Written by Hongyu Zhao, MD, PGY-2 and Qing Meng Zhang, MD, PGY-2 at Kaiser Permanente…
With the changing attendings, I now have a female physician, Dr. Yumbe, as part of our team. It is very interesting to get a different perspective- in particular as she trained at UTI as an intern and has now returned.
On our last call day, we admitted a middle aged male with recently discovered positive HIV status who had travelled out of Lusaka to visit family. 5 days after his return, he presented to his local hospital with cyclic fevers, darkened urine and confusion. His blood smear showed 4+ parasitemia- likely plasmodium falciparum the parasite causing the more severe forms of malaria, including cerebral malaria. Because of he also presented with severe jaundice and elevated creatinine (a sign of partial renal failure), we were concerned that he would develop “black water” fever where hemolysis (destruction of red blood cells caused by parasite release) is so severe that the patient’s urine turns black and kidneys fail. Given his risk factors, my attending immediately admitted him to the ICU, despite his stable blood pressure and respiratory status. He did well, was transferred from the ICU and discharged within the week.
Since I was following the patient, we discussed him at length, including her rationale for transfer to the ICU. She said that in Lusaka and surrounding areas, malaria is rarely seen, but when it is, they don’t even do plasmodium strain identification- it is assumed to be falciparum and almost always a very severe case. Furthermore, malaria and the mosquito population used to be under better control than it is now. People with frequent exposure to malaria are thought to develop at least partial immunity- but in the past 20 years, since the control has been good, the community’s immunity is thought to be waning. Furthermore, in people with newly diagnosed HIV have their own risks with malaria. Studies performed Zambia showed that those with an initial CD4 count <300 are prone to increased risk of malaria infection, increased parasite load, and increased risk of recurrent infection.
Here many people present with AIDS defining illnesses as their first sign of HIV infection- as people did in the height of the AIDS epidemic in the US. I have seen now disseminated Karposi’s sarcoma, Herpes Zoster, HIV wasting syndrome, persistent diarrhea, vomiting, fungal nail infections, neutropenia, anemia, thrombocytopenia, and CNS toxoplasmosis all in patients with newly diagnosied HIV. I almost feel like I am beginning to be able to look at a patient and suspect HIV positive status just from their ill health and presenting complaints.
There are many other ways that the high rate of HIV infection and AIDS has affected the Zambian population- and none more ever-present than its potentiating effect on tuberculosis. One of the Zambian characteristics I have noticed is to be soft spoken and very calm, even about things that are very serious. When I asked my attending about the effect of HIV and TB on the disease climate and the recent trend, my attending said- “No, it is not very good. It is in fact, very serious.”
She explained that because initially HIV was diagnosed with AIDS defining illness (including those outlined in the WHO guidelines for identification of HIV positive individuals in areas where HIV testing is not available) and antiretroviral treatment only started when patients were severely ill, the patients were very compliant in taking their medications. However, now, with the ability to check CD4 counts and discuss when to start antiretroviral therapy, people have started on antiretrovirals without severe or debilitating conditions and the compliance to the medication regimens has decreased. There seem to be more antiretroviral therapy defaulters (what the hospital calls people who have stopped taking their medications) who present with AIDS defining illness and then are must start on second or third line treatment.
Tuberculosis was always difficult to treat, and decreasing exposure is thought to be tantamount in decreasing the chance of infection. With the number of persons with immune systems suppressed by HIV infection and developing infectious TB, there is more community exposure. The group of patients who present with serious tuberculosis infection- the classic wasting and night fever lung infection, Pott’s disease- TB in the bone, or milliary TB- where it has spread to multiple organs, now includes all people with suppressed immune systems, newly diagnosed HIV cases, the elderly and the young. And there is, of course, the slow and insidious increase in the rate of multiple drug resistant tuberculosis strains as people fail to complete their treatment and spread bacteria which has been exposed and developed resistance the first line tuberculosis treatment.
Though more eloquent people than I have spoken about the disastrous effects of high rates of HIV positive individuals in a population, especially on the control of tuberculosis, at UTH it is demonstrated daily. People come in very sick and here, we treat the infection prior to starting antiretroviral therapy to avoid precipitating IRIS (Immune reconstitution syndrome, where patients with a previously suppressed immune system will respond well to antiretroviral treatment and then develop serious or morbid complications from the body’s response to infections that the immune system previously lacked the strength to attack). This means they must survive the initial infection to start HIV treatment, or, in cases where concern for TB is high, they must survive 2 weeks of antibiotics for tuberculosis in order to start on highly active retroviral therapy. That does not always occur.
These difficulties are compounded by the fact, now that I am getting to know the population we see a bit better, that people here only come into the hospital when they are very close to death. This is particularly frustrating for the physicians who may find a woman with low blood pressure and newly diagnosed HIV who actually has Addison’s crisis due to TB infection of the adrenal glands rather than sepsis, and for whom emergent treatment may be less effective had she presented and been diagnosed with TB or HIV prior to her symptomatic hypotension.
I have also been working for long enough to see the number of patients who are severely ill and pass even while hospitalized. Sometimes, as for my patients with CLL with conversion to ALL who I wrote about on a previous blog, a nurse will come get the physician for a “change in status” and it is unclear how the event occurred. Sometimes the physicians and nursing will be present at the bedside. Last week we attempted CPR and resuscitation on a patient who had a change in status right after returning from a procedure. Though we had all the knowledge and everyone was trained in what to do, the patient still expired.
The physicians here work very hard to take care of their patients, and they have a huge number of very ill patients for which to care. On the cheerier side, glucose strips are restocked, and my new nick name is McGyver because I’ve always got my (bottomless?) bag of medical tools. I’ve also had the pleasure of seeing several of the patients who we had recently discharged or admitted, going home much improved or even seeing them for a follow up visit looking remarkably well. It is very satisfying to see life-saving medicine working even on severe and serious cases.
And now, I’ve taken enough time to write this entry and I should be getting back to work. My team (now down to just one intern and one attending due to a partial strike in the hospital) will be working the overnight admission shift.