Mariana Bridi da Costa, a 20-year old Brazilian model, tragically died early Saturday morning from Pseudomonas aeruginosa urosepsis.
How can this happen?
Miss Bridi da Costa initially presented on December 30th, and was diagnosed with kidney stones. An ultrasound, plain film, or CT scan likely would have been done to confirm the diagnosis. I assume that a urinalysis was also performed, and if so, may have pointed to a urinary tract infection on that day.
Treatment of kidney stones typically consists of fluids and pain control. Depending on the size and location, a urologist may need to be consulted to extract the stone via a procedure, or break it up with shock waves. Antibiotics are normally not prescribed in uncomplicated cases.
In any case, she was apparently sent home, and presented again on January 3rd in septic shock. This is a condition involving life-threateningly low blood pressure brought about by an infection that has spread to the bloodstream.
Patients in this scenario are critically ill, requiring intravenous medications to maintain the blood pressure, and several broad-spectrum antibiotics to treat the infection. In Miss Bridi da Costa’s case, the responsible bacteria was Pseudomonas aeruginosa.
On January 23rd, it was reported she had to have her hands and feet amputated, presumably from continued spread of the infection. She passed away days later.
Pseudomonas aeruginosa is one of the most virulent bacteria that exists. It is resistant to many antibiotics, and can rapidly mutate to become resistant to newer drugs. Normally, more than one antibiotic has to be prescribed to ensure its eradication.
It is almost always contracted within the hospital, causing about 10 percent of the two million hospital-acquired infections each year in American hospitals. The presence of a urinary catheter or undergoing urologic procedures – such as a cystoscopy – can lead to Pseudomonas-associated urinary tract infections.
In this case, the fact that the infection was caught within the community is worrisome, and exceedingly rare. Assuming that she was not immunocompromised, she may have had previous colonization with the Pseudomonas in her genitourinary tract. Bacteria then could have ascended through the urethra to the kidneys, and from there, into the blood stream.
Once in the blood, infection that remains untreated causes a significant inflammatory response, leading to possible blood clots, or results in the blood vessels within the extremities to shut down, causing the tissue to become necrotic. Amputation would then be necessary.
I suspect that earlier treatment, such as when she initially presented on December 30th, may have made a difference. Ciprofloxacin, a common antibiotic used to treat urinary tract infections, does have activity against Pseudomonas. By the time she presented with sepsis, her prognosis became exceedingly poor, with studies showing up to a 40 to 50 percent mortality rate.
Although most infectious disease specialists acknowledge that contracting a Pseudomonas infection outside the hospital is not common, this is a sobering reminder that drug-resistant infections are not only possible, and may be on the rise. We are already seeing an increase in the number of methicillin-resistant Staphylococcus aureus (MRSA) and Clostridium difficile cases within the community.
Inappropriate antibiotic use is a major culprit, but it’s a problem that’s often dismissed. So the next time you go to the doctor’s office thinking you need an antibiotic for a cold, think of Mariana Bridi da Costa.
Related posts:
- What Mozart can teach us about suberbugs and antibiotic resistance
- Getting rid of a cold without antibiotics
- Medicare is no longer paying for complications
- A nuclear bomb to kill a fly
- Primary care is a lousy term
- Too many doctors are calling in antibiotics over the phone
- Medicare ceases to pay for medical errors
{ 12 comments }
It is unlikely that she required amputation because of the infection in and of itself. More likely is the case that she was given extra-ordinarily high doses of vasopressors which lead to profound peripheral vascular vasoconstriction, ultimately shutting off critical blood flow to her extremities.
You’re analysis of the problem is definetely correct. But I would add that the other problem that remains widespread is the innapropriate management of patients with severe sepsis and septic shock. I am not saying that this patient was mis-managed. I just want to make a point that there is a huge international campaign to improve the medical therapy and early identification of these patients. The SCCM has been leading this campaign and is making a good impact.
JFS
I would think the pseudomonas infection was not community-acqired, but aquired in the hosptial during her admission Dec 30.
Either way, its tagic.
BTW, Congrats on the best med blog award.
Pseudomonas is a community-acquired organism as well as an opportunistic infectious organism in hospitals. It is common in infectious keratitis associated with contact lens wear, overwear and abuse.
I agree with Dr. Sucher. The amputation of her hands and feet was probably the result of vasopressors used to treat her septic shock.
News reports also said she underwent bilateral nephrectomies and a partial resection of her stomach during her hospitalization.
DIC/ inflammatory syndrome or vasopressors?
Tragic either way.
Vasopressors. There is no doubt in my mind. It is an unfortunate well known consequence of vasoconstrictor administration for patients with septic shock. Fortunately it doesn’t happen often, but I have seen it multiple times. The bilateral nephrectomies is very unusual, but in medicine unusual things can occur and I would not comment on it. Stomach resection would be even more unusual, and if true would be a result of uncontrollable stress ulcer hemorrhage. Something that is extremely rare in the U.S. now for many many reasons.
But this is all really off the point. I Kevin’s point is well noted.
Thanks,
JFS
I was shocked when I had heard about this. It’s sad when something tragic like this happens.
People don’t really appreciate this, but one of the things that makes MRSA so deadly is that it is resistant to many antibiotics that normal commensal bacteria are not resistant to and those bacteria normally suppress the MRSA. If I may speculate as to what may have happened. She may have been colonized with MRSA but the MRSA were kept in check by her normal commensal flora; she took an antibiotic for her kidney stones, the antibiotic then wiped out her normal flora but didn’t wipe out the MRSA (because it was resistant), then with the open niche and the normal commensals gone, the MRSA could expand, express quorum sensing compounds, express virulence factors and cause sepsis.
I think that the infection can proceed extremely rapidly because there is nothing keeping the MRSA in check because all the competing bacteria have been wiped out. A large part of what keeps pathogens at bay is the normal commensal bacteria. Knock them out and you are effectively immunocompromised.
People need to appreciate that they can appear (and be) perfectly healthy, but if they are colonized by MRSA and take an inappropriate antibiotic they may develop sepsis and die in just a few days. It isn’t that an antibiotic “can’t hurt”, it can kill you via the scenario I outlined.
daedalus2u:
The news reports that the patient’s infecting organism was pseudomonas aeruginosa, a gram-negative rod bacterium, and usually resistant It was NOT MRSA which is a drug-resistant gram-positive organism common in the community.
Does instrumentation in urological procedures introduce pseudomonas to previously well, immunocompetent patient? The various pan-resistant strains of this nasty GN rod colonized in respiratory and urinary tracts of ambulatory hosts suggests missing data. Here's a case (purely anecdotal but interesting) the patient, an essentially well 42 yr old F. had recurring UTI with hematuria and flank pain secondary to left renal calculi x3 approx 8mm in upper pole. C&S revealed sulfa susceptible E-Coli hence Bactrim DS bid x 7 days was completed. The pt. then underwent Left ESWL followed by placement of double J-pigtailed stent to facilitate stone passage. Pt was discharged home from SDS Uro in stable condition, with standard instructions to strain all urine, begin vigorous oral hydration and Cipro 500 bid x7d and use of sched II analgesia prn. Despite the pain medication and due to intractable stent colic, the pt. called the surgeon who instructed her to remove the stent via the distal end which he had taped to her upper leg. It was this surgeons SOP to tape his stents thusly for precisiely this purpose. Within 48 hours the pt was confused, lethargic, fervescent at 104 with a white count of 38, with dramatic pallor reported by her family and and was having continuous, uncontrollable rigors. She was then re admitted to surgery via Uro svc. with a Dx of urosepsis. Blood and urine cultures pending, imagine revealed steinstrasse urosepsis. After being re-stented, ID was called in on consult and treatment with gentimicin was begun. At this point the patient was inadvertently administered a tenfold overdose of the ototoxic/nehphrotoxic /vestibulotoxic aminoglycoside despite the presence of a dosing pharmacy. 800mg was given instead of the customary adult dose of 80mg. Peak and trough was ordered but never drawn. Notes stated that the patient was a 'hard stick'. Central line/pressors were never not recommended by ID because renal function remained adequate and the patient had become more alert and oriented. Xigris was considered but then discounted as the patient did well. By hospital day 3 -urine and blood C&S revealed revealed a multidrug resistant pseudomonas a. which was ONLY susceptive to the third generation cephalosporin FORTAZ! The pt., by then then responsive in the unit, was stepped down , continued to improve, but suffered a permanent central bilateral vestibular paresis (secondary to aminoglycoside toxicity). Although the pt's urinary tract is colonized with this MDR pseudonomas she is otherwise well. Annual KUB reveals a q2/3 year re-appearance of calculi which are suspected of being the nidus of persistent infection. Prior to ESWL which the pt. must undergo approximately every 2/3rs she must have home IV Fortaz 1 gm bid, x 7 days. Immediately s/p last infusion prior to ESWL her urine was clean. Within three months of that, the pseudomonas is BACK but the patient does not become ill. It is a true colonization. Take home for me is that this organism and other GM rods which kill so quickly (along with the pressors/Xigris mentioned by the other providers) exhibits hehavior which is different in each host. This has the net effect of making use of the therapeutic armamentarium an increasingly complex nightmare. Have any of you used Xigris? Outcomes? I don't know about the status of Brazillian health care and even less about the details of this poor girls' demise at the hands of infectious disease. I want to think everything was done for her. But like many of you, In my less optomistic moments, I often wonder if ID won't get us all in the end?
Thank you for this post Dr. Pho– I lost my wonderful husband due to an intracerebral hemorrhage that resulted in poorly controlled BP which was caused by septic shock, shortly after having a cystoscopy with placement of a suprapubic catheter. Long story short, DH was a C7 quad with a long Hx of bladder infections because of his neurogenic bladder. He finally had enough infections, as they were impossible to forsee & he always ended up in autonomic dysreflexia. He had cheated death numerous times in the past so we NEVER expected his death to result from a proceure that is commonly done on an outpatient basis, and was something we had hoped would prevent future infections.
i feel that she could have lost her feet and hands because of dic causing thrombosis and gangrene. Sometimes a vasculitis can occur secondary to a systemic infection.
vasopressors seems attractve but i have never seen that happen in my 15 years of practice
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