Hepatorenal syndrome misdiagnosis may be reduced using inferior vena cava ultrasound to assess intravascular volume and guide management.

Hepatorenal syndrome (HRS) is a diagnosis of exclusion defined as acute kidney injury (AKI) with cirrhosis and ascites, with serum creatinine unresponsive to standardized volume administration and diuretic withdrawal. Persistent intravascular hypovolemia or hypervolemia may contribute to AKI and be revealed by inferior vena cava ultrasound (IVC US), which may guide additional volume management. Twenty hospitalized adult patients meeting HRS-AKI criteria had IVC US to assess intravascular volume after receiving standardized albumin administration and diuretic withdrawal. Six had IVC collapsibility index (IVC-CI) ≥50% and IVCmax ≤0.7 cm suggesting intravascular hypovolemia, 9 had IVC-CI <20% and IVCmax >0.7 cm suggesting intravascular hypervolemia, and 5 had IVC-CI ≥20% to <50% and IVCmax >0.7 cm. Additional volume management was prescribed in the 15 patients with either hypovolemia or hypervolemia. After 4-5 days, serum creatinine levels decreased ≥20% without hemodialysis in 6 of 20 patients - 3 with hypovolemia received additional volume, and 2 with hypervolemia plus one with 'euvolemia' and dyspnea were volume restricted and received diuretics. In the other 14 patients, serum creatinine failed to persistently decrease ≥20% or hemodialysis was required indicating that AKI did not improve. In summary, fifteen of 20 patients (75%) were presumed to have intravascular hypovolemia or hypervolemia by IVC ultrasound. Six of the 20 patients (40%) improved AKI by 4-5 days of follow-up with additional IVC US-guided volume management, and thus had been misdiagnosed as HRS-AKI. IVC US may more accurately define HRS-AKI as being neither hypovolemic nor hypervolemic, and guide volume management, decreasing the frequency of HRS-AKI misdiagnosis.

Eltrombopag-Induced Thrombocytosis and Thrombosis in Patients With Antiphospholipid Syndrome and Immune Thrombocytopenic Purpura.

Antiphospholipid syndrome (APS) may be either as a primary or in association with an underlying systemic autoimmune etiology (36.2%), particularly systemic lupus erythematosus (SLE). Thrombocytopenia is infrequently observed in APS patients, with an occurrence of 22% to 42% with the frequency of thrombocytopenia, higher in APS and SLE combination than in primary APS. There have been some controversial reports regarding the treatment of APS syndrome with thrombocytopenia with TPO agonists. We like to report a case with APS syndrome with severe thrombocytopenia treated with TPO-RA and developed severe thrombocytosis and thrombosis. Our case represented the first case of TPO-RA in treating APS syndrome developed severe thrombocytosis and our case also concurred that use of TPO-RA agents should be strongly discouraged in APS until larger studies clarify the safety of TPO-RA agents in APS.

Comparison of Respiratory Variations of Subclavian Vein and Inferior Vena Cava in Hospitalized Patients with Kidney Disease.

BACKGROUND: Accurate assessment of relative intravascular volume is critical for appropriate volume management of patients with kidney disease. Respiratory variations of inferior vena cava (IVC) diameter have been used and may correlate with those of subclavian vein (SCV) by bedside ultrasound. The purpose of this study was to assess the relationship between SCV and IVC respiratory variations by bedside ultrasound in a large group of hospitalized patients with acute and/or chronic kidney disease. METHODS: We compared 160 paired SCV and IVC bedside ultrasound studies from 102 semi-recumbent hospitalized adult patients with kidney disease. Patient encounters in which the SCV or IVC could not be clearly visualized were excluded. Collapsibility index=(Dmax-Dmin)/Dmax*100%; D=venous diameter. RESULTS: Relationships between SCV collapsibility index and IVC collapsibility index were not different for longitudinal and transverse views of the SCV. Correlation of SCV collapsibility index with IVC collapsibility index was 0.75 for mechanical ventilation (n=65, P<0.0001) and 0.67 for spontaneous breathing (n=95, P<0.0001). IVC collapsibility index cut-offs <20% for hypervolemia and >50% for hypovolemia corresponded to SCV collapsibility index cut-offs of <22% and >39%, respectively, for both mechanical ventilation and spontaneous breathing encounters. Using these cut-offs for SCV collapsibilities, assessment as hypervolemia versus not-hypervolemia had maximal sensitivity and specificity for predicting respective IVC collapsibility cut-offs of 88% for mechanical ventilation and 74% for spontaneous breathing, and assessment as hypovolemia versus not-hypovolemia had maximal sensitivity and specificity of 91% and 70%, respectively. Concordance, defined as agreement between assessment using SCV CI and assessment using IVC CI, was 85% for mechanical ventilation and 72% for spontaneous breathing when differentiating hypervolemia versus not-hypervolemia and was 89% and 71% respectively when differentiating hypovolemia versus not-hypovolemia. CONCLUSION: Assessment using SCV collapsibility index in the semi-recumbent position has a reasonable concordance with assessment using IVC collapsibility index for both spontaneous breathing and mechanical ventilation, in a wide range of hospitalized patients with concurrent kidney disease, and may be a useful adjunct to assess relative intravascular volume in patients with kidney disease.

Changes in cardiac output with hemodialysis relate to net volume balance and to inferior vena cava ultrasound collapsibility in critically ill patients.

Cardiac output may increase after volume administration with relative intravascular volume depletion, or after ultrafiltration (UF) with relative intravascular volume overload. Assessing relative intravascular volume using respiratory/ventilatory changes in inferior vena cava (IVC) diameters may guide volume management to optimize cardiac output in critically ill patients requiring hemodialysis (HD) and/or UF.We retrospectively studied 22 critically ill patients having relative intravascular volume assessed by IVC Collapsibility Index (IVC CI) = (IVCmax-IVCmin)/IVCmax*100%, within 24 h of cardiac output measurement, during 37 intermittent and 21 continuous HD encounters. Cardiac output increase >10% was considered significant. Net volume changes between cardiac outputs were estimated from "isonatremic volume equivalent" (0.9% saline) gains and losses.Cardiac output increased >10% in 15 of 42 encounters with IVC CI <20% after net volume removal, and in 1 of 16 encounters with IVC CI ≥20% after net volume administration (p = 0.0136). All intermittent and continuous HD encounters resulted in intradialytic hypotension. Net volume changes between cardiac output measurements were significantly less (median +1.0 mL/kg) with intractable hypotension or vasopressor initiation, and net volume removal was larger (median -22.9 mL/kg) with less severe intradialytic hypotension (p < 0.001). Cardiac output increased >10% more frequently with least severe intradialytic hypotension and decreased with most severe intradialytic hypotension (p = 0.047).In summary, cardiac output may increase with net volume removal by ultrafiltration in some critically ill patients with relative intravascular volume overload assessed by IVC collapsibility. Severe intradialytic hypotension may limit volume removal with ultrafiltration, rather than larger volume removal causing severe intradialytic hypotension.

Relationship of inferior vena cava collapsibility to ultrafiltration volume achieved in critically ill hemodialysis patients.

BACKGROUND: Ultrasound (US) assessment of intravascular volume may improve volume management of dialysis patients. We investigated the relationship of intravascular volume evaluated by inferior vena cava (IVC) US to net volume changes with intermittent hemodialysis (HD) in critically ill patients. METHODS: A retrospective cohort of 113 intensive care unit patients in 244 encounters had clinical assessment of intravascular volume followed by US of respiratory/ventilatory variation of IVC diameter, and had HD within 24 h. IVC collapsibility index (IVC CI)=(IVCmax-IVCmin)/IVCmax*100%. Volume management was guided by clinical data plus IVC US findings. Intradialytic hypotension (IDH) was categorized by severity from none to inability to tolerate HD. RESULTS: Linear regression correlating n-weighted proportions of encounters achieving net volume removal of ≥0.5 L, ≥1.0 L, ≥1.5 L, and ≥2.0 L strongly correlated across the range of IVC CI (R2=0.87-0.64). Sensitivity and specificity analysis showed IVC CI was a better predictor than IVCmax of achieving net ultrafiltration (UF) volumes. Mean central venous pressure, pulmonary artery occlusion pressure, and cardiac output were poor predictors by logistic regression and receiver operating curve analyses. IVC CI <20% was the approximate optimal cutoff for achieving ≥0.5 L to ≥2.0 L net UF volumes. Net volume change achieved tended to be less than recommended and may have been limited by the development of IDH. Severity of IDH did not correlate with UF rate in mL/kg/h. χ2 analysis showed pre-US clinical intravascular volume assessments had poor concordance with IVC CI categories. CONCLUSION: IVC US may be a useful tool for predicting whether critically ill patients will achieve volume removal with HD.