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Pulmonary-renal syndromes: Experience from an Indian Intensive Care Unit.

Rajagopala S, Sagar BK, Thabah MM, Srinivas BH, Venkateswaran R, Parameswaran S - Indian J Crit Care Med (2015)

Bottom Line: Clinical characteristics of patients with "definite PRS" were compared with those with "PRS mimics".Patients with PRS had more alveolar hemorrhage, hypoxemia and higher mortality (69%) when compared to "PRS mimics".Multicentric studies are needed to further characterize the burden, etiology, treatment protocols, and outcomes of PRS in India.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Dhanvantri Nagar, Puducherry, India.

ABSTRACT

Background: The etiology of patients presenting with pulmonary-renal syndrome (PRS) to Intensive Care Units (ICUs) in India is not previously reported.

Aims: The aim was to describe the prevalence, etiology, clinical manifestations, and outcomes of PRS in an Indian ICU and identify variables that differentiate immunologic causes of PRS from tropical syndromes presenting with PRS.

Materials and methods: We conducted a prospective observational study of all patients presenting with PRS over 1-year. Clinical characteristics of patients with "definite PRS" were compared with those with "PRS mimics".

Results: We saw 27 patients with "provisional PRS" over the said duration; this included 13 patients with "definite PRS" and 14 with "PRS mimics". The clinical symptoms were similar, but patients with PRS were younger and presented with longer symptom duration. Ninety-two percent of the PRS cohort required mechanical ventilation, 77% required vasopressors and 61.5% required dialysis within 48 h of ICU admission. The etiologic diagnosis of PRS was made after ICU admission in 61.5%. Systemic lupus erythrematosus (54%) was the most common diagnosis. A combination of biopsy and serology was needed in the majority (69%, 9/13). Pulse methylprednisolone (92%) and cyclophosphamide (61.5%) was the most common protocol employed. Patients with PRS had more alveolar hemorrhage, hypoxemia and higher mortality (69%) when compared to "PRS mimics".

Conclusion: The spectrum of PRS is different in the tropics and tropical syndromes presenting with PRS are not uncommon. Multicentric studies are needed to further characterize the burden, etiology, treatment protocols, and outcomes of PRS in India.

No MeSH data available.


Related in: MedlinePlus

Composite image of the chest radiograph (left) and computed tomography (CT) of the chest (right) of patient 1 with showing bilateral lower lobe consolidation with corresponding asymmetric ground glass opacities and crazy-paving on CT. A clinical diagnosis of alveolar hemorrhage (DAH) was made
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Figure 1: Composite image of the chest radiograph (left) and computed tomography (CT) of the chest (right) of patient 1 with showing bilateral lower lobe consolidation with corresponding asymmetric ground glass opacities and crazy-paving on CT. A clinical diagnosis of alveolar hemorrhage (DAH) was made

Mentions: Patients were diagnosed with “PRS” provisionally at ICU admission if they fulfilled all the below; acute illness (≤4 weeks) with evidence of renal and lung involvement at ICU admission, “active urinary sediment” on urine examination and pulmonary involvement consistent with diffuse alveolar hemorrhage (DAH) or vasculitis. “Active urinary sediments” was defined by the presence of at least one of the below; albuminuria (≥3+ on dipstick testing, >300 mg on 24-h collection or a urine protein/creatinine ratio >45 mg/mol), red blood cells (RBCs) or casts (RBCs or leukocyte casts) in urine microscopy examination with or without azotemia.[8] DAH was defined by the presence of at least two of the following; chest infiltrates consistent with DAH, hemoglobin ≤11 g/dL, and hemoptysis. In the absence of hemoptysis or a definite drop in hemoglobin, bronchoalveolar lavage fluid (BALF) showing grossly bloody returns or increasing bloody aliquots or hemosiderin-laden macrophages ≥20% was used as criteria for DAH.[9] All patients with “provisional PRS” who did not have a clear diagnosis at presentation underwent an echocardiogram, ultrasound of the kidneys, and appropriate bacterial cultures; the need for peripheral smears and antigen (histidine-rich protein 2) testing for malaria, IgM enzyme-linked immunosorbent assay (ELISA) for leptospirosis, nested PCR for scrub typhus or other appropriate tests was decided by the treating intensivist. Patients initially labeled as “provisional PRS,” but with no definite evidence of DAH or had a nonimmune etiology for PRS on subsequent evaluation were labeled as “PRS mimics” [Figure 1]. In patients with “definite PRS,” evaluation for the underlying etiology of PRS was initially performed with a panel of anti-nuclear antibody by indirect immunofluorescence (IIF), antinuclear cytoplasmic antibodies (ANCA) by IIF, anti-GBM antibodies by ELISA and complement levels (C3, C4). Appropriate guided-biopsies were performed from involved target organs (kidneys and/or lungs) to further characterize the individual diagnosis of PRS.[1011] Treatment was initiated when the syndromic diagnosis of “definite PRS” was made with pulse methylprednisolone 1 g daily for 3 days, followed by 1 mg/kg/day enteral prednisolone and IV cyclophosphamide 750 mg/m2 in the absence of infection or recent major gastrointestinal bleeding. Pantoprazole was administered to all patients during steroid therapy. The dose of cyclophosphamide was modified for an estimated eGFR <10 mL/min to 75% of the estimated dose. Six hundred mg mesna IV in three divided doses was administered in all patients along with cyclophosphamide. Rituximab was not used because of unavailability. Plasmapheresis (hemonitics PCS® 2 centrifugal pump) was initiated with 1.5 plasma volume exchanges (60 mL/kg) in the presence of definite DAH or serum creatinine >5.6 mg/dL and “definite PRS;” fresh frozen plasma (FFP) was used as replacement. Four percent albumin was also used when available. The ICU treating team in concurrence with the nephrology team initiated hemodialysis. Hemodialysis was performed by intermittent hemodialysis over 4 h or sustained low-efficiency dialysis over 9–12 h, when hemodynamically unstable. The decision on the number of sessions of plasmapheresis and hemodialysis and subsequent immunosuppression was decided in consensus with the rheumatology and nephrology teams. Bleeding was managed with random donor platelets or single donor platelets, FFPs, cryoprecipitate and packed red cell transfusions (RBCs) as guided by the results of platelet count, hemoglobin, prothrombin time, activated partial thromboplastin time, and fibrinogen levels. Prothrombin concentrates or activated factor VIIa were not used due to unavailability. Asymptomatic platelet counts ≤20,000/ml were treated prophylactically to a count greater than this level. Packed RBCs were transfused if ongoing major bleeding or if hemoglobin was ≤7 g/dL to a level greater than this.


Pulmonary-renal syndromes: Experience from an Indian Intensive Care Unit.

Rajagopala S, Sagar BK, Thabah MM, Srinivas BH, Venkateswaran R, Parameswaran S - Indian J Crit Care Med (2015)

Composite image of the chest radiograph (left) and computed tomography (CT) of the chest (right) of patient 1 with showing bilateral lower lobe consolidation with corresponding asymmetric ground glass opacities and crazy-paving on CT. A clinical diagnosis of alveolar hemorrhage (DAH) was made
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4478672&req=5

Figure 1: Composite image of the chest radiograph (left) and computed tomography (CT) of the chest (right) of patient 1 with showing bilateral lower lobe consolidation with corresponding asymmetric ground glass opacities and crazy-paving on CT. A clinical diagnosis of alveolar hemorrhage (DAH) was made
Mentions: Patients were diagnosed with “PRS” provisionally at ICU admission if they fulfilled all the below; acute illness (≤4 weeks) with evidence of renal and lung involvement at ICU admission, “active urinary sediment” on urine examination and pulmonary involvement consistent with diffuse alveolar hemorrhage (DAH) or vasculitis. “Active urinary sediments” was defined by the presence of at least one of the below; albuminuria (≥3+ on dipstick testing, >300 mg on 24-h collection or a urine protein/creatinine ratio >45 mg/mol), red blood cells (RBCs) or casts (RBCs or leukocyte casts) in urine microscopy examination with or without azotemia.[8] DAH was defined by the presence of at least two of the following; chest infiltrates consistent with DAH, hemoglobin ≤11 g/dL, and hemoptysis. In the absence of hemoptysis or a definite drop in hemoglobin, bronchoalveolar lavage fluid (BALF) showing grossly bloody returns or increasing bloody aliquots or hemosiderin-laden macrophages ≥20% was used as criteria for DAH.[9] All patients with “provisional PRS” who did not have a clear diagnosis at presentation underwent an echocardiogram, ultrasound of the kidneys, and appropriate bacterial cultures; the need for peripheral smears and antigen (histidine-rich protein 2) testing for malaria, IgM enzyme-linked immunosorbent assay (ELISA) for leptospirosis, nested PCR for scrub typhus or other appropriate tests was decided by the treating intensivist. Patients initially labeled as “provisional PRS,” but with no definite evidence of DAH or had a nonimmune etiology for PRS on subsequent evaluation were labeled as “PRS mimics” [Figure 1]. In patients with “definite PRS,” evaluation for the underlying etiology of PRS was initially performed with a panel of anti-nuclear antibody by indirect immunofluorescence (IIF), antinuclear cytoplasmic antibodies (ANCA) by IIF, anti-GBM antibodies by ELISA and complement levels (C3, C4). Appropriate guided-biopsies were performed from involved target organs (kidneys and/or lungs) to further characterize the individual diagnosis of PRS.[1011] Treatment was initiated when the syndromic diagnosis of “definite PRS” was made with pulse methylprednisolone 1 g daily for 3 days, followed by 1 mg/kg/day enteral prednisolone and IV cyclophosphamide 750 mg/m2 in the absence of infection or recent major gastrointestinal bleeding. Pantoprazole was administered to all patients during steroid therapy. The dose of cyclophosphamide was modified for an estimated eGFR <10 mL/min to 75% of the estimated dose. Six hundred mg mesna IV in three divided doses was administered in all patients along with cyclophosphamide. Rituximab was not used because of unavailability. Plasmapheresis (hemonitics PCS® 2 centrifugal pump) was initiated with 1.5 plasma volume exchanges (60 mL/kg) in the presence of definite DAH or serum creatinine >5.6 mg/dL and “definite PRS;” fresh frozen plasma (FFP) was used as replacement. Four percent albumin was also used when available. The ICU treating team in concurrence with the nephrology team initiated hemodialysis. Hemodialysis was performed by intermittent hemodialysis over 4 h or sustained low-efficiency dialysis over 9–12 h, when hemodynamically unstable. The decision on the number of sessions of plasmapheresis and hemodialysis and subsequent immunosuppression was decided in consensus with the rheumatology and nephrology teams. Bleeding was managed with random donor platelets or single donor platelets, FFPs, cryoprecipitate and packed red cell transfusions (RBCs) as guided by the results of platelet count, hemoglobin, prothrombin time, activated partial thromboplastin time, and fibrinogen levels. Prothrombin concentrates or activated factor VIIa were not used due to unavailability. Asymptomatic platelet counts ≤20,000/ml were treated prophylactically to a count greater than this level. Packed RBCs were transfused if ongoing major bleeding or if hemoglobin was ≤7 g/dL to a level greater than this.

Bottom Line: Clinical characteristics of patients with "definite PRS" were compared with those with "PRS mimics".Patients with PRS had more alveolar hemorrhage, hypoxemia and higher mortality (69%) when compared to "PRS mimics".Multicentric studies are needed to further characterize the burden, etiology, treatment protocols, and outcomes of PRS in India.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Dhanvantri Nagar, Puducherry, India.

ABSTRACT

Background: The etiology of patients presenting with pulmonary-renal syndrome (PRS) to Intensive Care Units (ICUs) in India is not previously reported.

Aims: The aim was to describe the prevalence, etiology, clinical manifestations, and outcomes of PRS in an Indian ICU and identify variables that differentiate immunologic causes of PRS from tropical syndromes presenting with PRS.

Materials and methods: We conducted a prospective observational study of all patients presenting with PRS over 1-year. Clinical characteristics of patients with "definite PRS" were compared with those with "PRS mimics".

Results: We saw 27 patients with "provisional PRS" over the said duration; this included 13 patients with "definite PRS" and 14 with "PRS mimics". The clinical symptoms were similar, but patients with PRS were younger and presented with longer symptom duration. Ninety-two percent of the PRS cohort required mechanical ventilation, 77% required vasopressors and 61.5% required dialysis within 48 h of ICU admission. The etiologic diagnosis of PRS was made after ICU admission in 61.5%. Systemic lupus erythrematosus (54%) was the most common diagnosis. A combination of biopsy and serology was needed in the majority (69%, 9/13). Pulse methylprednisolone (92%) and cyclophosphamide (61.5%) was the most common protocol employed. Patients with PRS had more alveolar hemorrhage, hypoxemia and higher mortality (69%) when compared to "PRS mimics".

Conclusion: The spectrum of PRS is different in the tropics and tropical syndromes presenting with PRS are not uncommon. Multicentric studies are needed to further characterize the burden, etiology, treatment protocols, and outcomes of PRS in India.

No MeSH data available.


Related in: MedlinePlus