, up to now (6 months post-revision, Figure 1C). We suspect that the local PLE in the Roux loop arose from local congestion of lymphatic outflow. Conclusion: Here, we report diagnosing a thus far unknown cause of PLE following LTx in a child. The Roux loop was found to be the site of albumin loss using early SPECT-CT recordings during an albumin scan. Notably, this was in the absence of relevant portal hypertension. Surgical revision of the Roux loop has stopped the PLE up to now, 6 months post-revision (Figure presented).

Idiopathic cyclic edema is a type of generalized edema that mainly affects women. Diagnosis is made by the patient’s clinical history and an evaluation of the accumulation of weight during the day. The objective of this study is to report the clinical control of lymphedema associated with idiopathic cyclic edema using calcium dobesilate. A 55-year-old female patient reported generalized edema for years in that she woke up in the morning with her legs swollen and the edema worsened during the day. The physical examination revealed generalized edema. After four days of treatment with calcium dobesilate, the patient returned to the Clínica Godoy, Brazil, with less edema and reductions in body weight and the amount of extracellular and intracellular fluid. With further treatment, there was a total reduction of the edema. It is concluded that calcium dobesilate helps to control lymphedema secondary to idiopathic cyclic edema.

International audience; Introduction: Systemic capillary leak syndrome (SCLS) is a rare disease characterized byrecurrent episodes and a triad of “leak attacks”: hypovolemic shock, generalized edema, hemoconcentration and paradoxical hypoalbuminemia. Case study and discussion: Here we report a case of pediatric idiopathic SCLS with an episode of cough and fever followed two days later by myalgia, livedo, acrocyanosis, and five days later by edema, tachycardia, hypotension, and generalized tonic-clonic seizure. Moreover, we provide evidence for an LPS-induced overproduction of interferon-gamma and interleukin-17 by the patient's peripheral blood mononuclear cells one year after the attack.Conclusion: This observation suggests the involvement of IL-17 in the pathogenesis of this disease.

Generalized edema is a major presenting clinical feature of children with nephrotic syndrome (NS) exemplified by such primary conditions as minimal change disease (MCD). In these children with classical NS and marked proteinuria and hypoalbuminemia, the ensuing tendency to hypovolemia triggers compensatory physiological mechanisms, which enhance renal sodium (Na(+)) and water retention; this is known as the "underfill hypothesis." Edema can also occur in secondary forms of NS and several other glomerulonephritides, in which the degree of proteinuria and hypoalbuminemia, are variable. In contrast to MCD, in these latter conditions, the predominant mechanism of edema formation is "primary" or "pathophysiological," Na(+) and water retention; this is known as the "overfill hypothesis." A major clinical challenge in children with these disorders is to distinguish the predominant mechanism of edema formation, identify other potential contributing factors, and prevent the deleterious effects of diuretic regimens in those with unsuspected reduced effective circulatory volume (i.e., underfill). This article reviews the Starling forces that become altered in NS so as to tip the balance of fluid movement in favor of edema formation. An understanding of these pathomechanisms then serves to formulate a more rational approach to prevention, evaluation, and management of such edema.

Introduction Idiopathic systemic capillary leak syndrome is a rare and fatal disease due to the unexplained episodic attacks of capillary leakage of plasma from the intravascular into the interstitial space. The attack consists of three phases, a prodromal phase, peripheral leak phase and recruitment phase. During the peripheral leak phase, generalized edema, mainly in the trunk and extremities, with hemoconcentration and hypoalbuminemia occurs, while usually the visceral organs like lungs, brain, heart and kidneys seem not to be involved. Treatment of the acute phase is supportive, focusing on adequate but not overzealous fluid resuscitation, because pulmonary edema usually occurs in the recruitment phase. Case presentation A 65-year-old Japanese woman was admitted to our hospital because of severe hypovolemic shock with metabolic acidosis and hemoconcentration and hypoalbuminemia. Although she was considered to be in the peripheral leak phase of idiopathic systemic capillary leak syndrome, which could not be diagnosed during the treatment, the generalized edema worsened further, severe flash pulmonary edema progressed rapidly after fluid resuscitation and she died. The autopsy showed generalized edema, especially alveolar pulmonary edema without endothelial apoptosis. Conclusions Because hypovolemic shock and fatal pulmonary edema may progress rapidly together even in the peripheral leak phase of idiopathic systemic capillary leak syndrome, we should keep in mind this rare and fatal disease and recognize the pathophysiology to treat it effectively when the patient has hypovolemia with metabolic acidosis.

Motoko Kanzaki,1 Jun Wada,1 Yoko Kikumoto,1 Shigeru Akagi,1 Kazushi Nakao,3 Hitoshi Sugiyama,2 Hirofumi Makino11Department of Medicine and Clinical Science, 2Department of Chronic Kidney Disease and Peritoneal Dialysis, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan; 3Internal Medicine, Hiroshima City Hospital, Hiroshima, JapanBackground: In nephrotic syndrome, the combination of furosemide and albumin infusion is a standard regimen to treat systemic edema. The efficacy of synthetic human atrial natriuretic peptide (hANP) for nephrotic syndrome to ameliorate the systemic edema and retain renal functions has not been fully demonstrated.Trial design: We conducted a prospective, randomized, controlled, open-label clinical trial. Patients were randomly assigned by a stratified biased coin design.Methods: A total of 12 patients with nephrotic syndrome between the ages of 20 to 79 years were enrolled and randomly assigned to either the conventional (CON) group treated with furosemide and albumin, and hANP group, in which carperitide was administered in addition to the conventional therapies. The primary end points were: (1) the differences in serum creatinine levels, and (2) the reduction of total dosage of furosemide and albumin by the treatments of hANP. Secondary end points were body weight, systolic blood pressure, heart rate, serum protein, albumin, and urinary protein excretion.Results: A total of 13 patients were enrolled, and one patient was excluded due to severe pneumonia. In both hANP (n = 7) and CON (n = 5) groups, body weight was reduced after 2-week treatments. Serum creatinine levels at follow-up significantly increased compared with baseline. The increase in serum creatinine levels (Δ serum creatinine) was smaller in the hANP group compared with the CON group (P = 0.31). The serum uric acid, serum urea nitrogen, and urinary protein excretion were reduced in the hANP group, and increased in the CON group, though these differences were not statistically significant. The usage of hANP significantly reduced the total dosage of furosemide (P < 0.05) during the treatment periods. No adverse effects were observed.Conclusions: The concomitant use of synthetic hANP with conventional therapies is beneficial for reducing the dosage of loop diuretics, and the elevation of serum creatinine and uric acid may be avoided.Keywords: furosemide, generalized edema, human natriuretic peptide, nephrotic syndrome&nbsp

The present case study is on a 16-year-old woman who was suffering from nephrotic syndrome after recovery from complete type of hydatiform mole. She was admitted in hospital because of proteinurea and hematuria. Then she was showing a generalized edema compatible with neprhotic syndrome. In her past medical history she had a suction curettage for hydatiform mole. After she received 4 courses chemotherapy, she completely recovered and βhCG has fallen from 12127 IU/L to under 10 IU/mL. Then she showed generalized edema, proteinurea and hematuria compatible with nephritic syndrome. After six courses chemotherapy the symptoms of nephrotic syndrome and invasive mole diminished, she released from hospital and scheduled for follow-up.

A 24-yr-old, 65-kg, 152-cm primigravida woman with severe pre-eclampsia and a history of asthma was admitted at 38 weeks’ gestationfor magnesium administration and oxytocin induction of labor. Herlaboratory studies and physical examination were within normal limitsexcept for proteinuria, hypertension, and moderate generalized edemawithout obvious facial edema at admission. Because of her preeclamp-sia, an epidural catheter was easily inserted early before onset of activelabor or pain. Three hours later, the patient had a witnessed tonic–clonic eclamptic seizure, which subsided shortly after administrationof 4 mg intravenous lorazepam and assisted mask ventilation. Becauseof recurring fetal heart rate deceleration, an urgent cesarean deliverywas planned. However, the patient was combatively uncooperativedespite a bilateral T4 anesthetic level achieved epidurally while heroxygen saturation remained 100% and blood pressure was 140/85mmHg. The patient was noted to have a Mallampati class I airway withmoderate generalized edema and mild facial edema. Rapid sequencegeneral anesthesia induction was performed with successful atrau-matic intubation on the first attempt, followed by verification of bilat-eral symmetrical breath sounds. Maintenance of anesthetic consisted ofvolume-controlled mechanical ventilation, 50% oxygen, 50% nitrousoxide, 1–2% sevoflurane, midazolam, and opioid without the need foradditional neuromuscular blocker other than succinylcholine at induc-tion. Intraoperative blood pressure and heart rate were maintainedwithin 20% of preoperative values while oxygen saturation was main-tained at 99–100%, end-tidal carbon dioxide between 30–35 mmHg,and airway pressures less than 25 cm H

The occurrence of nephrotic syndrome following a bee sting is rarely reported in the literature. Hypersensitivity is believed to be the precipitating factor for the renal disease. We report a two-year-old boy, who developed generalized edema and decreased urine output, seven days after a bee sting. Physical examination and laboratory findings were consistent with nephrotic syndrome; and corticosteroid treatment induced prompt remission with resolution of clinical symptoms and normalization of laboratory findings. There was no relapse of the disease during a one-year follow up.

A 7-year-old girl presenting with an 8-week history of fatigue, myalgia, dyspnea, and generalized, nonpitting edema of the extremities, face, chest, and abdomen, is reported from the Walter Reed Army Medical Center, Washington, DC.

Various manifestations after bee sting have been described. Local reactions, such as pain, wheal, flare, edema and swelling, are common and generally self-limiting. Uncommonly manifestations like vomiting, diarrhea, dyspnea, generalized edema, acute renal failure, anaphylactic shock, myocardial infarction, hypotension, collapse, pulmonary hemorrhage, acute hemorrhagic pancreatitis, and atrial fibrillation may occur. We report a 59 year-old man who sustained ischemic stroke and multi-organ dysfunction following multiple bee stings. Keywords: Bee sting, Acute stroke, Emergency department