ARF Case Study Linda Winn, RN, MSN Ed. Acute Respiratory Failure: Case Study.
An interesting case of ARF
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Transcript of An interesting case of ARF
First Admission on 21/3/03
Mr.Gandhi,36yr old male, with symptoms of chronic cough and expectoration, heamoptysis and fever ,was diagnosed to have sputum +ve pulmonary TB.He was started on ATT on 8/3/03.3 weeks later the pt was admitted in the ward with h/o dyspnoea, oliguria, facial puffiness and pedal edema for 10 days.On evaluation of his clinical profile and lab data, he was diagnosed to have renal failure. His inv.reports as follows,
Lab reports RFTBld urea 153 mg/dlSr creat 21.1 mg/dlSr electrolytesNa+ 138 mg/dlK+ 3.9 mg/dl Sr uric acid 8 mg/dlSr phosphate 7.4
mg/dl
Urine analysisAlb +Sugar nilEpi cells 2-4Pus cells 4-624 hr urine pr 40
mg/LUrine c/s no growth
continued Complete
heamogramHb% 10.6 g%Pcv 32%TC 8600DC P61 L36 E3ESR 80/140Platelets 1 lak cells
LFTTotal bilirubin
1.0mg/dlSGOT 32 IU/dlSGPT 25 IU/dl Bld glucose 80 mg/dl Total protien 5.6 g% Total cholesterol 200
mg%
continued
Sr HIV –ve Sr HBsAg –ve VDRL NR ECG WNL CXR bil apical infiltrations s/o PT USG abd bil medical renal disease non specific
hepatomegaly
Treatment given ATT was stopped 60 cycles of PD given After stopping ATT and PD, his RFT
values were as follows (2003)Date 21/
322/3 28/
331/3
03/4 09/4
Urea mg/dl 153 186 168 98 86 48
CreatinineMg/dl
21.1
12.8 8.0 4.5 2.4 1.5
Second Admission on 24/9/06
The pt was readmitted 3yrs later with h/o fever with chills ,vomiting, loin pain, oliguria, heamaturia, puffiness of face, pedal edema. His past history revealed that he discontinued ATT after the last admission. Again he developed the symptoms of TB and was found to be sputum +ve and was restarted on ATT(18/09/06).
On examination
Pt was febrile.Had puffiness of face and pedal edema.
His BP was 160/90mmhg.Had basal creps in his lung fields
Lab Reports RFTBld urea 168 mg/dlSr creat 11.1 mg/dlSr electrolytesNa+ 138 mg/dlK+ 3.9 mg/dl Sr uric acid 8.3 mg/dlSr phosphate 6.3
mg/dl
Urine analysisAlb ++Sugar nilEpi cells 1-2Pus cells 10-12RBC’s 25-27/hpfBile salts&pigments
nil
Continued Complete
heamogramHb% 12.0 g%Pcv 36%TC 7200DC P54 L43 E3ESR 28/60Platelets 1.2 lak cells
LFTTotal bilirubin
1.0mg/dlSGOT 31 IU/dlSGPT 40 IU/dl Bld glucose 127
mg/dl Total protien 5.6 g% Total cholesterol 256
mg%
Continued
ECG WNL CXR bil apical infiltrations s/o PT USG abd bil medical renal disease non specific
hepatomegaly
Diagnosis
Acute Renal Failure Rifampicin Induced The occurence of renal failure
again ( second time ) definitely proves that Rifampicin is the cause.
Treatment given ATT was continued without rifampicin 7 cycles of HD given After stopping rifampicin and HD, his RFT
values were as follows (2006)
Date 26/9 28/9
05/10
09/10
12/10
16/10
Urea mg/dl 168 105 118 158 78 28
CreatinineMg/dl
11.0 10.7
9.0 7.1 2.0 1.2
Similar cited articles
Covic A, Goldsmith DA et al. Rifampicin induced ARF: a series of 60 patients.Nephrol Dial Transplant1983; 13:924-929
Muthukumar T et al.ARF due to rifampicin:a study of 25 patients.Am J Kidney Dis. 2002 oct;40(4):690-6
Discussion From the data of TRC chetpet, Of treating more
than 8000 pulm & extrapulm pts with rifampicin containing regimen from early 1970’s ,3cases of probably rifampicin induced ARF has been reported.
A data from nephrology department of MMC states that rifampicin induced ARF constituted 2.5% of all cases of ARF during the study period of 1990-2000.
ARF due to rifampicin usually occurs in pts receiving intermittent or interrupted therapy & rarely with continuous therapy.
Clinical picture The pt usually presents with gastrointestinal
and flu like symptoms and clinical signs of intravascular heamolysis.
Post-rifampicin ARF is characteristically ass. with autoimmune heamolysis, thrombocytopenia, DIC, hepatic injury &tubular defects, thus creating a polymorphic picture.
Frequent lab findings are anemia, leukocytosis, thrombocytopenia, hypergammaglobulinemia& evidence of hepatic injury.
Renal toxicity of rifampicin Acute tubulointerstitial nephritis and/or
tubular defects. Isolated or superimposed glomerular
injury presenting either with a RPGN or a frank nephrotic syndrome.
The presentation is usually oligoanuria. And the urinalysis reveals sterile leukocyturia, protienuria, heamaturia & heamoglobinuria.
Immune induced rifampicin toxicity
Acc. Of antirifampicin Abduring drug free interval
(I Ag - RBC’s & tubular epi)
Readministration of drug
Intense immune reaction
Intravascular heamolysis Immune complex deposition in blood vessels & interstitium
heamoglobinuria ATN AIN
Diagnosis of post-rifampicin ARF
The specific time course of events, in association with a previous normal renal function and absence of other potential causes for ARF, establishes rifampicin as the sole etiology.
Routine examination for antirifampicin Ab & renal biopsy are not considered essential for positive diagnosis.
Prognosis Clinical course is very favourable with
very rare mortality. Prognostic factors: duration of anuric
phase& the severity of the immunological abnormalities and inflammatory syndrome(heamolysis, leucocytosis& hypergammaglobulinemia)