Malaria
I offer the following quote from the Oxford Handbook of Tropical Medicine: “Malaria, a protozoan disease transmitted by anopheline mosquitos, is the most important parasitic disease of humans. As many as 3 billion in endemic areas are at risk of malaria and approximately 500 million clinical cases occur annually. Between one and three million die annually, largely African infants and young children.” That last fact was brought home to me in dramatic fashion today when a nine month old with malaria was brought into the clinic in near death condition. It is possible that we may have saved him, but it is equally possible that he may not survive. His life literally hangs in the balance. More about that child later, but first a brief discussion of malaria is in order.
We who live in a world devoid of malaria cannot possibly appreciate the destructive and debilitating power of this disease. It was only when I lived and worked in Burundi that I did understand that power. It is, at best, a nasty and unpleasant disease; it is at worst, a disease quite capable of killing a child. The numbers (one to three million deaths per year) bear out that statement. The number of children that I have seen with this disease is countless. They come into the clinic with a typical look: a very ill-appearing look; a look which says that everything hurts (which it does); a look which begs for help. I show you one such child.
We, at the clinic, have the means to help these children. We have medications to treat the disease. Most Burundians afflicted with malaria cannot afford these or any medications. The most commonly used medication to treat malaria here is quinine. The cost of one week (the usual course of treatment) of quinine is approximately a dollar and a half. That amount is nothing to us, yet that same amount might as well be a million and a half dollars to a Burundian. That’s why he suffers through his all-too-frequent episodes of malaria without the hope of getting better quickly. That is also true for most of the children in Burundi. It is only a relative few who have access to the services of the clinic here in Kigutu, services that include the dispensing of malaria medication to those who cannot afford that medication.
May 25th, 2011:
The doctor at the outside clinic diagnosed him with “probable malaria,” but did not treat the baby, possibly because the mother could not afford the medication.
Malaria, in its most severe form, is often fatal. I saw that severe form today. The child was brought in virtually unresponsive. He cried only with deep pain. He hardly uttered a cry when we took blood, or even when an I.V. was inserted. His breathing was fast and labored, with each breath coming with an audible grunt. His nose flared out as he breathed (another sign of respiratory distress). Most remarkable was his color. Last year, I learned how to judge anemia the old fashioned way: by looking at the color of a child’s conjunctiva and nail-beds. We did not have a machine last year to test a child’s hemoglobin. This year, we do. That test would only confirm what I saw clinically: this child was profoundly anemic. His conjunctiva and his nail-beds were a chalk-like white. His tongue was white. The blood test confirmed what I saw: his hemoglobin was 3.7 (normal is 12-15). His heart was beating extremely fast (about 130-140 beats/minute) to compensate for his lack of blood. That compensation was ineffective, for the direct effects of the malaria infestation and the subsequent anemia had caused the child to develop something called “acute respiratory distress syndrome.” His lungs were not working. That’s why his breathing was so labored: to attempt to get enough oxygen to his soon-to-be failing body.
The child’s spleen was markedly enlarged, which was further proof that his anemia was the result of severe hemolysis (breakdown) of his red blood cells. I show you now pictures of the child, as he was early this afternoon. I think the pictures will give you an idea of the gravity of the situation.
We did not know for certain that the child had malaria, but the entire picture was consistent with severe malaria. We did a quick blood test which confirmed the diagnosis.
The child was in urgent need of a transfusion, but the clinic is not capable of doing a transfusion. We cannot keep blood on hand, because we do not have the refrigerator capacity of storing that blood. There is an extremely limited supply of blood in the entire country. That supply is distributed by a central source in Bujumbura. The nearest hospital that had the capability of performing a transfusion was in Rumonge, a 45 minute drive down the treacherous mountain path that passes for a road here. That hospital only had Type B blood. If our patient did not have Type B blood, the nearest hospital that might be able to accommodate him was more than two hours further away. It was unlikely that he would survive that prolonged a journey. We were in luck, for the child was Type B.
We had to stabilize him even before we could even think of transferring him. Assuming the mother was correct in her assertion that the child had been in that condition for five days, it was highly unlikely that he had anywhere near adequate fluid intake over those days. He needed fluid, but that was a double-edged sword. Giving him too much fluid, based on his degree of anemia, would cause him to develop certain heart failure. Not giving him enough could cause organ shutdown. We calculated what we thought was an appropriate amount.
We also needed to start treatment of the malaria. That meant loading him with a higher-than-usual dose of quinine, based on the severity of the anemia. We did so in a limited amount of fluid. I should, at this point, acknowledge the skills of the nurses who somehow got a working I.V. into this desperately ill child.
The other problem was that the child had a cough. Severe malaria often causes the child to be immuno-compromised. There was a reasonable chance, in view of the cough, that the child had developed a secondary pneumonia. Therefore, we gave him a dose of Ceftriaxone, a broad spectrum antibiotic.
The good news was that the child was successfully transferred to the hospital in Rumonge. Initially, the hospital was reluctant to take him, because the mother had no money to pay for their services. However, ultimately, they did, and, from what I understand, the child did receive the transfusion. What transpired after that, I do not know. I wait with the rest of you to see if the child did survive the grievous insult brought on by that ubiquitous (at least, ubiquitous here in Africa) parasite that goes by the name of malaria.
May 26th, 2011;
I have just now received the news that Festus Ndayisimiye has improved. Dr. Melino spoke with the doctor taking care of him in Rumonge, and the doctor reports that the blood transfusion had the desired effect. Festus is now out of danger, and it is expected that he will make a complete recovery.
Festus was lucky. The only blood available to him in Rumonge was Type B. This is a relatively uncommon blood type in the United States, with only about 10% of the population being Type B. Here in Burundi, it is slightly more common: the preliminary research I did shows that slightly less than 20% of the population are Type B. That meant that there was only a one in five chance that the hospital in Rumonge would have blood compatible with Festus’s blood. The next closest hospital with blood was over two hours away. I doubt that Festus would have made it that far.
Festus won his own version of the lottery yesterday. He beat the odds. His 20% chance of survival came home a winner.
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