Bilateral Pitting Pedal Edema Research Articles

Bilateral renal lymphangiectasia: a rare renal cystic disease managed by minimal invasive approach—a case report

BackgroundRenal cystic diseases are one of the commonest renal lesions encountered in clinical practice. Although common, most of the cysts are solitary, benign, asymptomatic and seldom clinically significant. But, renal lymphangiectasia is an exception. These are rare lymphatic malformation seen around the kidneys and in the retroperitoneum. It masquerades clinically like ADPKD and renal tumors and radiologically like a complex renal cyst. Although the cyst is benign, it possesses a significant impact on the quality of life. Because of its rarity, the management of this condition has not been well defined in the literature. A clinician must be aware of this rare condition and able to differentiate it from other similar conditions to aid in appropriate management. Hence, we present a case report of a female with bilateral renal lymphangiectasia managed successfully by laparoscopic excision.Case presentationA 34-year-old hypertensive female came with complaints of bilaterally progressive flank masses for 3 months and breathlessness for 2 weeks. On examination, she had bilateral pitting pedal edema, bilateral palpable renal mass and ascites. She had nephrotic range proteinuria, hypoalbuminemia and normal renal function. Imaging showed 22-cm bilateral peri-renal and hilar multi-loculated cystic lesions, suggestive of bilateral renal lymphangiectasia. Antihypertensives and percutaneous interventions were not successful in relieving her symptoms. Subsequently, she was managed with laparoscopic excision on both sides. After surgery, she had an uneventful postoperative period and good symptomatic relief. No recurrence of the lesion found in follow-up CT imaging after 18 months.ConclusionsRenal lymphangiectasia is a rare yet clinically significant cystic lesion of the kidney. It can be diagnosed confidently by noninvasive imaging modalities. Medical treatment offered for mild symptomatic disease. Patients with severe symptoms need surgical intervention especially if it is not responding to medical management. Minimal invasive approach is feasible and successful in the management of this voluminous disease.

Abstract 11703: A Rare Case of Redo MitraClip Failure Requiring Salvage Mitral Valve Replacement

Presentation: A 74-year-old lady with history of hypertension, COPD, severe pulmonary hypertension, HFpEF, redo MitraClip placement for severe mitral regurgitation (MR) secondary to mitral valve (MV) prolapse presented with four months of progressive dyspnea and bilateral lower extremity swelling. Vitals were significant for hypotension and tachycardia. Examination revealed a holosystolic murmur at the apex, crackles in bibasilar lung fields, and 3+ bilateral pitting pedal edema. Work-up: TTE revealed EF of 65%, enlarged right ventricle, flattened interventricular septum, multiple mitral clips attached to the MV leaflets, and an eccentric MR jet. TEE revealed severe left atrial dilation, severe MR with eccentric and posteriorly directed regurgitant jet and mal-coaptation of MV leaflets with three MitraClips attached (Figure 1-3). Management: For recurrent severe mitral regurgitation resulting in decompensated heart failure, options included another redo MitraClip procedure versus surgical MV replacement. After extensive discussion with the multidisciplinary team and the patient, a decision was made to proceed with surgical MV replacement accepting a high operative risk with STS risk score of >8%. Intraoperative findings revealed one inverted MitraClip with posterior leaflet detachment and two other clips that had densely scarred into the posterior leaflet leaving an unrecognizable MV (Figure 4). A 29 mm Epic Plus bioprosthetic MV was placed successfully. After a prolonged postoperative course, her clinical status improved. Conclusion: In patients who have failed the MitraClip procedure, significant destruction and fibrosis of the leaflets leaves surgical MV replacement being the only reasonable option. Surgical risk must be determined in conjunction with a multidisciplinary team as MV repair is performed at advanced centers in high-risk patients with good results. This can reduce the number of redo MitraClip and salvage MV surgery.

A RARE CASE OF PROLONGED HASHITOXICOSIS INDUCED CARDIOMYOPATHY

Hashitoxicosis is the initial hyperthyroid phase of the patients with Hashimoto′s thyroiditis and usually this phase lasts for one to two months.We had a rare case of Hashimoto′s thyroiditis with prolonged phase of Hashitoxicosis and Hashitoxicosis induced cardiomyopathy. A 27 year old male presented with 6 months history of heat intolerance, sweating, tremors, weight loss and 3 week history of shortness of breath,palpitations and swelling of lower limbs. On examination, patient had exophthalmos, bilateral pitting pedal edema, goitre, tremors, tachycardia, tachypnea, raised JVP, S3, pansystolic murmurs in mitral and tricuspid areas. Thyroid prole showed elevated T3, T4 and suppressed TSH. Anti-TPO antibodies were elevated. USG neck and FNAC were suggestive of Hashimoto′s thyroiditis. 2D Echo showed dilated cardiomyopathy. Patient was started on anti thyroid drugs, diuretics and advised for follow up.

Considerations in Complications Arising from the Management of Pemphigus Vulgaris: A Case Report

Background: This paper reports a case of pemphigus vulgaris in a middle-aged male with oral lesions and skin eruptions
 Objective: To highlight the complications of prolonged steroid therapy.
 Case Report
 A 48-year old male presented with an eight-month history of recurrent mouth ulcers. There was positive history of cutaneous ulcers on the upper extremities, back and genital areas. Patient had been placed on long term steroid therapy prescribed by general practitioners. General examination showed bilateral pitting pedal oedema, moon face and low blood pressure. Intra-oral examination revealed multiple irregular shaped ulcers and erosions with erythematous floor on the buccal mucosa, labial mucosa, floor of the mouth, soft palate and anterior pillar fauces. The dorsum of the tongue had areas of ulcerations with necrotic slough. An impression of pemphigus vulgaris was made based on high index of clinical suspicion and patient was commenced on azathioprine 50mg and prednisolone 40mg daily for a week. Topical use of clobetasol ointment (0.05%) was also commenced to be applied twice daily. There was improvement with the oral lesions on a one-week review. The dose of prednisolone was then stepped down to 20mg daily for one week and 0.2% chlorhexidine mouth rinse twice daily was introduced.
 Punch biopsy of an intact labial mucosa was done on a subsequent visit and histopathology examination confirmed the diagnosis of pemphigus vulgaris. Patient was referred to the cardiologist on account of the hypotension and bilateral pedal oedema which was suggestive of complications of long-standing steroid use.
 Patient was placed on maintenance dose of prednisolone 10mg and azathioprine 50mg daily, and topical steroid oral rinse.
 Conclusion: This study reports a case of pemphigus vulgaris with oral and skin lesions in a middle-aged male. Patient developed some complications due to the prolonged duration of steroid therapy. Regular patient monitoring, adjustment of steroid therapy combined with adjuncts like steroid-sparing drugs are essential to minimizing the steroid-induced adverse effect

Biventricular thrombi in a patient with methamphetamine induced dilated cardiomyopathy

A 39-year-old male with a 20-year history of cannabis and methamphetamine abuse presented to the ER with progressive shortness of breath, orthopnea, and bilateral leg swelling.Temperature 36.8°C, pulse 116/min, blood pressure 125/89 mmHg, respiratory rate 18/min, oxygen saturation 93% on room air. He had 2+ bilateral pitting pedal edema, elevated JVD, and S3. He had elevated BNP and creatinine, low magnesium, and potassium. UDS was positive for Amphetamine and THC (Marijuana) but normal Ethanol level. EKG was sinus rhythm, PVCs, and non-specific T wave changes; CXR showed cardiomegaly with pulmonary vascular congestion. CT chest revealed an indeterminate well-circumscribed filling defect in the right ventricle’s apex concerning for a thrombus versus neoplastic nodule. Transthoracic Echocardiography (TTE) findings of biventricular dilatation, global hypokinesis, right and left apical thrombus, a 5 X 3.2 cm mass in the right ventricle, Left Ventricular Ejection Fraction (LVEF) of 15 to 20%, grade 2 diastolic dysfunction, and Pulmonary Artery Systolic Pressure (PASP) of 40 mmHg (Figure 1a & 1b). He had widely patent coronary arteries on left heart catheterization, but Right heart catheterization showed elevated pulmonary capillary wedge pressure. Thrombophilia screen was negative, and there was no Deep Venous Thrombus (DVT) on lower extremity venous Doppler ultrasound.

Case Report on Chiari Syndrome

Chiari Malformation is a rare condition. A condition known as Chiari malformation occurs when brain tissue spreads into the spinal canal. When a portion of your skull is excessively small or malformed, it presses on your brain and forces it downward. Chiari malformation is a rare occurrence, although the increased use of imaging testing has resulted in more diagnosis.
 Case Presentation: A 18-year-old boy was admitted to the hospital with the following symptoms: Tingling sensation, numbness over left hand since 2 to 3 months. Neck bend toward right side, pain in left hand since 6 month. Difficulty during eating by hand since 2 to 3 month. On physical examination, indicated a bright attentive person with pale conjunctiva and no symptoms of icterus. He had a tachycardia, bilateral pitting pedal edema and a swollen abdomen with shifting dullness, all of which pointed to as cites. He had a history of intermittent abdominal pain. On admission he complaint of new onset of dyspnea on exertion, fatigue and abdominal swelling. The rest of all physical examination was normal, with no skin changes and an intact arterial pulses in all four extremities.
 Conclusion: The primary focus of this case study is on professional management and outstanding nursing care, which may provide the holistic care that Chiari Syndrome necessitates while also effectively managing the challenging case. After a full recovery, the patient's comprehensive health care team collaborates to help the patient regain his or her previous level of independence and satisfaction.

Hepatic vein thrombosis secondary to COVID-19

COVID-19 is known to cause both arterial and venous thromboembolism. Although a lot of attention is being given to those presenting with myocardial infarction and stroke, splanchnic vein thrombosis which includes portal, mesenteric, splenic, and hepatic vein thrombosis is often underreported. A 21-year-old female presented with progressive abdominal distension and obstipation for the past 2 weeks. The patient was diagnosed as a case of moderate COVID-19 illness 2 weeks before the onset of these symptoms and recovered on receiving treatment according to the COVID protocol. Physical examination revealed pallor and bilateral pitting pedal edema up to ankles. Systemic examination revealed uniformly distended abdomen with signs of free fluid and tenderness in the right hypochondrium. Hematological investigations showed moderate-grade microcytic hypochromic anemia. Biochemically, indirect hyperbilirubinemia and transaminitis with moderately elevated D-dimers and Lactate dehydrogenase (LDH) was noted. Radiological imaging of the abdomen (including USG with doppler and CT contrast Scans) revealed gross ascites, nutmeg appearance of liver with completely obscured hepatic veins indicating no flow of blood, multiple intrahepatic portosystemic collaterals and a partially thrombosed inferior vena cava with no evidence of portal hypertension. All other workup to rule out other causes of hepatic vein thrombosis was inconclusive. The patient was treated with low-molecular-weight heparin and then continued with oral warfarin at discharge. On a 4-week follow-up, the patient showed marked clinical improvement with partial resolution of presenting symptoms.

LEFT VENTRICULAR NONCOMPACTION: AN UNUSUAL CAUSE OF HEART FAILURE

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Left ventricular noncompaction (LVNC) is a cardiomyopathy characterized by prominent trabeculae and deep intertrabecular recesses in communication with the ventricular cavity. LVNC affects up to 1.3% of the population and is responsible for 3-4% of all heart failure syndromes. CASE PRESENTATION: A 76-year-old male presented to the emergency department due to increasing dyspnea. He endorsed lower extremity swelling and orthopnea. He was tachypneic and hypoxemic. Lung auscultation revealed bibasilar crackles. Bilateral pitting pedal edema was noted. BNP was elevated at 861 pg/mL and troponins were elevated at 0.6 ng/L. Electrocardiogram demonstrated normal sinus rhythm with T-wave inversions in the inferolateral leads. Chest radiograph showed cardiomegaly, vascular congestion and bilateral pleural effusions suggestive of congestive heart failure syndrome. Transthoracic echocardiogram revealed left ventricular ejection fraction of 25-30%. Prominent trabeculae and deep interventricular recesses were noted, concerning for LVNC. Coronary angiography showed moderate nonobstructive coronary artery disease without need for percutaneous coronary intervention. His clinical condition improved with diuretic therapy, blood pressure control, and initiation of guideline-directed medical therapy. During his hospitalization, telemetry captured 6 beats of non-sustained ventricular tachycardia. Lifevest was placed to evaluate need for ICD implantation after optimization of medical therapy. He was scheduled for follow up echocardiogram in 3 months and counseled on the need for family screening. DISCUSSION: LVNC is thought to be a congenital cardiomyopathy caused by failure of cardiac sinusoids to compact during embryogenesis. However, studies demonstrate development of LV trabeculations on serial echocardiograms suggesting LVNC may be an acquired cardiomyopathy. Predisposition to trabeculation development may be genetically determined, LVNC has a 30% rate of familial recurrence. Excessive preload and afterload are thought to contribute as the development of trabeculations is noted in chronic renal failure and valvular heart disease. Criteria for diagnosis of LVNC vary and are not universally agreed upon. Thus, a multi-modality imaging approach involving echocardiography and cardiac MRI is recommended. LVNC is associated with significant complications, 56% of patients will develop heart failure syndrome and up to 40% will require heart transplantation. Additionally, 11% of patients undergo ICD implantation for ventricular arrhythmias and 7.6% of patients die of sudden cardiac death. Risk of thromboembolism ranges from 21-38%, likely due to turbulent flow through intertrabecular recesses. Three-year mortality rate is estimated at 14%. CONCLUSIONS: LVNC is a relatively common cardiomyopathy with significant morbidity and mortality. We urge clinician awareness to facilitate prompt diagnosis and management. Reference #1: Bhatia, Nisha L., et al. “Isolated Noncompaction of the Left Ventricular Myocardium in Adults: A Systematic Overview.” Journal of Cardiac Failure, vol. 17, no. 9, 2011, pp. 771–778., doi:10.1016/j.cardfail.2011.05.002. Reference #2: Tian, Julia, et al. “Left Ventricular Noncompaction: A Rare Case of Nonischemic Cardiomyopathy.” Case Reports in Cardiology, vol. 2019, 2019, pp. 1–3., doi:10.1155/2019/5637638. Reference #3: Gati, Sabiha, et al. “Adult Left Ventricular Noncompaction.” JACC: Cardiovascular Imaging, vol. 7, no. 12, 2014, pp. 1266–1275., doi:10.1016/j.jcmg.2014.09.005. DISCLOSURES: No relevant relationships by Gopika Dasari, source=Web Response No relevant relationships by Anneka Hutton, source=Web Response No relevant relationships by Eli Levine, source=Web Response No relevant relationships by Shaheen Mizyed, source=Web Response

Lipid Inclusions in Cardiac Myocytes - A Rare Case of Cardiolipotoxicity

Introduction The heart oxidizes fatty acids for its energy production. However, excessive accumulation of lipids due to various processes such as obesity, diabetes, heart failure (HF), myocardial ischemia, or infarction can result in damage to the heart tissue, also known as cardiolipotoxicity. Case A 69-year-old gentleman with a history of non-ischemic cardiomyopathy, right ventricle failure, permanent atrial fibrillation, ventricular tachycardia and cardiac cirrhosis presented to the hospital with exertional dyspnea, orthopnea, and decreased functional capacity. Physical exam was pertinent for elevated jugular venous distension, bibasilar rales, and bilateral pitting pedal edema. Laboratory findings were significant for brain type natriuretic peptide 1641 pg/ml, hemoglobin A1c 6.1%, total cholesterol 79 mg/dl, triglyceride 84 mg/dl, low density lipoprotein (LDL) 53 mg/dl, and high density lipoprotein (HDL) 9 mg/dl. Chest x-ray demonstrated mild pulmonary vascular congestion. Electrocardiogram showed atrial fibrillation and right bundle branch block. Transthoracic echocardiogram showed normal left ventricular systolic function with ejection fraction of 55%, severely dilated right ventricle with severely reduced systolic function and markedly dilated right and left atrium. Right heart catheterization showed findings consistent with mild pulmonary hypertension from diastolic HF and severe tricuspid regurgitation. Endomyocardial biopsy showed intracellular accumulation of significant amorphous material in most cardiac myocytes. Electron microscopy revealed fat lobules and inclusion bodies within the myocytes, consistent with cardiolipotoxicity (figure 1). Guideline directed medical management of HF was initiated and patient was subsequently discharged home. Discussion Due to various stressors such as HF, myocardial ischemia, infarction or atrophy, there is increased expression of genes involved in glucose metabolism rather than fatty acid oxidation. This leads to increased accumulation of lipids in the failing myocardium, thereby leading to cardiolipotoxicity. Increased lipid accumulation causes cardiac steatosis thereby leading to ER dysfunction, contractile dysfunction, and cell death. Our case describes a distinct metabolic phenotype of myocardial dysfunction for which no definite cause or treatment has been identified. Further research is required to advance our knowledge on cardiac metabolism in normal myocardium as well as in patients with HF, which could result in development of novel therapeutic interventions and strategies in these patients.

A rare case of Hypothyroidism in a male presenting as Polyserositis

Introduction: Primary hypothyroidism presenting with isolated ascites, pericarditis, or pleural effusion though rare, is well known. The combination of all three, however, is extremely rare and poorly recognised; hence delaying the diagnosis. Case Report: A 40 yr old male presented with progressive abdominal distension, swelling of the lower limbs, facial puffiness, loss of appetite, constipation, hoarseness of voice, and weight gain over 6 months. Physical examination revealed facial puffiness, periorbital oedema, bilateral pitting pedal edema, dry skin with sparse body hair and macroglossia. Systemic examination revealed muffled heart sounds, dullness on percussion in the lower lung fields bilaterally with absence of breath sounds in the same areas, distended abdomen with signs of free fluid, abdominal wall edema, and delayed relaxation of ankle jerk. ECG showed low voltage QRS complexes in all the leads. Chest X-Ray showed bilateral minimal pleural effusion with a massive Cardiomegaly. USG abdomen revealed moderate Ascites with no evidence of portal hypertension. A 2-D echo showed pericardial effusion and global hypokinesia with preserved ejection fraction of 60% (Fig 3). Ascitic fluid showed a high protein content 3.1g/dL, 59% lymphocytes, 36% monocytes, 5% mesothelial cells and no neutrophils. LDH was 107 IU/L. Thyroid profile showed T3 150 μIU/ml. TPO was negative. The patient was started on an escalating dose of Levothyroxine from 25 to 100 mcg. Diuresis was given. The patient was discharged on and continued with Levothyroxine 100mcg daily for continued use. On a 4 week follow up, the patient had significantly improved with resolution of tissue edema and pleural effusion with minimal pericardial effusion and ascites.

Ecthyma gangrenosum on the face of a malnourished child with Pseudomonas sepsis: Simulating Cancrum oris.

IntroductionEcthyma gangrenosum (EG) is a cutaneous lesion commonly caused by Pseudomonas aeruginosa that involves mainly the lower limbs and gluteal region, seen more in immunosuppressed patients with neutropenia. Cancrum oris (Noma) is a gangrenous necrosis of the face that begins as a gingival ulcer and progresses rapidly to destroy contiguous tissues in malnourished children.Case PresentationThis article reports a case of facial EG which was similar to Noma in a malnourished child: a 16-month old girl with fever, cough, weight loss, watery stool and swelling on right cheek. She was febrile, pale, wasted with bilateral pitting pedal oedema. She had a solitary circumscribed round necrotic lesion, with surrounding hyperaemia on the right malar area which extended to destroy the right ala nasi. No intra-oral rashes but she had left ear discharge. She received blood transfusion, antibiotics, antiseptic wound care and nutritional rehabilitation.Management and OutcomeSwabs of the lesion and ear discharge both revealed Gram-negative bacilli and culture yielded P. aeruginosa. Retroviral, Mantoux and Gene Xpert tests were negative. She had moderate anaemia, normal white blood cell count, and neutropaenia. Parenteral ceftriazone was changed to ciprofloxacin based on sensitivity results and lack of clinical response. The wound healed with residual scarring and partial destruction of right ala nasi.DiscussionAlthough this patient had facial necrosis to suggest Noma, she did not have initial oral involvement, and clinical features such as Pseudomonas sepsis and neutropaenia suggested EG. Facial necrosis in malnourished children may be due to EG.

Clinical spectrum of severe acute malnutrition among children admitted to nutritional rehabilitation centre of a tertiary care hospital with special reference to incidence of bilateral pitting pedal oedema in children with severe acute malnutrition

Background: Malnutrition is a major cause of morbidity and mortality in under five children globally, according to global nutrition report 2016, forty five percent of deaths in under five children are linked to malnutrition. The objective of this study was to study the clinical spectrum in children with Severe Acute Malnutrition (SAM) admitted to nutritional rehabilitation center of a tertiary care hospital.Methods: Children between the age group of 6 months to 5 years admitted in the nutritional rehabilitation centre during the period of 1 year (from April 2016 to March 2017) meeting our inclusion criteria were included in the study. We retrospectively reviewed the medical records of these children. Clinical spectrum of SAM was compared with comparison group.Results: A total of 100 cases were included in the study. Ninety five percent of children met the criteria of weight for height less than 3SD, 45% of children met the criteria of Mid Upper arm Circumference (MUAC) less than 11.5 cms and 5% of children met the criteria of bilateral pitting pedal oedema. Mean age of presentation of children in the present study was 15.8 months among which 45% were males and 55% were females. Major symptoms of the study group were fever, cough, hurried breathing, loss of appetite and loose stools with 79%, 45%, 27%, 26% and 23% as respective frequencies. Pneumonia (43%) was the major comorbidity among children admitted with severe acute malnutrition. Diarrhoea (21%), meningitis (8%), urinary tract infection (6%) were the other co-morbidities present in the study group.Conclusions: Pneumonia and diarrhoea are the major co-morbidities present in children with SAM. Majority of children fulfil the criteria of weight for height ≤3SD for diagnosis of SAM. There is a low incidence of oedematous malnutrition in the present study.

Aids-related kaposi’s sarcoma in a four year old child: the challenge of a missed opportunity

Background : AIDSrelated Kaposi’s sarcoma (KS) is an AIDS-defining illness and is now increasingly recognized in children infected with HIV. Many of these cases are missed due to low index of suspicion. Vertical transmission of HIV is the commonest route of transmission in children and this is preventable by early maternal antenatal diagnosis, early commencement of HAART by the mother and adoption of the safest possible mode of delivery. The index case did not benefit from these services, making her acquire HIV and then develop AIDS-defining illness (KS) at a tender age of 4 years. Aim and objective: The study is aimed at emphasizing the need for all pregnant women to have antenatal screening as soon as pregnancy is confirmed so as to prevent vertical transmission of HIV to the unborn child. It is also aimed at creating awareness in clinical practice so as to increase index of suspicion among clinicians when evaluating chronically ill children. Case Description: GG was a 4year old girl who presented at 108 Nigerian Air force Hospital, Abuja with non-itchy skin rashes of two weeks duration, generalized body swelling, cough and haematochezia of one week duration, and fever of four days duration. She was a paternal orphan having lost her father a year prior to presentation to Acquired immunodeficiency syndrome (AIDS)-related illness. Her mother also tested positive to Human Immunodeficiency virus (HIV) and has been on highly active anti-retroviral therapy (HAART) for a year. Physical examination revealed moderate pallor, bilateral pitting pedal oedema, and matted non-tender peripheral lymphadenopathy. There were papular and nodular skin lesions with a reddish solid lesion on the hard palate. She tested positive to HIV. Abdominal ultrasound scan revealed moderate hepatomegaly with ascites, while chest x-ray showed bilateral interstitial pneumonitis, right hilar lymphadenopathy, right pulmonary nodule and ipsilateral pleural effusion. Excisional biopsy of one of the skin nodules confirmed the diagnosis of Kaposi’s sarcoma. She was commenced on HAART and antibiotics, with a unit of blood transfused. Her condition deteriorated, which necessitated referral to university of Abuja Teaching Hospital where she eventually died after a day of admission. Conclusion : Paediatric AIDSrelated KS is becoming increasingly common in Nigeria and as such, high index of suspicion is required while evaluating pediatric patients. This, coupled with early commencement of HAART is required to avert the pitfalls observed in this case; bearing in mind that childhood AIDSrelated KS is lethal. Keywords : Generalized lymphadenopathy; Kaposi’s sarcoma; Missed opportunity; Paediatric AIDS; Skin rashes

NON PITTING TYPE PEDAL EDEMA WITH LITHIUM: A CASE REPORT

<p><strong>Objective: </strong>To report a case of lithium induced bilateral nonpitting pedal edema.</p><p><strong>Methods: </strong>The clinical data of a bipolar affective disorder patient with current episode of mania and psychotic symptoms who experienced bilateral non pitting pedal edema with lithium.</p><p><strong>Results: </strong>The patient was a 29 yr old female who developed bilateral non-pitting type pedal edema with lithium therapy with normal plasma lithium level (0.72mEq/l). She is a known case of bipolar affective disorder (BPAD) was admitted to psychiatry department with episode of mania with psychotic symptoms. She had history of drug induced hypersensitivity reaction with eosinophilia and systemic symptoms (DRESS) with oxcarbazepine and so the drug was discontinued and was started on tablet lithium 400 mg twice daily. On admission here, the dose of lithium was increased to 1200 mg/day. The patient gradually improved but she developed bilateral non-pitting pedal edema. Serum lithium concentration was normal and there were no other early symptoms of lithium toxicity. But as the patient's distress further increased with increasing pedal edema, it was decided to stop lithium altogether and to maintain the patient on tablet quetiapine 800 mg therapy for BPAD. Within one week of stopping lithium the edema on both her feet decreased significantly. Causality was assessed by naranjo causality assessment scale and a probable relationship was obtained between lithium and pedal edema with a score of 6.</p><p><strong>Conclusion: </strong>This case emphasises that regular physical examination and laboratory investigations are important for patients who are on lithium therapy. Clinicians should always be careful while initiating lithium treatment in a patient with respect to the initial dose and dose escalation even after a period of successful therapy with lithium, as minor dose escalation can cause major changes in the serum lithium concentration and thereby the patient’s tolerability to lithium.</p>

A case study report of denovo lymph node occurance of myeloid sarcoma

Myeloid sarcoma (MS) as a rare localized solid tumor mass consists of myeloblasts or immature myeloid cells was found in an extramedullary site of a 4 year male child who was suffering with fever, abdominal distension since 4 months and swelling of legs from 1month . On examining pallor, bilateral cervical and inguinal lymphadenopathy, bilateral pitting pedal edema, Hepatosplenomegaly & ascites found. On investigation anemia with leukocytosis, thrombocytopenia was found. USG abdomen showed multiple non necrotic lymphnodes. Bone marrow aspiration suggestive of JMML, lymphnode biopsy showed myeloid sarcoma and was confirmed by immune histochemistry (IHC) markers LCA, KP-1(CD68), myeloperoxidase are positive.Immunophenotyping is useful in differentiating myeloid sarcoma from lymphoma and leukaemia. Child was treated with 3/7 regimen of cytoarabinoside, daunorubicin.

A Case of Interosseous Membrane Calcification.

A 69-year-old male presented with complaints of progressive easy fatigability, low back ache and pain in the right forearm for the past one year. He had associated swelling of legs for the past three months and had noticed a decrease in his urine output. He never had any other associated joint pains, burning micturition or oral ulcers. He was hypertensive and was on medical treatment, with no other co-morbid illnesses. Examination revealed pallor and bilateral pitting pedal oedema. Vitals were within normal limits. Systemic examination was unremarkable. Musculoskeletal examination revealed bony tenderness over the L3 – L4 spine with no obvious swelling and tenderness over the lower half of the right forearm. There were no visible deformities.

English

Autoimmune hemolytic anemia is uncommon. The estimated overall (not age-adjusted) annual incidence is about 1 case per 100,000 populations; after age 60 years, the annual incidence reaches 10 per 100,000. The disorder can occur at any age, but most patients are older than 40 years. About 65% of patients with primary autoimmune hemolytic anemia are women, and almost all cases that complicate systemic lupus erythematosus occur in women. A 65 years old male presented with generalized weakness, breathlessness on exertion, swelling of lower limbs and pain abdomen of 6 months duration. He was previously admitted elsewhere on several occasions (within past 3-4 months) with similar complaints, and had received multiple blood transfusions. On clinical examination, patient had pallor and bilateral pitting pedal edema. Abdominal examination revealed massive Splenomegaly (12 cm below left costal margin), moderate Hepatomegaly. Investigations revealed Hb% of 8.6 g/dl, Platelet count = 1 lakh/cmm, ESR = 120 mm, retic count -2.2 %. Peripheral smear showed evidence of hemolysis. Serum LDH was high, Serum bilirubin predominantly indirect hemoglobin= 2, S. Haptoglobin below 6.63. These findings suggested hemolysis as a cause of his anemia and splenomegaly. Further evaluation was done to find out the cause of hemolysis in this elderly male. Hb Quantification using HPLC was normal. Serum G6PD activity was normal. ANA was negative. Hams test was negative. Direct & Indirect Coomb's tests were positive. Bone marrow examination showed erythroid hyperplasia. CT Abdomen showed hepatosplenomegaly. Upper GI endoscopy and colonoscopy were normal. Based on these findings a diagnosis of warm antibody type auto immune haemolytic anaemia (AIHA), probably of idiopathic type, was made and patient was started on steroid therapy. After 2 weeks, repeat haemoglobin was 12.8 gm%, WBC count was 7020/cumm reflecting response to steroid therapy. Severe AIHA can be a medical emergency. Red cell transfusion poses a special problem as the transfused cells are rapidly destroyed, but can be life- saving and in the meantime steroids can exert their effect. This unique situation requires good liaison and understanding between the clinical unit and the serology lab. Thus it is very important to diagnose this condition and treat accordingly. Untreated, chronic auto immune hemolysis progresses to severe anaemia and associated complications. It is important to consider the diagnosis of autoimmune hemolysis in elderly males also, although this condition is usually seen in females. It is important to rule out malignancies and connective tissue disease in elderly presenting with

Very early complication of rheumatic heart disease (valvuloplasty for severe mitral valve stenosis for 6 year old male patient)

Rheumatic heart disease continues to contribute greatly to the burden of cardiovascular disease in Yemen, It’s usual to see a lot of advance RHD cases in adult in Yemen but in pediatric it is rare to see such advance case specially under the age of eight. Case report A.M, a 6 year old Yemeni male child was seen in September 2012 with history of recurrent breathlessness which started about 4 years earlier. His symptoms worsened in the previous three weeks when he became breathless at rest, had paroxysmal nocturnal dyspnea, huge abdominal distention, bilateral leg swelling and cough productive of whitish sputum. Past history was not significant for recurrent sore throat but he was diagnosed to have RHD at age of 3 year old without any farther follow up and irregular using to long acting penicillin. He was the second child in his family; both parents are in a very low income group. There was no family history of the disease in any of his siblings. Examination revealed that the child looked marasmic, pale, was chronically ill, and had a tinge of jaundice with bilateral pitting pedal edema. A cardiovascular system examination revealed a pulse rate of 101 per minute, regular and small volume, blood pressure of 90/60 m mmHg, elevated jugular venous pressure, displaced apex beat which was located at 5th intercostal space anterior axillary line, loud first and second heart sounds opening snap and mid diastolic rumbling murmur with systolic murmur at left parasternal border. The respiratory rate was 26 cycles per minute and bilateral crepitations. Other examination findings were visible dilated abdominal vein, a tender, pulsatile hepatomegaly of 3 cm below the right coastal margin and massive ascites. An echocardiography showed densely thickened mitral valves with severe commissural fusion leading to doming of the mitral valve in diastole, markedly dilated left atrium, normal left ventricular eject ion fraction, markedly dilated right atrium and right ventricle. Colour flow showed severe tricuspid regurgitation and severe pulmonary hypertension. The calculated mitral valve area is 0.6 cm square and pressure gradient max/mean (14/6 mmHg) respectively. ECG sinus rhythm normal axis and dilated LA with RBBB Complete blood count showed low HB 9 mg/dl with normal a white cell count. The chest X-ray revealed cardiomegaly with a double cardiac shadow positive mitralization sign. He was placed on diuretics (furosemide and low-dose spironolactone) Angiotensin Converting Enzyme inhibitor (Lisinopril), intranasal oxygen, intravenous heparin and antibiotics. And was prepared for percutaneous mitral valvuloplasty On the third day of admission, The PMVP was done with good out come the mitral valve area increase from 0.6 to 1.8 cm 2 and decrease in the pressure gradient to 6/4 mmHg and the pulmonary hypertension to mild. After that patient condition get better with improving to the dyspnea, the child become more active start to eat and play more frequent than before with decrease to the abdominal distension and the patient discharge to home in good condition and advice to follow up the hospital after six month. Discussion Rheumatic heart disease, no doubt remains a disease with great morbidity and mortality in most low and middle income countries specially in Yemen despite been having almost eradicated in high income countries, it affects the young population of our community whom presented late most of the time with complication due to the shortage of the medical service in the most of the regain of Yemen specially the remote areas. The case being presented typifies the cost of late presentation in patients with rheumatic heart disease. its usual in our country to see such cases in late stage and complicated but it’s rare to see a 6 year old child presented with severe mitral stenosis and he needed PMVB even it is successful procedure that saved his live but all that could be prevented from happening in the first place by a simple preventive program which we do not have in our country.

Pseudomesotheliomatous Adenocarcinoma of Lung: A Diagnostic Dilemma

A 52 years old farmer developed left-sided chest pain 4 months prior to admission that was dull aching, episodic, lasting for 1 to 2 minutes, relieved of its own and increased on deep inspiration. He was found to have left-sided pleural effusion. Pleural fluid analysis revealed straw colored fluid with positive stain for acid fast bacilli at Civil Hospital, Rupnagar. He was enrolled under Revised National Tuberculosis Control Programme (RNTCP) for directly observed antitubercular treatment (DOTS) as a new case. Despite 2 months of treatment, there was no symptomatic improvement and repeat evaluation showed a persistent large pleural effusion. Therapeutic thoracocentesis (2-3 times) was done followed by intercostal chest tube insertion 2 months prior to admission with drainage of approximately 200 to 300 ml of hemorrhagic fluid per day. Over a period of 2 weeks preceding admission, severity of chest pain gradually increased. Six days prior to admission, he developed high grade fever associated with rigors and chills. Breathlessness started 4 days prior to admission, was acute in onset, progressing during this time period to being present at rest and not associated with orthopnea or wheeze. There was no history of cough, expectoration, hemoptysis, swelling of feet, decreased urine output or altered sensorium. There was no significant illness in the past. He was a nonsmoker with no addictions. On initial evaluation, he was conscious and oriented. He had tachycardia (130/min), normal blood pressure (130/70 mm Hg) and tachypnea (40/min) with use of accessory muscles of respiration. Pallor, bilateral pitting pedal edema and small right supraclavicular lymph nodes were noted. Examination of the chest revealed presence of a chest tube, reduced chest wall movements with signs of volume loss on the left side, dull note on percussion with reduced intensity of breath sounds in the left infraclavicular and left mammary areas. The clinical findings were consistent with those of pleural effusion. Per abdomen, the liver was palpable 2 cm below right subcostal margin with no other specific features. Spleen was not palpable, there was no tenderness or free fluid and bowel sounds were present. Rest of the systemic examination was unremarkable.

Hunter syndrome presenting as heart failure: A case report

Introduction: Hunter syndrome (Mucopolysaccharidosis type II, MPS II) is a genetic disorder associated with deficiency of lysosomal enzyme iduronate­2­sulfatase and impairment of glycosaminoglycans (GAGs) metabolism. Hunter syndrome is well described in medical literature but less is known about heart failure. We are presenting a rare case of Hunter­syndrome with heart failure. Case Report: A 17­year­old boy presented to emergency department with chief complaint of dyspnea on exertion for last seven days. He also had history of progressive abdominal swelling since five years of age. On examination, he was tachypneic with raised jugular venous pressure and bilateral pitting pedal edema. His head was dolicocephalic in shape with coarse facial features. His abdomen was distended with hepatosplenomegaly and an umbilical hernia. He has one younger brother with similar clinical profile and one normal younger sister. Suspecting mucopolysaccharidosis, we performed a skeletal survey. A lateral X­ray of the skull showed an enlarged and J­shaped sella turcica. Patient’s and his brother’s enzyme assays for iduronate­2­sulfatase were markedly low. Based on the clinicoradiological and enzyme assay diagnosis of Hunter syndrome (MPS II) was made. Conclusion: Various clinical and radiological features are typical of MPS II. A detailed clinical evaluation and radiological investigations help in diagnosis of MPS II. The enzyme assay is required to confirm the diagnosis.