Myelofibrosis‐associated massive splenomegaly: A cause of increased intra‐abdominal pressure, pulmonary hypertension, and positional dyspnea

Ziakas, Panayiotis D.; Voulgarelis, Michael; Felekouras, E; Anagnostou, Dimitra; Tzelepis, George E.

doi:10.1002/ajh.20388

Cited by 18 publications

(12 citation statements)

References 20 publications

(20 reference statements)

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“…Unfortunately the incidence of thrombosis in polycythaemia vera and essential thrombocytosis has been difficult to establish; however, at presentation the reported incidence of thrombosis in essential thrombocytosis and polycythaemia vera varied from 11% to 25% and from 12% to 39%, respectively [23][24][25][26][27]. More recent series tend to describe lower incidence figures that are probably a result of both a lead time bias in diagnosis and improved therapy.…”

Section: Chronic Thromboembolic Pulmonary Hypertensionmentioning

confidence: 99%

Pulmonary hypertension in patients with chronic myeloproliferative disorders

2015

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Pulmonary hypertension (PH) is a major complication of several haematological disorders. Chronic myeloproliferative diseases (CMPDs) associated with pulmonary hypertension have been included in group five of the clinical classification for pulmonary hypertension, corresponding to pulmonary hypertension for which the aetiology is unclear and/or multifactorial. The aim of this review is to discuss the epidemiology, pathogenic mechanism and treatment approaches of the more common forms of pulmonary hypertension in the context of CMPD's: chronic thromboembolic pulmonary hypertension, precapillary pulmonary hypertension and drug-induced PH. @ERSpublications Epidemiology, pathogenic mechanism and treatment approach of PH in patients with chronic myeloproliferative diseases http://ow.ly/Q1QX4

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Section: Chronic Thromboembolic Pulmonary Hypertensionmentioning

confidence: 99%

Pulmonary hypertension in patients with chronic myeloproliferative disorders

2015

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“…In the venous circulation, characterised by a low shear rate state, hyperviscosity may cause a major disturbance to blood flow and increased risk of thrombosis. At higher shear rates in the arterial circulation the rise in red cell mass displaces the platelets towards the vessel wall, increasing platelet activation and platelet-platelet interactions [21]. Furthermore, red blood cell abnormalities which occur in polycythaemia vera and essential thrombocytosis may lead to the formation of red blood cell aggregates that directly contribute to flow disturbance and thrombosis and platelet activation, especially in small vessels [25,36,37].…”

Section: Aetiologymentioning

confidence: 99%

“…The possible association of PH with CMPD has been suggested by case reports and small case series [9,10,[11][12][13][14][15][16][17][18][19][20][21][22]. However, the exact incidence and prevalence of PH in this population remains poorly defined.…”

Section: Epidemiologymentioning

confidence: 99%

“…Essential thrombocytosis patients with microvascular disturbances have decreased platelet survival and evidence for platelet-mediated thrombotic processes, such as increased urinary thromboxane B2 [21]. Inhibition of platelet cyclooxygenase-1 by aspirin is followed by improving microvascular disturbances with correction of shortened platelet survival time and reduction of thromboxane B2 excretion to normal levels [25 41, 43].…”

Section: Aetiologymentioning

confidence: 99%

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Pulmonary hypertension in patients with chronic myeloproliferative disorders

Adir

Humbert²

2010

European Respiratory Journal

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Pulmonary hypertension (PH) is a severe haemodynamic disorder in which the pulmonary artery pressure is persistently elevated, leading to right-sided heart failure and death. Recently, chronic myeloproliferative diseases associated with pulmonary hypertension were included in the group 5 category, corresponding to PH for which the aetiology is unclear and/or multifactorial.In this review we will describe the distinct forms of PH in the context of the myeloproliferative diseases chronic thromboembolic pulmonary hypertension and pre-capillary PH mimicking pulmonary arterial hypertension. The epidemiology, mechanisms and treatment approaches will be discussed.

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“…Sepsis and infectious complications aggravating intestinal and capillary permeability favor fluid accumulation. Extramedullary hematopoiesis as seen with chronic myeloid leukemia can also result in hepatosplenomegaly [84], chronic IAH, and chronic (irreversible) pulmonary hypertension. The mechanisms of veno-occlusive disease seen after stem cell transplantation may be triggered by or related to increased IAP [85].…”

Section: Intra-abdominal Hypertension In the Haematology Patientmentioning

confidence: 99%

Intra-abdominal hypertension and abdominal compartment syndrome in burns, obesity, pregnancy, and general medicine

Malbrain¹,

Keulenaer²,

Oda³

et al. 2015

Anaesthesiol Intensive Ther

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Intra-abdominal hypertension (IAH) is an important contributor to early organ dysfunction in trauma and sepsis. However, relatively little is known about the impact of intra-abdominal pressure (IAP) in general internal medicine, pregnant patients, and those with obesity or burns. The aim of this paper is to review the pathophysiologic implications and treatment options for IAH in these specific situations. A MEDLINE and PubMed search was performed and the resulting body-of-evidence included in the current review on the basis of relevance and scientific merit. There is increasing awareness of the role of IAH in different clinical situations. Specifically, IAH will develop in most (if not all) severely burned patients, and may contribute to early mortality. One should avoid over-resuscitation of these patients with large volumes of fluids, especially crystalloids. Acute elevations in IAP have similar effects in obese patients compared to non-obese patients, but the threshold IAP associated with organ dysfunction may be higher. Chronic elevations in IAP may, in part, be responsible for the pathogenesis of obesity-related co-morbid conditions such as hypertension, pseudotumor cerebri, pulmonary dysfunction, gastroesophageal reflux disease, and abdominal wall hernias. At the bedside, measuring IAP and considering IAH in all critical maternal conditions is essential, especially in preeclampsia/eclampsia where some have hypothesized that IAH may have an additional role. IAH in pregnancy must take into account the precautions for aorto-caval compression and has been associated with ovarian hyperstimulation syndrome. Recently, IAP has been associated with the cardiorenal dilemma and hepatorenal syndrome, and this has led to the recognition of the polycompartment syndrome. In conclusion, IAH and ACS have been associated with several patient populations beyond the classical ICU, surgical, and trauma patients. In all at risk conditions the focus should be on the early recognition of IAH and prevention of ACS. Patients at risk for IAH should be identified early through measurements of IAP. Appropriate actions should be taken when IAP increases above 15 mm Hg, especially if pressures reach above 20 mm Hg with new onset organ failure. Although non-operative measures come first, surgical decompression must not be delayed if these fail. Percutaneous drainage of ascites is a simple and potentially effective tool to reduce IAP if organ dysfunction develops, especially in burn patients. Escharotomy may also dramatically reduce IAP in the case of abdominal burns.

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Myelofibrosis‐associated massive splenomegaly: A cause of increased intra‐abdominal pressure, pulmonary hypertension, and positional dyspnea

Cited by 18 publications

References 20 publications

Pulmonary hypertension in patients with chronic myeloproliferative disorders

Pulmonary hypertension in patients with chronic myeloproliferative disorders

Pulmonary hypertension in patients with chronic myeloproliferative disorders

Intra-abdominal hypertension and abdominal compartment syndrome in burns, obesity, pregnancy, and general medicine

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