Pretibial Myxedema - Case Report

Pretibial Myxedema - Case Report
Jeanie Chung-Leddon,MD,PhD
Dermatology Online Journal
7(1): 18Department of Dermatology, New York University

PATIENT: 75-year-old woman
DURATION: One month
DISTRIBUTION: Left shin

History

The patient noticed a non-tender, erythematous nodule on the left shin approximately one month ago. The lesion grew slowly in size, and new lesions developed near the original nodule. She denied a history of trauma to the leg, fevers, chills, sore throat, cough, night sweats, or weight loss. Indomethacin 25 mg three times daily for two weeks was administered with no resolution of the lesions. She has been taking levothyroxine since radiation treatment to the thyroid for Grave's disease.

Physical Examination

On the left lateral and anterior aspect of the shin, there were three, erythematous, indurated nodules and plaques with no ulcers. The lesions were neither warm nor tender to the touch. Bilateral exophthalmos was noted but there was no appreciable thyromegaly or nodularity in the thyroid.

Laboratory Data

Complete blood count showed a white cell count of 7.5 x 109/L, hemoglobin 12.5 gm/dl, hematocrit 37.6%, and platelets 251x 109/L. Streptozyme test was negative; thyroid function tests and free T4 levels were normal. There were no infiltrates noted on a chest radiograph, however a purified protein derivative test was positive at 48 hours.

Histopathology

The upper dermis was thickened by extensive deposits of mucin that separated the collagen fibers. The epidermis and papillary dermis were spared.

Diagnosis

Pretibial myxedema

Comment

Pretibial myxedema can be present in either Grave's disease or hypothyroidism. Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsa of the feet.[1] The lesions can be morphologically variable, but commonly they consist of pink, flesh-colored to violaceous nodules. The skin can also present with a diffuse brawny edema without the nodules or in rare cases with elephantiasis nostras . In Grave's disease, myxedema tends to occur in the presence of ophthalmopathy at a later stage in the disease. One half of the cases of myxedema occur after the patient becomes euthyroid with treatment. Other manifestations of thyrotoxicosis include warm, moist and smooth skin, often accompanied by persistent flushing of the face, redness of the elbows, and palmar erythema. Other presentations can include chronic urticaria, alopecia areata, generalized pruritus, and hyperpigmentation.

Primary hypothyroidism or Hashimoto's thyroiditis can have similar myxedematous involvement in a diffuse or acral distribution. Facial changes can be characteristic with a broad nose, thick lips, large tongue, sticky secretions on the eyelids, and droopy eyelids.

Myxedema in both hyperthyroid and hypothyroid conditions results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin. The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts.[2,3] The fibroblasts in the orbital and pretibial dermis share antigenic sites that underlie the autoimmune process that causes Grave's disease. This cross-reaction may contribute to the development of myxedema occurring long after euthyroid status is achieved through treatment.

Treatment for myxedema is difficult. Systemic or intralesional glucocorticoids, topical glucocorticoids under occlusion or high-dose intravenous immunoglobulin have been reported to offer some relief.[4,5]

References

1. Fatourechi V, Pajouhi M, Fransway AF. Dermopathy of Graves disease (pretibial myxedema).Review of 150 cases. Medicine (Baltimore). 1994 Jan;73(1):1-7. PubMed

2. Chang TC, Wu SL, Hsiao YL, Kuo ST, Chien LF, Kuo YF, Change CC, Chang TJ. TSH and TSH receptor antibody-binding sites in fibroblasts of pretibial myxedema are related to the extracellular domain of entire TSH receptor. Clin Immunol Immunopathol 1994;71(1):113-20. PubMed

3. Stadlmayr W, Spitzweg C, Bichlmair AM, Heufelder AE. TSH receptor transcripts and TSH receptor-like immunoreactivity in orbital and pretibial fibroblasts of patients with Graves' ophthalmopathy and pretibial myxedema. Thyroid. 1997 Feb;7(1):3-12. PubMed

4. Volden G. Successful treatment of chronic skin diseases with clobetasol propionate and a hydrocolloid occlusive dressing. Acta Derm Venereol 1992;72(1):69-71. PubMed

5. Antonelli A, Navarranne A, Palla R, Alberti B, Saracino A, Mestre C, Roger P, Agostini S, Baschieri L. Pretibial myxedema and high-dose intravenous immunoglobulin treatment. Thyroid 1994;4(4):399-408. PubMed

Dermatology On Line

Ultrasound Findings of Acute Idiopathic Scrotal Edema

Ultrasound Findings of Acute Idiopathic Scrotal Edema

A. Craig Thomas
Mark P. Cain
Anthony J. Casale
Richard C. Rink

Department of Urology, Indiana University School Of Medicine
Corresponding Author:Mark P. Cain, MDRiley Hospital for Children
Suite 1739702 Barnhill DriveIndianapolis, IN 46202
mpcain@iupui.edu
(317)274-7446Fax: (317) 274-7481

Idiopathic scrotal edema is an uncommon cause of acute scrotal problems in children. This is a diagnosis that can be confirmed with color Doppler ultrasound, thus obviating the need for surgical exploration.1-4 Although the literature documents the benefit of Doppler ultrasound in identifying blood flow to the testis in these patients, there is little mentioned with regards to the scrotal wall changes on ultrasound.5-7

We submit ultrasound findings in three boys that presented to us with characteristic findings of idiopathic scrotal edema, each of which had significant scrotal wall subcutaneous edema on ultrasound examination.All three patients presented with acute onset of scrotal swelling and erythema. Scrotal ultrasound demonstrated similar findings in all three patients, including normal appearing testicular parenchyma and excellent blood flow to both testes. There was significant peritesticular edema with the appearance of considerable fluid in the scrotal wall (see Figure 1 and 2), with marked thickening of the subcutaneous tissues.

There was also a significant increase in the vascularity of the scrotal skin and subcutaneous tissues. One patient was admitted overnight for IV antibiotics due to the severity of the scrotal wall edema. Two patients received oral Benadryl for the presumed diagnosis of idiopathic scrotal edema. Recovery was uncomplicated, with complete resolution of symptoms within 48 hours in all 3 patients. The findings of significant scrotal wall edema on ultrasound examination of patients with idiopathic scrotal edema are most likely underreported in the literature. This is consistent with the disease process and together with findings of normal testicular blood flow, would assist in confirming the diagnosis in patients with suspected idiopathic scrotal edema, and permit conservative management with the avoidance of unnecessary scrotal exploration.

Bibliography

Grainger AJ, Hide, GH, Simon TE: The ultrasound appearances of scrotal oedema. European J of Ultrasound 8: 33-37, 1998.
Lerner RM, Mevorach RA, Hulbert WC, Rabinowitz R: Color Doppler US in the evaluation of acute scrotal disease. Radiology 176: 355-358, 1990.
Rabinowitz R, Hulbert WC: Acute scrotal swelling. Urologic Clinics of North America 22: 101-105, 1995.4.
Sasso F, Nucci G, Palmiotto F, et al.: Acute idiopathic scrotal oedema: rare disorder or difficult diagnosis?. International urology and nephrology 22: 475-478, 1990.
Melekos MD, Asbach HW, Markou SA: Etiology of acute scrotum in 100 boys with regard to age distribution. J Urol 139: 1023-1025, 1988.
Najmaldin A, Burge DM: Acute idiopathic scrotal oedema: incidence, manifestations and aetiology. Br J Surg 74: 634-635, 1987.Brandes SB, Chelsky MJ, Hanno PM: Adult acute idiopathic scrotal edema. Urology 44: 602-605, 1994.

Journal of Urology

Insulin-Induced Edema

Insulin-induced oedema in children and adolescents.

J Paediatr Child Health. 2006 Oct;42(10):655-7

Oedema is an uncommon complication of insulin therapy, which has only rarely been reported in childhood. We describe a case of a 12-year-old girl with newly diagnosed type 1 diabetes, who presented with oedema of the lower extremities and periorbitally, one day after the initiation of insulin treatment. Other causes of oedema were excluded. Following administration of frusemide, oedema resolved within ten days. An extended review of the literature revealed only nine cases of insulin-induced oedema in children and adolescents aged 16 years or less.

In conclusion, insulin-induced oedema should be considered during the introduction of insulin therapy in children and adolescents with newly diagnosed type 1 diabetes. Loop diuretics and ephedrine may be beneficial when spontaneous resolution does not occur.

PMID: 16972977 [PubMed - in process]

* * *

Generalized edema following insulin treatment of newly diagnosed diabetes mellitus


Juliusson PB,
Bjerknes R,
Sovik O,
Kvistad PH.
Barneklinikken Haukeland Sykehus 5021 Bergen. pjul@haukeland.no

BACKGROUND:

Generalised oedema after introducing insulin therapy is an infrequent complication, usually appearing when large doses are used in underweight patients. The pathophysiology is unclear.

MATERIALS AND METHODS:

Two patients from two different hospitals are presented by case histories. A limited literature search was performed.

RESULTS:

Patient 1. A 13-year-old girl was admitted with polyuria and polydipsia and a weight loss of 15 kg over six months. She had ankle oedema, dry scaling skin, weight 31.6 kg (2 kg below 2.5th centile), marked hyperglycaemia (60 mmol/l), and ketonuria without acidosis. After one day with insulin infusion she was treated with subcutaneous injections, reaching after a few days a dose of 2 U/kg/day. She gradually developed generalised oedema and gained 20 kg over two weeks. From day 8 after admission she was treated with furosemide and from day 16 also with ephedrine. S-albumin reached a nadir of 25 g/l. The oedema gradually disappeared. The patient was discharged after one month, weighing 42 kg, and with a daily insulin dose of 88 U. Patient 2. A 14-year-old girl presented with decreased vision over a period of six months. She felt otherwise healthy and had no weight loss. Bilateral cataract and hyperglycaemia (20.7 mmol/l) were detected. There were normal serum electrolytes and no acidosis. After administration of insulin (increased up to 1.5 U/kg/day) she gradually developed generalised oedema, gaining 8.5 kg over nine days. S-albumin fell from 36 g/l to 28 g/l. She was treated with furosemide and the oedema gradually disappeared in the course of one month. None of the patients had proteinuria, liver failure or hyperaldosteronism, but both experienced transient and unexplained muscle pain and neuralgic pain in the legs.

INTERPRETATIONS:

One of the cases with newly diagnosed diabetes and generalised oedema presented here, supports suggestions in the literature of an association between marked weight loss and large insulin doses. However, as shown by the other case presented, this association is not obligate.

PMID: 11332378 [PubMed - indexed for MEDLINE]

Acute Vasogenic Edema Induced by Thrombosis of a Giant Intracranial Aneurysm

Acute Vasogenic Edema Induced by Thrombosis of a Giant Intracranial Aneurysm: A Cause of Pseudostroke after Therapeutic Occlusion of the Parent Vessel

American Journal of Neuroradiology 24:1237-1239, June-July 2003

Dima Hammouda, Philippe Gaillouda, Alessandro Olivib and Kieran J. Murphya
a Department of Interventional Neuroradiology, the Johns Hopkins Medical Institutions, Baltimore, MDb Cerebrovascular Surgery, the Johns Hopkins Medical Institutions, Baltimore, MD
Address reprint requests to Philippe Gailloud, MD, Interventional Neuroradiology, Department of Radiology and Radiological Sciences, the Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287

Abstract

Summary: A 16-year-old male adolescent presenting with acute retro-orbital pain underwent emergent internal carotid occlusion for a giant cavernous aneurysm. Three weeks later, the patient complained of headache and right hemiparesis, which suggested an acute stroke. CT and MR imaging revealed vasogenic brain edema without infarct. The symptoms rapidly resolved with steroid therapy. Follow-up CT showed resolution of the edema. The imaging characteristics, clinical implications, and etiology of vasogenic edema occurring after thrombosis of a giant intracranial aneurysm are discussed.

Introduction

Giant intracranial aneurysm thrombosis, occurring either spontaneously or after therapeutic occlusion of the parent vessel, may become symptomatic by exerting mass effect on surrounding neural and vascular structures. In rare instances, expansion of the thrombosed aneurysm can eventually lead to an ischemic event in the adjacent brain parenchyma (1). On the other hand, the association of aneurysmal thrombosis with vasogenic brain edema, although exceptional, may wrongly suggest the diagnosis of brain infarction (2, 3). We present a case of symptomatic temporal lobe edema occurring 3 weeks after therapeutic occlusion of the internal carotid artery (ICA) for the treatment of a giant cavernous aneurysm. The imaging characteristics, etiology, and clinical implications of vasogenic edema following aneurysmal thrombosis are discussed.

Case Report

A 16-year-old male adolescent with no remarkable medical history presented to the emergency department with acute left retro-orbital pain. CT scans documented a mass lesion in the left cavernous sinus region; the mass invaded the sphenoid sinus and the middle cranial fossa. Digital subtraction angiography (DSA) revealed a giant aneurysm arising from the cavernous portion of the left ICA, extending medially and superiorly into the middle cranial fossa and inferiorly into the sphenoid sinus (Fig. 1). After successful completion of a carotid occlusion test, therapeutic occlusion of the left ICA with a silicone detachable balloon (Target Therapeutics, Natick, MA) was performed and followed by the proximal delivery of three Guglielmi detachable coils (Target). Control angiograms obtained after ICA occlusion showed no opacification of the aneurysmal cavity despite the presence of brisk collateral flow toward the left cerebral hemisphere via both the anterior and posterior communicating arteries. The immediate follow-up findings were unremarkable. A postprocedural CT scan obtained 2 days after ICA occlusion showed a heterogeneous increase in attenuation within the aneurysmal cavity, consistent with ongoing thrombosis. The patient was discharged home 72 hours after the procedure. He was examined twice during the following week for episodes of mild epistaxis. Each time, the clinical findings were unremarkable. A repeat head CT scan obtained 10 days after the procedure continued to show a thrombosed aneurysmal cavity, less heterogeneous in appearance, but without other interval changes. Three weeks after the intervention, the patient complained of severe headache and a right hemiparesis of sudden onset that suggested a left-sided ischemic event. A left temporal-lobe hypoattenuation was documented by CT (Fig 2). The aneurysmal cavity was hypoattenuating centrally and hyperattenuating peripherally. Its size (3.5 cm) was unchanged when it was compared on the previous CT scans. Emergency brain MR imaging confirmed the presence of a 3.5-cm left parasellar mass consistent with the thrombosed aneurysm. In the left temporal lobe, the white matter immediately surrounding the aneurysm appeared hypointense on T1-weighted images and hyperintense on T2-weighted and fluid-attenuated inversion recovery images (Fig 3). The cortical gray matter was spared. Diffusion-weighted (DW) imaging and apparent diffusion coefficient maps were unremarkable, with no evidence of cytotoxic edema (Fig 4). The imaging characteristics were compatible with vasogenic edema. The patient’s symptoms rapidly regressed with steroid therapy, and the patient was discharged home 3 days later with no residual neurologic signs or symptoms. Except for the thrombosed aneurysmal cavity, findings on a CT scan obtained 2 months later were normal. The patient was neurologically intact at the 12-month follow-up visit.

Discussion

Occurring as a consequence of intracranial aneurysm thrombosis, stroke has been described and attributed to different mechanisms. One mechanism is extension of the thrombus from the aneurysmal cavity into the parent vessel, as Brownlee et al described (4). In their report, spontaneous thrombosis extended from an unruptured aneurysm in the anterior communicating artery into the left middle and both anterior cerebral arteries. An alternative mechanism is compression of the parent artery by a large thrombosed aneurysm followed by secondary thrombus formation within the parent vessel. This process has been documented in a case of spontaneous thrombosis of a middle cerebral artery aneurysm (J. Simon et al, unpublished data, 2001). Stroke can also be observed during or after coiling of an endovascular therapeutic aneurysm. This occurrence may be due to release of clot fragments from a partially thrombosed aneurysmal cavity into the cerebral circulation. Although these thromboembolic events can have dramatic consequences, they appear to remain clinically silent in most instances (5). Brain infarction can also occur after therapeutic occlusion of the parent vessel aimed at excluding the aneurysmal cavity from the circulation. A careful angiographic evaluation of the potential collateral supply, as well as the performance of an occlusion test before definitive vessel occlusion, are essential in keeping the risk of such a complication as low as possible.

On the other hand, an ischemic event can complicate an otherwise successful treatment. In this situation, the mechanisms are similar to those associated with spontaneous aneurysm thrombosis; that is, compression of the parent artery by the expanding aneurysm (1) or extension of the thrombus into the lumen of the parent vessel.

Our 16-year-old patient presented with a giant aneurysm of the left ICA that was treated by occluding the parent vessel with a combination of detachable balloon and coils, after a successful balloon occlusion test. The first follow-up CT scan obtained 2 days after the procedure showed a heterogeneous increase in attenuation within the aneurysmal cavity compatible with ongoing thrombosis. The patient was discharged neurologically intact. A second routine follow-up CT study performed 10 days later revealed a decrease in heterogeneity, again consistent with evolving thrombosis of the aneurysm. Three weeks after the intervention, the patient returned, complaining of acute headache and a sudden onset of right hemiparesis. The diagnosis of a left hemispheric stroke was immediately suspected in the emergency department, and it was initially suggested by a large temporal-lobe hypoattenuation depicted on CT scans. However, careful analysis of the CT findings showed sparing of the cortical gray matter; this finding was inconsistent with an ischemic process. The appearance of the aneurysmal cavity was consistent with ongoing thrombosis, and its size was unchanged. Brain MR imaging further clarified the nature of the lesion by confirming the absence of cortical involvement. Normal DW images documented the noncytotoxic origin of the white matter edema and therefore ruled out the diagnosis of acute stroke. On the basis of the imaging findings, steroid therapy was immediately started, with a rapid improvement of the patient’s symptoms. He was discharged home 3 days later with no residual symptoms.

The imaging appearance of the aneurysm after occlusion of the ICA (ie, decreasing intraaneurysmal heterogeneity on the successive CT scans) suggests progressive thrombosis of the aneurysmal cavity; this process was completed at about 3 weeks, when the patient was admitted to the hospital for the episode of acute vasogenic edema. This time course is consistent with the pattern of thrombus formation that Strother et al (6) documented in giant aneurysms after occlusion of the parent vessel. In their study, serial MR images showed an increase in mass effect at the time of thrombus completion, which took place as late as 6 weeks after the procedure. A similar phenomenon was considered in our patient, who presented with acute symptoms 3 weeks after ICA occlusion. However, no enlargement of the aneurysmal cavity was observed, and no other sign of increased mass effect was depicted on the CT or MR images. Massive vasogenic edema has also been associated with spontaneous thrombosis of otherwise asymptomatic giant intracranial aneurysms (7, 8). An increase in the size of the aneurysm after thrombosis with secondary breakdown of autoregulation and swelling of the adjacent brain parenchyma was proposed as a potential mechanism (2). Compromise of venous drainage in the vicinity of the enlarged aneurysmal cavity could also play a role in such instances. In a recent study, the CBF in the area of perianeurysmal vasogenic edema was found to be reduced, with a return to baseline values after the edema resolved. The authors suggested that the enlargement of acutely thrombosing aneurysms result in loss of vasoresponsivity and ischemia (9). Again, these potential mechanisms seem unlikely in our patient, when we consider the absence of aneurysm enlargement and increased mass effect. The development of an inflammatory process in the brain parenchyma surrounding the thrombosed aneurysm has been suggested as an alternate explanation for the edematous reaction. However, no chemical mediators have yet been linked to perianeurysmal vasogenic edema (10), for which the exact mechanism remains unclear at this time.

Conclusion

Symptomatic vasogenic edema can be observed in the brain parenchyma surrounding a thrombosed intracranial aneurysm. Although infrequent, vasogenic edema must be included in the differential diagnosis of strokelike symptoms occurring in the context of spontaneous or therapeutically induced thrombosis of an intracranial aneurysm. MR imaging is important in establishing the definitive nature of the event by demonstrating vasogenic rather than cytotoxic edema on DW images. In our experience, steroid treatment has been proved effective in reducing the extent and clinical impact of the edematous reaction.

References:

Blanc R, Weill A, Piotin M, Ross IB, Moret J. Delayed stroke secondary to increasing mass effect following endovascular treatment of a giant aneurysm treated by parent vessel occlusion. AJNR Am J Neuroradiol2001; 22 :1841 –1843[Abstract/Free Full Text]

Heros RC, Kolluri S. Giant intracranial aneurysms presenting with massive cerebral edema. Neurosurgery1984; 15 :572 –577[Medline]

Yamada K, Shrier DA, Tanaka H, Okawara SH. Cerebral giant aneurysm with extensive vasogenic edema. Radiat Med1998; 16 :305 –307[Medline]

Brownlee RD, Tranmer BI, Sevick RJ, Karmy G, Curry BJ. Spontaneous thrombosis of an unruptured anterior communicating aneurysm: an unusual cause of ischemic stroke. Stroke1995; 26 :1945 –1949[Abstract/Free Full Text]

Rordorf G, Bellon RJ, Budzik RE, et al. Silent thromboembolic events associated with the treatment of unruptured cerebral aneurysms by use of Guglielmi detachable coils: prospective study applying diffusion weighted imaging. AJNR Am J Neuroradiol2001; 22 :5 –10[Abstract/Free Full Text]

Strother CM, Eldevik P, Kikuchi Y, Graves V, Partington C, Merlis A. Thrombus formation and structure and the evolution of mass effect in intracranial aneurysms treated by balloon embolization: emphasis on MR findings. AJNR Am J Neuroradiol1989; 10 :787 –796[Abstract]

Sadik AR, Budzilovich GN, Shulman K. Giant aneurysm of the middle cerebral artery: a case report. J Neurosurg1965; 22 :177 –181

Nadjmi M, Ratzka M, Wodarz M. Giant aneurysms in CT and angiography. Neuroradiology1978; 16 :284 –286[Medline]

Ushikoshi S, Kikushi Y, Houkin K, Miyasaka K, Abe H. Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils: case report. Neurol Med Chir1999; 39 :524 –529

Nakayama Y, Tanaka A, Ohshiro S, Yoshinaga S. Extensive edema in the thalamus caused by thrombosed basilar artery aneurysm. Neurol Med Chir1998; 38 :274 –277

Anti-inflammatory, analgesic and anti-edema effects of Lafoensia pacari extract and ellagic acid.

Anti-inflammatory, analgesic and anti-oedematous effects of Lafoensia pacari extract and ellagic acid.

J Pharm Pharmacol. 2006 Sep;58(9):1265-73.

Rogerio AP,
Fontanari C,
Melo MC,
Ambrosio SR,
de Souza GE,
Pereira PS,
Franca SC,
da Costa FB,
Albuquerque DA,
Faccioli LH.

Faculdade de Ciencias Farmaceuticas de Ribeirao Preto, Universidade de Sao Paulo, Departamento de Analises Clinicas, Toxicologicas e Bromatologicas, Av. do Cafe s/n, Ribeirao Preto, SP, 14040-903, Brazil.

Lafoensia pacari St. Hil. (Lythraceae) is used in traditional medicine to treat inflammation. Previously, we demonstrated the anti-inflammatory effect that the ethanolic extract of L. pacari has in Toxocara canis infection (a model of systemic eosinophilia). In this study, we tested the anti-inflammatory activity of the same L. pacari extract in mice injected intraperitoneally with beta-glucan present in fraction 1 (F1) of the Histoplasma capsulatum cell wall (a model of acute eosinophilic inflammation). We also determined the anti-oedematous, analgesic and anti-pyretic effects of L. pacari extract in carrageenan-induced paw oedema, acetic acid writhing and LPS-induced fever, respectively. L. pacari extract significantly inhibited leucocyte recruitment into the peritoneal cavity induced by beta-glucan. In addition, the L. pacari extract presented significant analgesic, anti-oedematous and anti-pyretic effects. Bioassay-guided fractionation of the L. pacari extract in the F1 model led us to identify ellagic acid. As did the extract, ellagic acid presented anti-inflammatory, anti-oedematous and analgesic effects. However, ellagic acid had no anti-pyretic effect, suggesting that other compounds present in the plant stem are responsible for this effect. Nevertheless, our results demonstrate potential therapeutic effects of L. pacari extract and ellagic acid, providing new prospects for the development of drugs to treat pain, oedema and inflammation.

PMID: 16945186 [PubMed - in process]

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