Monday, 19 August 2013


The pic is a preop X-ray of a little boy's left foot (yes, left - I had unwittingly flipped the film over when I took the photo). He presented two weeks after accidentally kicking a fence while playing football (such a dangerous sport!), a week after his mother had found and removed a wooden splinter sticking out of his great toe just adjacent to the toenail, and a few days after he developed three sinus tracts over the dorsum of his foot that subsequently discharged frank pus. As you can (hopefully) clearly see, there is a transverse fracture running through the epiphysis of his proximal phalanx. What was worse was that when we took him to theatre for washout and debridement, it was an open fracture; the proximal edge of the toenail had lifted off, revealing the bony structures underneath. The little box at the corner of the pic shows the epiphysis of the proximal phalanx on the left and the entire distal phalanx on the right (looks rather similar to a tooth, right?); these bone fragments were found to be completely detached from the neighbouring soft tissue once the nail was removed. At any rate, he's probably headed for a partial amputation, poor kid.

Two days ago, we had two deaths, both boys under the age of five years. The first was dead on arrival; he had been admitted at our facility for over two weeks back in June with developmental delay, stunted growth, pectus carinatum (pigeon chest), and an incidental finding of malaria, which was treated but never really made a complete recovery. At any rate, he represented with respiratory distress, was seen at another clinic that morning and got referred to us. However, due to it being Saturday, he was left sitting outside the clinic (which is closed on weekends) for around half an hour before I was notified of his presence and by the time he was brought to the ward, had already passed on, presumably from a primary respiratory arrest.

And neither's even the complex case I wanted to discuss. The second boy, aged 2 years and 8 months, has got to be one of the most complicated cases I've encountered in my brief career and, in my humble opinion, would have warranted ICU admission posthaste as well as a postmortem back home (but unfortunately, such resources are unavailable here). He presented in a pre-terminal state - obtunded with minimal response to external stimuli, bradypnoeic (RR 8/min) with a Kussmaul's respiratory pattern, as well as generalised oedema. In fact, he was so puffy that none of us could obtain intravenous access and we had to rapidly make the decision to insert an intraosseous line. On the (correct) hunch that hypoglycaemia could have contributed to his moribund state, we gave a bolus of 50% dextrose with immediate improvement in his respiratory effort.

Over the course of the afternoon, more history was elicited; the oedema was first noticed a MONTH prior to presentation, which in turn was preceded by (non-bloody) diarrhoea, some oral as well as buttock sores and possibly a sore throat. On the other hand, his respiratory distress was an acute event, having only started that morning after breakfast. A CXR and quick ultrasound scan did not reveal any drastic effusions (pericardial, pleural or otherwise), consolidation, cardiomegaly, cardiac valvular pathology, hepatic/splenic lesions or ascites. We don't have biochemistry so we were unable to exclude renal or hepatic impairment but his urine output was borderline adequate and there was no obvious hepatosplenomegaly, jaundice or coagulopathy; urinalysis did reveal a mild degree of haematuria and proteinuria with white cell casts seen on microscopy. No paediatric sized blood pressure cuff either so his BP remains unknown.

At this stage, my top differentials were glomerulonephritis of some form (likely post-streptococcal) +/- malaria (smear proven two weeks ago with likely suboptimal treatment elsewhere). As you could probably tell, that wasn't the end of the story. As a matter of fact, it only got curioser and curioser (as Alice would put it). He then developed seemingly refractory hypoglycaemia; it was persistently low despite numerous boluses of dextrose. Was it due to leakage of the dextrose solution from the intraosseous line? A false reading since the samples were capillary in source and there was gross oedema giving a dilutional effect? Or something occult like central adrenal insufficiency? Not having any hydrocortisone, we trialled a stat dose of dexamethasone. Either way, despite our throwing everything we have at him, it was a case of too little, too late. Spontaneous respirations ceased eight hours later; throughout the whole admission, he had been (almost malignantly) tachycardic with laboured breathing and a decreased conscious state.

If it had in fact been GN, why was his respiratory distress so acute one month after the precipitating cause? If it was malaria causing severe hypoglycaemia, why was the smear at our lab negative when it should have shown at least some degree of parasitaemia? If it was APO secondary to some other cause (cardiac, hepatic or otherwise), why was it not shown on CXR? Why did the hypoglycaemia not respond to treatment? Could it have been HUS secondary to enterohaemorrhagic E.coli; if so, why was bloody diarrhoea absent? There were just so many points that didn't add up and it's left us confounded. Worse still, it's left his family with one less member. His mother wasn't even present to say goodbye as she was at home with a newborn. At least, he died surrounded by his father, grandmother and a cohort of aunts and uncles.

It reminded me of how finite our knowledge is, how limited our skills and talents are, how powerless we are in the face of death. The good news, thankfully, is that through the love of God incarnated in the body of Christ, we can transcend this mortality and know that this is not the end.

1 Corinthians 1:20-25 Where is the wise? Where is the scribe? Where is the disputer of this age? Has not God made foolish the wisdom of this world? For since, in the wisdom of God, the world through wisdom did not know God, it pleased God through the foolishness of the message preached to save those who believe. For Jews request a sign, and Greeks seek after wisdom; but we preach Christ crucified, to the Jews a stumbling block and to the Greeks foolishness, but to those who are called, both Jews and Greeks, Christ the power of God and the wisdom of God. Because the foolishness of God is wiser than men, and the weakness of God is stronger than men.

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