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Complications of hemodialysis access
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Mia Miller, Prakash Jayanthi, William Oppat
Development of high-output heart failure is an underappreciated complication in patients. As a fistula shunts blood from the arterial circulation to venous circulation bypassing capillary resistance, there is increased preload, as well as decreased systemic arterial flow. Fistula flow in a well-functioning fistula is approximately 700–1500 mL/min.73 Over time, this leads to left ventricular hypertrophy, reduced ejection fraction, and heart failure. Symptoms include tachycardia, elevated pulse pressure, dyspnea on exertion, fluid retention, and jugular venous distension.74 On physical examination, the fistula appears large with rapid flow and aneurysmal growth, often times referred to as a “mega-fistula”.75 Workup begins with an echocardiogram to document left ventricular function, and investigation to rule out other etiologies of high-output heart failure. Elevated levels of biochemical assays such as ANP and BNP confirm volume expansion. To determine high-output heart failure as the definitive cause, a right heart catheterization is required. Characteristic findings include pulmonary hypertension with normal pulmonary vascular resistance and high cardiac output with low-normal systemic vascular resistance.74
Developmental Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James H. Tonsgard, Nikolas Mata-Machado
Liver vascular malformations: High output heart failure.Portal hypertension.Jaundice.Portosystemic encephalopathy.
Vascular tumours and congenital vascular malformations
Published in Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland, Manual of Venous and Lymphatic Diseases, 2017
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland
Indications for intervention include:Cosmetically severe deformity.Severe functional impairment.Lesions located at a life-threatening region, such as adjacent to the airway,Lesions at a region threatening vital functions, such as visionLesions in a region with potentially high risk of complications, such as haemarthrosis.Disabling pain.Haemorrhage or lymph leakage.Secondary arterial ischaemia.Secondary complications from chronic venous hypertension.Infection, thrombosis, bone destruction or growth changes.High-output heart failure.
Impact of hyperthyroidism on in-hospital outcomes of patients with heart failure
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Kunjan Udani, Dveet Patel, Leslie Hart, Vinod Nambudiri
Reportedly, about one-third of patients may develop irreversible hyperthyroid cardiomyopathy [5]. Low output, or ‘true,’ heart failure can result from severe, longstanding hyperthyroidism and is characterized by decreased contractility, abnormal diastolic compliance, and pulmonary congestion. High output heart failure is characterized by paradoxical features including increased cardiac output and contractility [7]. Analysis of more than 25,000 participants from 6 prospective cohorts from the USA and Europe showed that the risks for hospitalizations and complications due to heart failure exacerbations were increased with both higher and lower TSH values [3]. The risk of developing heart failure is increased in patients with underlying heart conditions and the degree of heart failure may be dependent on the patient’s age and severity of hyperthyroidism. Untreated hyperthyroidism and persistent high-output state leads to irreversible ventricular dilation and chronic heart failure, which can result in a fatal outcome [7]. In our retrospective study, we focused on patients diagnosed with hyperthyroidism and aimed to determine its effects on mortality (primary endpoint) and length of stay (secondary endpoint) selectively in those patients with a concomitant diagnosis of heart failure.
Management of fluid status and cardiovascular function in patients with diffuse skin inflammation
Published in Journal of Dermatological Treatment, 2019
Arash Taheri, Amanda D. Mansouri, Parisa Mansoori, Rahimullah Imran Asad
Patients with chronic, widespread skin inflammation, such as erythroderma, usually develop their pathology and vascular changes gradually over time. First, there is a mild reduction in blood pressure. Patients with access to water and good nutrition will compensate for this reduction in blood pressure by retaining salt and water. Fluid retention leads to an increase in intravascular and extravascular volume and presents as peripheral edema. After adequate compensations, these patients have sufficient preload and venous return to the heart and do not require intravascular fluid infusion. However, the blood pressure of most of these patients remains lower than their baseline due to peripheral vasodilation in the skin. Most patients with good cardiac reserve function can compensate for peripheral vasodilation and blood shunting with increased cardiac output and blood pumping (1). They can maintain their blood pressure at a level sufficient for internal organ perfusion. However, if the heart cannot support increased cardiac output, the patients’ blood pressure may remain too low. Patients with heart failure or reduced cardiac reserve cannot pump more blood to compensate for the shunting of blood through the skin. The resulting hypotension and internal organ hypo-perfusion cause severe compensatory fluid retention, which leads to a significant increase in central venous pressure and pulmonary vascular pressure, decompensated congestive heart failure, and pulmonary edema (17). This condition is called high-output heart failure (12).
A rare case of Coombs-negative autoimmune haemolytic anaemia in pregnancy
Published in Journal of Obstetrics and Gynaecology, 2019
Kazuki Takasaki, Morikazu Miyamoto, Masashi Yoshida, Hiroaki Soyama, Masashi Takano, Kenichi Furuya
She was referred to our hospital at 26 weeks of gestation, with a haemoglobin level of 3.6 g/dl; lactate dehydrogenase, 1334 IU/L; and an indirect bilirubin 1.8 mg/dl. The percentage of reticulocytes was 9.86%. The peripheral blood smear findings revealed many erythroblasts but no malignant cell. The Coombs test, sugar water test, ham test and several virus tests, such as the test for the cytomegalovirus, were negative. Flow cytometry revealed normal levels of CD55- and CD59-positive red blood cells. At 27 weeks of pregnancy, the red-blood-cell-bound-IgG (RBC-IgG) levels increased to 63, which helped us clinch the diagnosis of Coombs-negative AIHA. At the same time, a high-output heart failure induced by severe anaemia developed. Immediately, we administered 0.5 mg/kg/day of prednisolone (PSL) and diuretics. Blood transfusion and oxygen administration were commenced as well, following which the haemolytic anaemia and heart failure improved markedly. At 34 weeks of gestation, severe foetal tachycardia and severe variable deceleration developed, because of which an emergency caesarean section (CS) was performed. A male child, weighing 1984 g was delivered, with an Apgar score of 9 and 9 at 1 and 5 min, respectively. Although the baby did not develop anaemia and haemolysis, he suffered from supraventricular tachycardia (SVT) and heart failure, necessitating dopamine administration and ventilatory support. He improved significantly and was discharged on the 27th day of life. The mother was discharged after 7 days of CS. Post-discharge, the dose of PLS was gradually decreased, with no recurrence. Her clinical course is shown in Figure 1.