Clinical features of hepatopulmonary syndrome in cirrhotic patients

Alizadeh, Amir Houshang Mohammad; Fatemi, Seyed Reza; Mirzaee, Vahid; Khoshbaten, Manoochehr; Talebipour, B; Sharifian, Afsaneh; Khoram, Ziba; Haj-sheikh-oleslami, Farhad; Gholamreza-shirazi, Masoomeh; Zali, Mohammad Reza

doi:10.3748/wjg.v12.i12.1954

Cited by 43 publications

(32 citation statements)

References 4 publications

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“…In this study, HPS was found in 9/40 (22.5%) patients. Despite that, 10/40 (25.0%) patients had IVD, however, without fulfilling the diagnostic criteria of the syndrome, which may represent a frustrated form of it, as the subclinical cases found in the study of Mohammad Alizadeh AH et al (25) .…”

Section: Discussionmentioning

confidence: 90%

“…In the present study, we found the IVD in 15 (71.4%) of 21 patients with SA and in 4/19 (21.1%) of those without such abnormalities (P<0.01). Mohammad Alizadeh AH et al (25) found the presence of IVD in 17/54 (31.4%) of researched patients, of these, 10/54 (18.3%) met criteria for the HPS and 7/54 (13%) had only IVD, defined as subclinical cases of the syndrome. In this study, HPS was found in 9/40 (22.5%) patients.…”

Section: Discussionmentioning

confidence: 98%

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Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Silvério

Guimarães

Elias

et al. 2013

Arq. Gastroenterol.

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Context Hepatopathies can significantly influence both veins and arteries, these changes may cause some cutaneous stigmas, such as spider angioma (SA) and some systemic vascular changes, such as those observed in hepatopulmonary syndrome (HPS). Based on this common pathophysiological root we can assume that the SA can be skin markers of HPS. Objective The objective of this study is to assess whether there is a relationship between the presence of SA and HPS. Methods Records of 40 patients with liver cirrhosis who underwent contrast echocardiography were evaluated, in which we researched the description of SA, physical examination, and other clinical and laboratory data. For diagnosis of HPS we use these signs of the disease: presence of liver disease (cirrhosis in the case), abnormalities in gas exchange by arterial blood gases, and evidence of pulmonary vasodilations by the contrast echocardiography. Results The SA were found in 21/40 (52.5%) patients and hepatopulmonary syndrome in 9/40 (22.5%). The HPS was observed in 8/21 (38.1%) of patients with SA and 1/19 (5.3%) patients were without this sign (P<0.01). We found no statistically significant difference between the SA and the presence of HPS with sex or age. Patients with SA had a higher hypoxemia [PaO2 84.8 ± 11.5 mmHg and 19.8 ± 14.7 mmHg alveolar-arterial gradient of oxygen (AAG)] than those without SA (PaO2 90.8 ± 10.7 mmHg and 10.9 ± 11.7 AAG mmHg) (P<0.05). Conclusion Our findings show a correlation between the presence of SA and HPS, suggesting that the SA may be cutaneous markers of HPS.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 98%

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Silvério

Guimarães

Elias

et al. 2013

Arq. Gastroenterol.

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“…Although chronic dyspnea is the predominant respiratory symptom in patients with liver disease [22] , there are scarce reports on its prevalence and measurement. These reports show contradictory data regarding the prevalence of chronic dyspnea, ranging from 0% to 95% [3,[23][24][25][26] . Nevertheless, none had assessed the severity of chronic dyspnea using such a widely accepted tool as the mMRC chronic dyspnea scale (Table 3).…”

Section: Discussionmentioning

confidence: 98%

Dyspnea and respiratory muscle strength in end-stage liver disease

Kaltsakas¹,

Antoniou²,

Palamidas³

et al. 2013

WJH

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AIM:To investigate the prevalence of chronic dyspnea and its relationship to respiratory muscle function in end-stage liver disease. METHODS:Sixty-eight consecutive, ambulatory, Caucasian patients with end-stage liver disease, candidates for liver transplantation, were referred for preoperative respiratory function assessment. Forty of these (29 men) were included in this preliminary study after applying strict inclusion and exclusion criteria. Seventeen of 40 patients (42%) had ascites, but none of them was cachectic. Fifteen of 40 patients (38%) had a history of hepatic encephalopathy, though none of them was symptomatic at study time. All patients with a known history and/or presence of co-morbidities were excluded. Chronic dyspnea was rated according to the modified medical research council (mMRC) 6-point scale. Liver disease severity was assessed according to the Model for end-stage liver disease (MELD). Routine lung function tests, maximum static expiratory (Pemax) and inspiratory (Pimax) mouth pressures were measured. Respiratory muscle strength (RMS) was calculated from Pimax and Pemax values. In addition, arterial blood gases and pattern of breathing (VE: minute ventilation; VT: tidal volume; VT/TI: mean inspiratory flow; TI: duration of inspiration) were measured. RESULTS:Thirty-five (88%) of 40 patients aged (mean ± SD) 52 ± 10 years reported various degrees of chronic dyspnea (mMRC), ranging from 0 to 4, with a mean value of 2.0 ± 1.2. MELD score was 14 ± 6. Pemax, percent of predicted (%pred) was 105 ± 35, Pimax, %pred was 90 ± 29, and RMS, %pred was 97 ± 30. These pressures were below the normal limits in 12 (30%), 15 (38%), and 14 (35%) patients, respectively. Furthermore, comparing the subgroups of ascites to non-ascites patients, all respiratory muscle indices measured were found significantly decreased in ascites patients. Patients with ascites also had a significantly worse MELD score compared to non-ascites ones (P = 0.006). Significant correlations were found between chronic dyspnea and respiratory muscle function indices in all patients. Specifically, mMRC score was significantly correlated with Pemax, Pimax, and RMS (r = -0.53, P < 0.001; r = -0.42, P < 0.01; r = -0.51, P < 0.001, respectively). These correlations were substantially closer in the non-ascites subgroup (r = -0.82, P < 0.0001; r = -0.61, P < 0.01; r = -0.79, P < 0.0001, respectively) compared to all patients. Kaltsakas G et al . Dyspnea and liver disease tor of mMRC score was RMS (r = -0.51, P < 0.001). In the subgroup of patients without ascites this relationship becomes closer (r = -0.79, P < 0.001), whilst this relationship breaks down in the subgroup of patients with ascites. The disappearance of such a correlation may be due to the fact that ascites acts as a "confounding" factor. PaCO2 (4.4 ± 0.5 kPa) was increased, whereas pH (7.49 ± 0.04) was decreased in 26 (65%) and 34 (85%) patients, respectively. PaO2 (12.3 ± 0.04 kPa) was within normal limits. VE (11.5 ± 3.5 L/min), VT (0.735 ± 0.287 L), and VT/TI (0.449...

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“…Manifestasi hipoksemia pada HPS berupa keluhan dispneu yang khas seperti platipneu dan orthodeoxia disertai dengan adanya tanda sirosis, seperti spider naevi, palmar eritem, asites merupakan patognomonis pada HPS. (7,8) …”

Section: Pendahuluanunclassified

Diagnosis Dan Tatalaksana Hepatopulmonary Syndrome

Elvira¹

2015

MKA

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AbstrakSirosis hepatis dan penyakit hati kronik merupakan penyebab kematian terbanyak di seluruh dunia. Tingginya angka morbiditas dan mortalitas sirosis berhubungan dengan komplikasinya yang bersifat sistemik. Salah satu komplikasi sirosis dapat mengenai paru berupa sindrom hepatopulmonar atau hepatopulmonary syndrome. Hepatopulmonary syndrome (HPS) didefinisikan sebagai trias yang terdiri dari kegagalan hati stadium lanjut, hipoksemia arterial serta dilatasi intravaskular pulmonar tanpa disertai penyakit kardiopulmonar. Patogenesis HPS masih belum diketahui pasti, namun diduga terjadi gangguan metabolisme zat vasoaktif paru yang menimbulkan vasodilatasi vaskuler paru. Manifestasi klinis HPS berupa dispneu yang khas dengan tanda kegagalan hati dan hipertensi portal. Modalitas diagnostik HPS adalah radiologi thorax, analisa gas darah, contrast enhanced echocardiography (CEE), nuclear scanning dengan Tc-99m dan angiografi paru. Penatalaksanaan HPS terutama bertujuan menurunkan vasodilatasi intrapulmonar, meningkatkan oksigenasi arterial dan mengurangi keluhan. Deteksi dini terhadap komplikasi sirosis mutlak diperlukan dalam mencegah dan mengurangi angka morbiditas dan mortalitas.

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Clinical features of hepatopulmonary syndrome in cirrhotic patients

Cited by 43 publications

References 4 publications

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Dyspnea and respiratory muscle strength in end-stage liver disease

Diagnosis Dan Tatalaksana Hepatopulmonary Syndrome

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