Bread and butter
The “bread and butter” medical conditions at SFH are malaria, tuberculosis, other respiratory tract infections, diarrhoeal disease, AIDS (and its myriad manifestations and complications), parasitic infestations (such as hookworm), and other bacterial infections (such as cellulitis and abscesses). Accidents and injuries account for many of the surgical admissions.
Some examples that were not “bread and butter” cases are described in the sections that follow.
Paralysed by a mad dog
A 52-year-old man, Mr Z, was admitted to SFH in mid-April with confusion and paralysis. In early February a dog bit both him and a small child at his village. The dog was believed to have rabies because of its strange behaviour. It was also said to have been (take a guess…) “foaming at the mouth”. The other villagers subsequently destroyed the dog. The small child was urgently taken to SFH for treatment. Mr Z, a peasant farmer, chose not to make the considerable journey to the hospital and remained at the village to work on the land.
Mr Z began to develop weakness in his right leg in early April, starting at the site of the dog bite. Two weeks later, at the time of admission, all of his limbs were flaccidly hypotonic (i.e. floppy like a rag doll) with absent reflexes and marked weakness. He was also disorientated. Sensation was difficult to assess, but Mr Z showed no response to painful stimuli in his limbs. Mr Z also had loss of anal sphincter tone and was doubly incontinent. As is typical of Zambians, his plantar reflexes were neither up nor down (*).
* There is a memorable quote in “Manson’s Tropical Diseases” on the subject of the toughness of African feet. It says that if Babinski had been African, he would never have become famous for his eponymous neurological sign. Usually the noxious stimulus of a metal bar running the length of a bare African sole shows no neurological response.
According to one of the nurses on the ward, Mr Z started to “bark like a dog” during the night. The next morning, on ward round, I was greeted by his lifeless body and his grief-stricken wife. Thankfully Mr Z’s torment was not prolonged. Mr Z’s illness was notified as a case of paralytic rabies, as well as a case of acute flaccid paralysis.
Hard as nails
One of the first patients I had the privilege of looking after at SFH was Mr P, a man in his fifties. He originally had a seizure and fell into a blazing fire, badly burning his left foot. The wound became infected, and sometime later Mr P developed stiffness in his neck. Within three or four days the rigidity encompassed his whole body and he began to experience agonising muscle spasms. Back in New Zealand, tetanus has almost “bogey man” status – in Zambia it was very real.
I first met Mr P almost two weeks after he was admitted to SFH. He had already been treated with antibiotics and tetanus antitoxin. Still, the slightest environmental disturbance could trigger a cascade of painful muscle spasms. He also had terrible trismus (“lockjaw”) – he could barely open his mouth wide enough to admit a straw. By this time his muscle mass had dissolved to almost nothing. As well as experiencing bursts of severe pain he was in danger of dying from aspiration pneumonia secondary to choking, or from infection of his burn or bed sores, or even from simply wasting away.
I gave his daily dose of diazepam a substantial boost to try to control the spasms that had now persisted for a couple of weeks. The next day he greeted me with a “thumb’s up” sign and said “Doctor, those medicines you gave me – they were super!”. Miraculously, Mr P steadily recovered from that point onwards. With the close attention of his wife at his bedside, Mr P survived tetanus without parenteral nutrition, intubation, mechanical ventilation, or the many other high-tech interventions that he would certainly have received in the West. His rigid jaw transformed into a rapid-fire set of lips. Soon he was pestering me for walking sticks and asking for more food.
I bumped into him a few weeks later when he was returning to clinic for review, so he could be gradually weaned off diazepam. His wife smiled and shook my hand and said, “thank you, Doctor Neek-sorn”, while Mr P, still riding in a wheelchair, vowed to track me down when he was stronger – so that he could be my “garden boy”!
“Lockjaw” – Mr P a few days after Paul and I arrived at St. Francis’ Hospital. For the photo Mr. P was asked to open his mouth as wide as possible. (Photo by Paul Young).
Running on empty
Anyone who has experienced medicine in Africa will be amazed at the haemoglobin levels that walk in through the door. The risks associated with blood transfusion are many (not to mention the expense), so the only indication for the administration of blood is to save someone’s life.
A 23 year old man, Mr N presented to SFH with malaria. He had tried taking chloroquine at home, having had symptoms of fever and headache for over a week. When I saw him he kept trying to sit up, despite experiencing obviously severe dizziness. Finally, the nurse and I were able to convince him to lie still on his bed. Looking at his conjunctivae in the afternoon darkness of the ward was like seeing a pair of crescent moons on a clear night. His blood slide showed heavy malarial parasitaemia (4+), and his haemoglobin concentration was measured at 2.5 g/dL. The “Oxford Handbook of Clinical Medicine” includes a page of laboratory values that can be rapidly fatal – included are haemoglobin concentrations less than 7.0 g/dL (#). Needless, to say Mr N was given a blood transfusion. He went on to make a remarkably rapid recovery after treatment with quinine.
# …when accompanied by a low mean cell volume or a history of bleeding. The presence of Plasmodium falciparum on a blood film is also on the “dangerous” list.
Sugar and alcohol
Mr L, a teacher in his early forties, was admitted in a confused, but rousable, state. He was jabbering loudly and incomprehensibly. The brief history obtained indicated that Mr L had been on a heavy drinking binge the day before. On the morning of his admission, his wife found him in the state described above. Mr L was administered a hefty bolus of glucose, along with a dose of thiamine. Later his random blood glucose returned the incredible value of 0.2 mM (less than about 2.5 mM is considered low) – thus he was diagnosed with alcohol-induced hypoglycaemia. His blood slide also showed a malarial parasitaemia of 1+; the significance of this was unclear given the likely background levels of parasitaemia in the Zambian population. Nevertheless, treatment with quinine (and lots more glucose) was also initiated.
A few days later Mr L was back to his normal self and ready to go home. Later I learnt from another teacher at the same school that Mr L had been depressed following his suspension from teaching duties. He was suspected of sexual misconduct with some of his female students.
The shrinking feet of the man from Malawi
Mr J had travelled to SFH from Malawi. He was admitted overnight. The brief admission note showed that he was in his thirties and had three presenting complaints: (1) “hungry”, (2) “shrinking feet”, and (3) “does not want to answer anymore questions”. A blood slide showed the presence of malarial parasites, and anti-malarial treatment was started. By the time I saw him the next day he was handcuffed to his bed – he had apparently been “scaring the nurses” during the night. A “psychiatric” referral was arranged. The psychiatric assessment was summarised by a list of three “impressions” at the bottom of the page: (1) “psychopath – aggressive type”, (2) “Ganser syndrome” (**), and (3) “Criminal”. He was given the universal treatment for psychiatric illness in Zambia, big doses of chlorpromazine. The next day he again had three complaints, this time they were: (1) “dry mouth”, (2) “sleepiness”, and (3) “too many drugs, and not enough food”.
** “Ganser syndrome –what the @#$% is that?”, I hear you cry in despair. The “Oxford Handbook of Clinical Specialties” has the following entry in the section “Some unusual eponymous syndromes”: “Disorientation plus pseudodementia with ‘approximate answering’, e.g. an answer to ‘What is the colour of the chair in the corner?’ might be: ‘What corner? I don’t know what a corner is. I don’t see a chair…’ … Often there is a preceding head injury.”…
I think that Mr J’s main problem was hunger, a problem shared by many people in Malawi during my time in Africa, a consequence of poor crop yields. He also seemed to have a well developed sense of humour, which led him towards a fate resembling something out of “One Flew Over The Cuckoo’s Nest”. Ultimately, Mr J agreed to continue taking his medicines when he was told he would be discharged in a few days. Soon after his discharge he returned begging for money to allow him to travel back to Malawi. He was told he might be able to hitch a ride on an ambulance returning to Chipata and was sent on his way.
Excerpts from the original case notes of Mr J’s psychiatric assessment (photo by Paul Young).
Organophosphates appear to be the favourite means of poisoning in Katete – whether the target is animal or human. Typically, a person’s dog will be poisoned and their crops will be raided the following night. Sometimes people are accidentally poisoned by drinking from a container that previously contained a pesticidal substance. Mr C, a 23 year old man, poisoned himself.
Mr C was admitted unconscious with a bradycardia (slow heart rate) of 48 beats per minute. His mouth was dripping with saliva and tears were streaming down his cheeks. His pupils were tightly constricted and his muscles were twitching rapidly. He was also incontinent of urine. His presentation was a textbook description of organophosphate poisoning.
Mr C was given frequent doses of atropine to keep his heart rate up, until his pupils were no longer constricted and his secretions decreased. He was also treated with diazepam. One of the nurses noticed blood in the urine after putting a condom catheter in place. Subsequent urinalysis showed the presence of Schistosoma haematobium, for which he was treated with a stat dose of praziquantel.
After a few days Mr C was ready to go home. What made Mr C poison himself? He attempted suicide after being accused of “impregnating” a girl.
“A Midsummer Night’s Dream”
One day I walked through the gates of SFH to be greeted by the “eeyore-ing” voice of what sounded like a demonic donkey. I scanned the courtyard and corridors with my eyes but could not find the source of this bizarre noise. Soon after starting the ward round the source found me – he was admitted to Saint Augustine.
Mr D was a young, healthy looking man in his twenties. He had a history of intractable hiccups that had been tormenting him (and everyone else within earshot of him) for over two months. The hiccups were quite violent, rapidly repetitive, and associated with a great deal of belching and tic-like facial movements. Interestingly, the hiccups subsided whenever Mr D had food in his mouth, and when he slept at night. Full clinical examination yielded no other abnormalities. A psychogenic cause was suspected.
It turned out that Mr D had been cursed by a local village woman. The purpose of the curse was to prevent Mr D from working on his father’s farm, and to ruin his marriage prospects (it was clearly working…). An attempt was made to reassure Mr D that there was nothing physically wrong with him and that the curse would only be effective as long as he believed in it’s power over him. Unfortunately, his conviction in the power of the curse was strong, and thus the curse was powerful. Mr D did concede, however, that the curse would wear off eventually. I tried (for his and everyone else’s benefit) to convince him that it might wear off sooner rather than later. He was also encouraged to keep working despite the hiccups, and even to try walking around with food in his mouth. The next day he was discharged, hiccups and all – his ultimate fate remains unknown.
Something other than pus
Medicine at SFH is not all weird and wonderful signs and symptoms. Many of the problems people face in Zambia are similar to those of people back home.
KS was a boy aged about twelve years old. He was admitted to St. Augustine with a vague history of palpitations and fevers. After a thorough history and examination, a physical basis for these symptoms was deemed unlikely. We suggested to him that sometimes people get palpitations when they are worried about something. Eventually, he said that he had just started studying at a new boarding school where he was being bullied and that he was missing his mother. His parents were contacted and they made the journey to SFH. KS’s parents showed great concern and thanked me for bringing their son’s problems to light. They said they would find a place for him at a day school closer to home.
“No problems, Doctor…”
Mr P was a 26 year old male patient at Saint Augustine. He had recently made an excellent recovery from a left lower lobe pneumonia after treatment with amoxicillin. However, in typical Zambian fashion, a new set of problems emerged. He now complained of urinary urgency (having to rush to the toilet), polyuria (passing large volumes of urine), polyphagia (even the patient in the bed beside him said that he ate like a hippo), and polydipsia (excessive thirst). The list grew even longer as he finally divulged what his most troubling problems were – pain and weakness in both lower limbs that prevented him from walking. He also said he was numb from the thighs down.
The mystery began to unravel when Mr P admitted that, although he has since stopped drinking alcohol (as many patients do when they are admitted to hospital…), for nearly three years he gulped down about two-and-a-half bottles of kachasu (think Zambian rocket fuel brewed from maize) each day. It turned out that he had decided to give up alcohol as he was now engaged to be married (I neglected to ask how many cows he paid for his bride-to-be).
Mr P was examined thoroughly, but no significant clinical findings were made until his neurological assessment. He had a wide-based gait, unsteadiness on Romberg’s test (standing with your feet together and eyes closed), mild lower limb weakness (equal distally and proximally), normal tone, brisk-normal deep tendon reflexes, and loss of pin-prick and proprioceptive sensation in a stocking distribution below the thighs.
I suspected a peripheral neuropathy resulting from alcohol misuse, vitamin deficiency (such as dry beriberi), or diabetes mellitus. He was started on B multivitamin tablets, and a fasting blood glucose concentration was measured – it was normal, effectively ruling out diabetes mellitus (despite the suggestive history).
Mr P was always the last patient I saw on ward round. I would stand scratching my head wondering what else I could do for him. Prophetically, after a couple of days a big box of thiamine arrived at SFH. Previously the only thiamine that could be given was in the tiny B multivitamin tablets, each tablet containing only 1 mg of thiamine. Unsure of the appropriate dose for treating dry beriberi, I started Mr P on 200 mg of thiamine daily, and gave him some pyridoxine as well just in case.
The weekend passed and on the Monday I came to the end of my ward round ready to find the best spot on my head to scratch. I asked Mr P if there were any problems, he said, “No problems, doctor…”. I stared at him in disbelief, and checked that I had heard him correctly. He smiled, hopped out of bed and quickly walked a short way up and down the ward. He was happily sent home – after being warned not to start drinking alcohol again.
Peripheral neuropathy-like symptoms are commonplace at SFH. Often they are attributed to the effects of HIV infection, and it is assumed that nothing can be done. However, I learnt from Mr P that all avenues must be exhausted before making such an assumption – or you might just miss a case of dry beriberi (thiamine deficiency) associated with excessive alcohol consumption…
Medicine for a Mzungu
Mr N was a medical student from a far off land in the South Pacific. After a few weeks at SFH he was finally convinced to join the SFH football team. After a few near-death experiences at training and a couple of comical cameos on match day, he was charitably given a place in the starting line-up for the big game against a team from a rival hospital. A large, typically enthusiastic crowd assembled as the livestock cleared the pitch and the referee signalled the start of the match.
Filling the right back position Mr N struggled against a fleet-footed winger who had the added bonus of football boots. Mr N quickly learnt that there are two types of footballers in Zambia – those with boots and those without. The SFH side struggled against their flamboyant opponents and were in disarray after conceding two rapid-fire first-half goals (sadly the referee failed to notice that three of the visitor’s forwards were off-side when he awarded first goal…).
After a rousing half-time talk – all of which was unintelligible to Mr N – the SFH team were rejuvenated. Roared on by the home crowd, a new-found enthusiasm and the will to win surged through the team. Miraculously, a valiant fight back brought the score level at two goals apiece. Then the real drama began to unfold.
The SFH team were awarded a corner after being camped in the opposition goal mouth for some time. Chaos ensued in the six-yard box as the ball was delivered in from the right. Somehow the ball was driven goal-ward by a SFH striker, only to be deflected wide by a defender’s fist. The referee courageously steeped forward and pointed to the penalty spot. The visiting players swarmed around him, vigorously pleading their case. A few minutes passed. Finally, the referee’s resolve broke down. Leaving the SFH boys dumbfounded, the referee reversed his decision and bizarrely awarded a free kick to the visitors. The show went on.
In the dying minutes of the match, the SFH team pushed all available men forward. The visitors cleared out of their penalty area and launched a counter-attack. Mr N, finding himself out of position, began to scurry back towards his own goal. However, an SFH midfielder, battling in defence, stole the ball from the visitors as they surged forward. Thinking quickly, he unleashed a long ball downfield. Mr N sharply turned as the ball soared overhead. Somehow he evaded the offside trap and found himself 30 meters from the opposition line, hurtling goal-ward with the ball at his feet.
Time stood still (as it tends to on such occasions). The crowd hushed (or perhaps they roared – one of the two…). The visitor’s keeper, sensing danger, rushed off his line. As Mr N met the pouncing keeper he instinctively pushed the ball to the keeper’s left with the outside of his right foot. The ball slipped past the stranded keeper and glided inside the near post.
Pandemonium followed in the form of a massive pitch invasion. Acrobatic Zambian children cartwheeled and back-flipped across the surface of the pitch, while the adults jumped for joy and sang loudly. Met with dissent by the visiting team, the referee signalled the end of the match. SFH were victorious, three goals to two.
For the rest of the week, Mr N was called upon by countless supporters who insisted on reliving the match-winning goal. Mr N however had other concerns, having sustained a bloodied and grazed knee during the match. As expected the wound became infected. Pus oozed from every crack in the skin. Mr N was left hobbling around with a painful golf-ball sized lymph node in his right groin. Reluctantly he started a course of antibiotics as the infection progressively worsened. Magically the medicine did it’s job and Mr N was walking freely again four days later.
NB. Anyone who doubts the verity of this story can write to Charles “Coach” Chupa at St. Francis Hospital. He will gladly provide you with a written deposition confirming the truth of the events I have described…
The St. Francis boys – nervous before the big game.
Opposing right backs. Note my soon to be infected right knee – I wish I had shin pads like my Zambian colleague…
Please note that this was originally written in 2002.