Volume 186 - Issue 3
An unusual cause of severe metabolic acidosis
Authors: Mark A Boyd and Stephen Hedger
Med J Aust 2007; 186 (3): 158-159. || doi: 10.5694/j.1326-5377.2007.tb00846.x
Published online: 5 February 2007
Published online: 5 February 2007
To the Editor: We read with interest the “Diagnostic Dilemma” by Peter et al.1 The case raises interesting management issues. The first is initiation of antibiotics. Despite 1 week of fever, rigors, haematuria and loin pain, we are informed that the patient was in no distress at initial assessment. In this situation there is, despite the anxieties of resident staff, no urgent need to administer antibiotics; hospitals are controlled, monitored environments in which observation, review and investigation can be undertaken, within reason, if a diagnosis is not immediately made. The second issue is antibiotic selection. The provisional diagnosis was a urinary tract infection, and ceftriaxone and gentamicin were administered. The justification for the use of two agents with a similar spectrum of antimicrobial activity is not given.2 Likewise, no justification is given for the use of a potent nephrotoxin in the presence of moderately severe acute renal failure.
Flucloxacillin was added “to broaden the gram-positive antibiotic cover”. It is not apparent why staphylococcal cover was sought at this stage. All cultures (blood, urine and pleural fluid) remained negative. At Day 14, ceftriaxone and gentamicin were changed to ticarcillin/clavulanic acid and ciprofloxacin “because of persistent fever and rising [white cell count]”; this decision in the absence of positive cultures is not explained.
The patient’s renal function deteriorated further and he became profoundly acidotic. In fact, the patient’s renal function had performed heroically, given administration of gentamicin for 2 weeks in the presence of acute renal failure at admission. In the intensive care unit, flucloxacillin was replaced with vancomycin; the rationale is not explained.
This case illustrates important points regarding antibiotic use. Despite significant renal impairment at admission, the patient was administered a 2-week course of a nephrotoxic antibiotic, which contributed to renal collapse. This situation would have been terminal if not for supportive intensive care. The treating team appears to have managed the patient as if sepsis were a given, and yet all cultures remained negative. This illustrates a basic but crucial teaching point — fevers, chills, rigors, raised inflammatory markers and neutrophilia do not necessarily equate with sepsis. If this experience reflects routine practice elsewhere (and it is our experience that it does), is it any wonder that we have reached an era in which we now encounter organisms so resistant that they are essentially untreatable?3
References
- Peter JV, Rogers N, Murty S, et al. An unusual cause of severe metabolic acidosis. Med J Aust 2006; 185: 223-225.
- Safdar N, Handelsman J, Maki DG. Does combination antimicrobial therapy reduce mortality in Gram-negative bacteraemia? A meta-analysis. Lancet Infect Dis 2004; 4: 519-527. 0_i1091782
- Peleg AY, Paterson DL. Multidrug-resistant Acinetobacter: a threat to the antibiotic era. Intern Med J 2006; 36: 479-482. 0_i1091785