I SURVIVED MY CHILDHOOD and adolescence, as did my brother. Many don’t. That’s not to say we didn’t have close shaves. We both had our share of those but each time we were saved by circumstances rather than by luck, by a safety net many don’t have.
My parents were Polish Jews, refugees to New Zealand who ate pork and made yoghurt out of sour milk. We lived in Wellington in a house always full of visitors with strange names. They were a mad and flamboyant lot.
My parents’ love for me and my brother was never in doubt, so despite our close calls and near death experiences my brother and I remain full of forgiveness and understanding for their failings as parents. They were brought up in another time, a time so full of turmoil and grief that even simple everyday tasks like cooking had to be learned afresh.
There were no parenting lessons in Auschwitz so who can blame my mother for my brother’s ‘failure to thrive’, a weight loss that continued for weeks after the new mum and her first-born returned home to their small house. Still struggling with the English language, my mother was unable to fully comprehend the instructions on how to mix his formula feed. Despite my brother’s best efforts, the thick goo that filled the bottle could not be sucked through the bottle’s teet. Poor Leslie, that combination of extreme exercise and underfeeding almost killed him, but he was saved at the last moment by the heroic Dr Harding, our GP—a patient man reliably attired in a three-piece suit and a hat. He came to our house for a morning and simply watched what my mother was doing and saw in an instant what the problem was.
My first brush with death happened a few years later when I was six weeks old. We lived in a little house in Palmer St near where the old Wellington Tennis Club once was. Mum was at home alone with me, Les was at a Catholic preschool—another close call—near the Basin Reserve and Dad was at work. It was winter and the house was cold. I was asleep in the front room when the curtains caught fire on the heater. Mum was at the back of the house in the kitchen. Luckily my father came home for lunch and saw the smoke. Yelling out, he rushed into the front bedroom, grabbed me from the cot and threw me out of the window onto the lawn, only to have my mother berate him because I might catch a cold. Say no more, now you have it.
At age six, Leslie was run over by a bus and ended up with a broken femur. He spent six weeks in Wellington Hospital, his leg in traction. In those days, hospitals were fearsome institutions run by strict but well-meaning people who knew best. Visiting, even to the children’s ward, was restricted to two hours in the afternoon and two hours in the evening. This became intolerable to my father, who used to climb the drainpipe to the first floor just to get a glimpse of my brother and for my brother to see him. Dad hated that place from then until his dying day. How odd it is then that both his sons have spent all their working lives in hospitals like that one in Wellington; I would like to think on a ‘mission from Dad’ to humanise them.
When I came back from a long stint working abroad, I finished off my postgraduate training in Auckland at a time when Auckland’s hospitals—Middlemore, Greenlane, Auckland and Princess Mary—were all part of the Auckland Area Health Board. That and the constant complaints about doctors’ car parking were perhaps the only two things that they had in common because on all other fronts they were very different places with very different cultures.
The head of the regional anaesthetic service at the time was a distinguished man called Dr Watt. Tall, handsome and wise, with silver hair and a sharp parting, he saw immediately that I was a Middlemore man and happy to do G-d’s work in South Auckland. I was no pointy-headed professor in platform heels that was for sure, so to Middlemore I went and to this day I remain grateful for his direction.
I say ‘G-d’s work’ because of the immediately obvious and seemingly ever rising tidal wave of need in South Auckland, especially in the area of child health where the impacts of poor education, housing and low household incomes played out in such an egregious way.
A stark illustration of that was in the early to mid 1990s with the emergence of the epidemic of childhood disease caused by the bacterium Neisseria meningitidis serotype B, also known as meningococcus. This bug lives in the nasal passages of up to 15 per cent of us and can be spread by sneezing, coughing or sharing saliva. Although the causes of an epidemic are complicated and involve a change in many factors, it is widely accepted that the tipping point for this epidemic was the removal of the housing benefit in 1991. This forced families to live together in overcrowded houses, thereby increasing the risks of exposure to many more people. It was also clear that an individual child’s chance of developing meningococcal disease was related to the number of adults living in the house.
Unsurprisingly, the highest infection rates were among Māori and Pacific Island children under five years of age, many of whom presented to Middlemore Hospital critically ill. The infection we called meningococcaemia described a systemic illness caused by this bacterium entering the blood stream that led to a rapidly progressive deterioration in organ function characterised by profound shock, respiratory failure, a depressed level of consciousness, and a tendency to bleed—initially causing a small pin-prick haemorrhage in the skin then the blotchy, blue, non-blanching bruise we call an ecchymosis. Children don’t have the reserves of adults so when they become critically ill and stop eating and drinking, as did all of these infants, they can quite quickly develop dangerously low calcium and glucose levels, which on their own can be life threatening if not immediately treated.
The illness can be hard to pick at first and presents with symptoms similar to that of the common cold and flu—fever, headache, nausea, runny eyes, sore throat, runny nose, and cough. Some children with these general symptoms were seen by medical staff and sent home only to return with more advanced disease later. Tragically, a smaller number died at home.
During those early months of the epidemic, we were seeing up to four infants and children with advanced disease every day in our emergency department at Middlemore Hospital. Some died and many were left with serious disability as a result of the disease causing blockages to the circulation of blood in small blood vessels leading to the loss of digits and, in some cases, whole limbs.
We learned very quickly from those deaths, becoming super aggressive in our management of those kids. So too did the general community. As word of the epidemic spread, families became increasingly vigilant. They brought their sick kids to the doctor and our emergency department much earlier and for a wider range of symptoms. Family doctors stepped up giving these kids shots of penicillin with one hand while they called for an ambulance with the other.
The epidemic peaked in 2001 with 650 cases (17.4 cases per 100,000 people), and finally was put to bed with an immunisation campaign in the mid-2000s. In total 252 deaths were attributed to meningococcal disease between 1991 and 2007.
How ironic that such a destructive and nasty disease can be caused by a bug that is so sensitive to penicillin, our first antibiotic, discovered by Alexander Fleming in 1928. Even in the worst cases of disease, three days of intravenous treatment with penicillin will rid the body of the meningococcal bacteria. If only that was enough to halt the progression of this terrible disease!
We human beings are a complicated mix of biochemistry and biology—a dynamic boiling soup of molecules and biochemical reactions, some pulling us to the left, some pulling us to the right; others pull us up, some pull us down. When we are well, that push and pull seems to keep us uniquely balanced in the centre, a concept we call homeostasis—a term to describe the property of a system in which variables are regulated so that internal conditions remain stable and relatively constant.
Critical illness and injury play havoc with that fine balance. So despite access to antibiotics that kill the bacteria that causes disease, the consequences of the infection can continue to progress.
When I explain this to the families of my patients, I sometimes use another analogy—that of dominoes. Think about a line of dominoes and off each and every domino in that line is another line, and off every one of those is another line.
The initiating disease is like a boot kicking over a few of those dominoes. As they fall, so too do more and more dominoes around them. The rate at which that happens and the extent to which the dominoes continue to tumble is related to factors unique to that patient like their genetic makeup, the intensity and nature of the insult they have been subjected to, and the timeliness, effectiveness and accuracy of our treatments.
Despite removing the boot, or killing the bacteria with antibiotics, the consequences of the disease or injury can continue and for some are life threatening and for others, fatal.
Josh has just celebrated his twenty-first birthday. He is a lovely young man, quite sporty and now at the end of his university studies. On the face of it, he is just like many young people of a similar age—but Josh is different. On close inspection, you might notice that he has lost the tips of his fingers on both hands and, when he wears shorts, you can see his prosthetic leg—his own lost to meningococcal disease when he was a baby.
He became ill when he was only five months old. His mother remembers it like it was yesterday. At about 5 o’clock one afternoon, Josh developed a fever, quickly becoming sleepy and irritable. Thinking he was hungry, his mum tried to feed him but Josh was too drowsy to care. By the time he arrived in the emergency department he had a temperature of 40, was breathing fast and was already struggling to maintain normal oxygen levels in his blood, a condition we call hypoxia. His heart was racing, his circulation was poor and he had cold blue fingers. When we press on the finger tip of a well child the skin will blanch. When we release the pressure, it should take less than three seconds to pink up. This is called the capillary refill time and, in Josh’s case, it took a sluggish six seconds.
It was obvious what the problem was. He, like so many before him, had meningococcal disease. The telltale petechial rash, at first sparse—just a few pinhead-sized, reddish-blue spots were present on his chest and abdomen. Although easy to miss at first, they became increasingly evident, and before our eyes some of his fingers and toes mottled and darkened.
It was 1997 and we were hitting our stride with this disease. We were over the soft and gentle approach to kids presenting like this—we’d already seen too many die. I took over the airway, giving him high-flow oxygen while another doctor slid a drip into a vein in his foot, taking bloods at the same time. His blood sugar was low so we topped him up with a push of 50 per cent dextrose, some calcium, 20 millilitres per kilogram body weight of fluid, and a big dose of antibiotic.
As we were doing all of that, we prepared to take over his breathing to allow us to treat him more aggressively. We gave him small doses of drugs to get him to sleep and to stop him moving. A breathing tube was then inserted through one of his nostrils into the back of his mouth, and on down between his vocal cords into his trachea. This was followed by a nasogastric tube which drained a ghastly black fluid from his stomach, almost certainly a collection of old blood and stomach acids that typically accumulate in very sick kids.
We put him on a ventilator and went to work giving him more fluid, inserting new lines and beginning infusions of drugs to improve his heart function and circulation.
Critical illnesses like this follow different phases before they resolve, one way or another. Initially, there is a dramatic spiral-ling down and progressive deterioration of organ function—a descent towards death that we chase hard to slow and stop by taking control of the patient’s physiology, using aggressive fluid resuscitation, drugs to improve the circulation, ventilation and acute dialysis to restore a more normal milieu for the patient’s organs to operate in. With luck that will be followed by a period of relative stability as we continue to support the various organs of the body with our machines and drugs in the hope that people will have the strength to regroup and get better and, with our help, fend off new assaults from infection and the complications of the various treatments.
Over the next few hours, we worked hard to keep up with the chaos that was Josh’s physiology—more and more fluid, plasma and platelets to replace the clotting factors in his blood that were being consumed in forming the clots blocking the small vessels in his fingers, toes and other parts of his body; higher and higher doses of drugs to improve his circulation and the performance of his heart; more support on the ventilator.
As time passed, his descent slowed and he became a little more stable. By the next morning the worst was over, but he was left with black fingers and a dusky left leg from mid-shin down. That phenomenon, called Purpura fulminans, is the result of small vessels becoming blocked with debris that results classically from infection with this deadly bug Neisseria meningitidis and seen also with its equally deadly friend, the group A streptococcus.
Three days after his admission, Josh was discharged from ICU to the paediatric ward, and later went on to have a below-knee amputation of his left leg as well as losing the tips of a few fingers on both hands. Two weeks later, he was back at home.
Meningococcal disease still occurs but it is now more commonly due to the group C variant of the bug and it is adolescents who are most at risk. Because it too is spread by droplets through sneezing, coughing and sharing drink bottles, overcrowding or close living is again a factor. Typically we see outbreaks in poorer parts of the country but also in places like university hostels. Northland, hit hard by an epidemic of the B strain in the nineties and early 2000s, had an outbreak of meningococcal C disease in 2011 that led to the region’s health board instituting a widespread and successful vaccination campaign to stop it.
Although some of the factors that tipped the balance to start those epidemics of meningococcal disease have changed, poverty, overcrowding and poor housing continue to contribute to an unacceptably high incidence of preventable childhood disease. This is both debilitating for children and their families but also hugely costly to our communities, and to you and me who ultimately fund our health and social services.
Winter brings an enormous influx of sick kids into our hospital. Of those with chest infections, most live in cold, damp, overcrowded houses. Our intensive care unit has a paediatric wing, which in winter is full most of the time. In there are little babies with respiratory infections from viruses with strange names like respiratory syncytial virus, influenza, parainfluenza, enterovirus and rhinovirus. These infections are also spread through droplets by coughing and sneezing.
One of the most prevalent illnesses caused by these viruses has a strange name—bronchiolitis: –itis means inflammation; bronchioles are the very small airways in our lungs; hence inflammation affecting the small airways. As a result of the inflammation, air that is easily breathed in cannot all be breathed out due to the inflamed airways. This leads to the chest becoming hyperinflated, making it harder and harder for kids to breathe. In the main, infants and young children are nose breathers and this disease will also make them snotty, further increasing their difficulty in breathing. Children who are strong and healthy can usually put up with this for longer and will do much better than smaller babies and those born prematurely.
When we began the round in the ICU one winter morning a few years ago, I recognised Margretta immediately. She was embarrassed to be back with her seven-month-old son—his sixth hospital admission with bronchiolitis. She worried that we would think she was a bad mum and that Rikki would be taken away from her. Despite our lobbying, their large family still lived in the same cold house.
Rikki, a small baby, was breathing hard and fast, his head bobbing with each breath. The monitor said 80 breaths a minute but still with a good oxygen saturation of 96 per cent. Once he was wrapped snugly in a colourful blanket, I slid in an IV, then took some bloods to send to the lab and a swab from the back of his nose to send for virology. One nurse steadied his head as another used a small suction catheter to clear out Rikki’s blocked nose. They then slipped in a nasogastric tube to keep his tummy empty so it wouldn’t press against his diaphragm and make his breathing even more difficult. Finally, he had another chest X-ray. Rikki didn’t like any of that—nor did his breathing.
Our next move was to make him drowsy with an old-fashioned drug called chloral hydrate, which we put down his nasogastric tube, and then we put him on bubble CPAP (continuous positive airway pressure).
Bubble CPAP is a simple, non-invasive way to support babies who are struggling to breathe. It delivers humidified oxygen to the child via a pair of soft nasal prongs. The expiratory limb of the circuit carrying the baby’s expired gas is placed in a reservoir open to air but under water at a depth of between 1 and 10 centimetres of water, thereby generating between 1 and 10 centimetres of continuous positive pressure in the breathing circuit.
It is incredible to see the relief this brings to these infants working so hard to breathe. As soon as we put Rikki on, now more sleepy and cooperative thanks to that small dose of chloral hydrate, his respiratory rate settled and his breathing required much less effort. Not only did he look more settled but so did we.
A good number of babies are admitted to hospital more than once each winter, and we will see those same children many times throughout their infancy. Unsurprisingly, those born either very small or prematurely seem to be at greatest risk of deterioration.
What we do in the hospital, giving oxygen and antibiotics and putting kids on ventilators, treats the end result but does nothing to address the causes of this recurring problem. Nor does the advice of well-meaning, prestigious people like the former Chief Medical Officer of the UK, who gave this advice to the people of Britain in 1999:
1.Don’t smoke. If you can, stop. If you can’t, cut down.
2.Follow a balanced diet with plenty of fruit and vegetables.
3.Keep physically active.
4.Manage stress by, for example, talking things through and making time to relax.
5.If you drink alcohol, do so in moderation.
6.Cover up in the sun, and protect children from sunburn.
7.Practise safer sex.
8.Take up cancer screening opportunities.
9.Be safe on the road: follow the Highway Code.
10.Learn first aid ABC—airways, breathing, circulation.1
Advice like this is easy to give and, in this case, I’m sure it was well meant. Others are less generous about the causes of ill health, blaming those individuals who fill our hospital wards, keep coming back to our emergency departments, or use our social services. We’ve all heard the rhetoric: ‘They are lazy.’ ‘Why don’t they get a job?’ ‘They don’t care.’ ‘They don’t love their children.’ ‘They don’t try hard enough.’
Soon after the CMO’s message to the people of Britain, I attended a talk in Wellington delivered by Ichiro Kawachi, a professor of Public Health at Harvard. He gave recommendations of a different sort. His advice for staying healthy differed, playing on the delusion that the queues at the doors of our social services were the result of poor choices. He urged:
1.Don’t be poor. If you can, stop. If you can’t, try not to be poor for too long.
2.Don’t have poor parents.
3.Don’t live in a poor neighbourhood.
4.Own a car.
5.Practise not losing your job and don’t become unemployed.
Ichiro points to many of the structural and social issues that need to be addressed if we are to have a more equal society. He also made it clear that, try as they might, many people need to be given a hand up and out of the hole they find themselves in. This is not the same as being forced out of one hole and into another.
When I was the Principal Medical Advisor to the Minister of Health and the Director General of Health, I schlepped up and down from Auckland to Wellington every other week. While there, I was given a hat to wear—across its hatband was written the letters ‘WoG’. Hmm, yes, I was. ‘WoG’ stood for ‘Whole of Government’. The hat was a reminder to members of the Ministry of Health executive team that we should be working more collaboratively with other agencies to address the complex real life problems we were faced with. Sadly, on its own that symbolic action was not enough—‘hat and hope’ was not a plan.
The barriers to this kind of transformative thinking and activity are many and significant. Budgets and agendas continue to be jealously protected within government departments, and our world continues to be ruled by the same old thinking that allows the problems we face to persist. As a result, the well-meaning, stroboscopic interventions of the public service continue and most of the root causes that drive our concerns remain unaddressed.
As for the hat, it quickly became my much needed protection from the sun, worn exclusively in the privacy of my own garden.
Hospital management is expensive and complex. However, this cost and complexity can be rationalised by the provision of good information about the changing demand for services. Middlemore, like many other modern hospitals, utilises historic data to accurately predict the changing demand for services across all of its departments. As part of that, a hospital status report is generated each day and more often than not it looks like this:
TODAY THE HOSPITAL IS FULL
—107 per cent of capacity
•Currently there are 100 patients in the Emergency Department of which 50 are waiting for an inpatient bed.
•There are 8 over-census patients in treatment rooms around the medical wards.
•There are 8 patients in the Gastro Clinic.
•There are 7 female adult patients in Kidz First Short Stay Unit.
•There are a further 17 patients expected in Day Surgery, 5 will require beds.
•The Discharge Lounge in Wd 34 E is full with 4 inpatients and this has the potential to delay discharges from Surgical Services today.
•There are 5105 minutes of acute surgery needing to be done and 34 patients are currently waiting.
•There were 298 patients through the emergency department yesterday, similar numbers are expected today.
•Nursing shortages as a result of sick leave are an issue.
The adult wards at my hospital are usually full but now, increasingly, with younger people suffering from life threatening complications of type 2 diabetes—a largely preventable disease associated with obesity.
Despite all the good things we have achieved as a nation why is it that we are not doing better at preventing the preventable? Should this not embarrass us? Does this not cost the health system millions of dollars and effectively prevent many people from making a productive contribution to their families, communities and our nation?
‘Of course’ is the answer to all of those questions!
Preventing disease requires a whole of society approach and ought to start with the well-being of families, pregnant women and children. During my time working in Samoa, I frequently did ward rounds with the paediatricians. All women, they were hard working, very skilled and capable of doing amazing things with not very much.
In the middle of a round one morning, a child came into the emergency department with an obvious problem with her breathing. She was two years old and had been unwell for two weeks, during which time she had been treated by traditional healers. We heard her before we saw her—a rhythmic high pitched squeaking noise with each breath, accompanied by an in-drawing visible at her throat and a sucking in of her abdomen in an effort to get air into her lungs. That noise is called stridor. It results from a narrowing of the airway at some point as air makes its way from the mouth to the upper trachea. Until an effective vaccine was introduced a little over twenty years ago, the commonest cause of stridor was epiglottitis—an infection of the epiglottis caused by a bacteria called Haemophilus influenzae.
The epiglottis itself is a strange U-shaped structure that lives deep in the throat and effectively guards the opening of the larynx, protecting us from inhaling our food as we swallow.
The child’s name was Vaelua, and she weighed only 8 kilograms. Vaelua had a temperature of 40 degrees Celsius and looked pale. I spoke to her then I prodded her, but she didn’t respond. She was already unconscious because of the build-up of CO2 in her blood. A lateral X-ray of her neck done earlier did not suggest epiglottitis but instead showed an enormous bulge of soft tissue clearly narrowing her airway around her larynx. It was also obvious that if we didn’t do something soon, Vaelua would stop breathing and die. That something had to be inserting a breathing tube into her airway to bypass the obstruction; but in emergency situations like this, fraught with danger, that can be next to impossible.
The principles of treatment in cases like this are to disturb the child as little as possible in case we lose the airway completely. Our priority is to get them to a skilled anaesthetist and surgeon in the operating theatre. Once there, we know from experience that the safest course of action is to keep the child breathing on their own while inhaling an anaesthetic vapour until they are deeply asleep. This allows the anaesthetist to see whether they can visualise the larynx and then insert a breathing tube past the obstruction.
I called the theatres and told them we were on our way. En route to the theatre suite, we pushed past people in corridors, ejected others from lifts and politely ignored the theatre orderly’s instruction for me to change into scrubs. To have done so would have cost Vaelua her life.
Once in theatre we followed the rules, but soon after arriving the child simply stopped breathing. The amount of oxygen in her blood dropped precipitously and her heart rate slowed dramatically. Our anaesthetist looked into Vaelua’s mouth to see whether we might get the breathing tube in from the top end but all he could see were swollen folds of tissue. As my colleague Dina began CPR, I looked toward Aleki, our surgeon, and together we talked him through his first ever emergency tracheostomy—a vertical incision in the neck, down through the strap muscles to expose the trachea, then one final slit into it to allow for the passage of the breathing tube.
I reckon the whole thing took no more than two or three minutes from the time she stopped breathing to the point where the tube was in and her life saved. We attached the tube to a ventilator bag and puffed 100 per cent oxygen into her lungs. As we did this, Vaelua’s heart rate rose and the oxygen saturation in her blood returned to a very healthy 100 per cent. Having secured the tube, we gave her antibiotics. Then using a syringe and needle, through her widely open mouth, we punctured into the abscess cavity and removed 70 millilitres of foul-smelling brown pus.
Vaelua came back to the ICU after that and remained on a ventilator for a couple of days to allow the swelling in her neck to go down. Then, on the third morning, we removed the breathing tube from the tracheostomy hole in her neck, covered it with gauze and tape and off she went, breathing normally again through her mouth and nose. Three days later, Vaelua went home.
Kids are definitely not small adults. Although we have the same bits—spleen, kidney, bone and brain—these organs do different things for us at different times of our lives; they can change shape as the child grows and respond differently in illness when we do things to them. The airway of a child is a case in point—small and narrow, the structures there are floppy and the relationships they have with each other are different. For those of us used to dealing with adults, all this can make for trouble. We did well with Vaelua. Yes we were lucky, but we were also prepared.
We know that many childhood diseases occur in our poorest households. The causes for this are not that complex or complicated. Putting wind behind Ichiro Kawachi’s sails is the transformative thinking behind the report ‘Solutions to Child Poverty in New Zealand’ released by the Office of the Children’s Commissioner in December 2012.2 Far from thinking that improving health is reliant on new technology or more doctors and a massive investment in new pharmaceuticals, the report recommended making moderate investments in four key areas. Namely, pay people a living wage, provide better housing, make nutritious food affordable and keep kids engaged at school. What a treat for a government to have such an expert group as this help with such an important issue. What a travesty the government of the day didn’t have the humility to accept those recommendations and the good sense to act on them.
In 2008, in a particularly poor part of Auckland, in a community of many single parents and large families, something really wonderful began. It started with a group of primary school teachers who had been struggling to bring their kids up to speed with simple reading, writing and arithmetic. Instead of arriving at school with a five-year-old’s reading level, most came with the reading level of a three-year-old. As a result, if they were to succeed at school these children would, in effect, need to learn at 1.5 times the pace of their peers. The teachers began an organisation called Manaiakalani that promoted learning in this impoverished community.
I met a group of these children in 2011 when they came to perform at the opening of Ko Awatea—a centre focused on health system innovation and improvement—on the campus at Middlemore Hospital. So here they were three years on leading a hilarious and, at the same time, moving performance of soliloquy, song, dance and storytelling that left the audience in stitches of laughter and in complete awe. These kids, once virtually illiterate, were now in command of their own destinies, connected to each other and the wider world to an extent that was simply mind-boggling. The children were passionate about learning and since then they, and other kids who have followed them, have gone on to achieve in all aspects of life.
Manaiakalani draws a whole range of magnificence to it. Children passionate about learning and now doing significantly better on national assessments. Parents willing to make sacrifices and invest in their kids like never before; teachers and schools prepared to disrupt what they’ve always done to enable student learning; community, philanthropic, commercial and government partners willing to invest. Why? Because Manaiakalani is profoundly different and making a difference. The programme is new and exciting, and enabling a shift and acceleration in student achievement.
—Pat Snedden, Manaiakalani chair
The work of the Manaiakalani Education Trust (www.manaiakalani.org) is a wonderful example of the potential all children have to succeed. It has shown that given the right guidance and assistance all children can do well, and that parents, no matter their circumstances, want the best for their children and will make sacrifices to ensure that they might succeed. Giving these children the chance to do that through learning will improve their health status as they age. It will also influence how they, in turn, will parent by showing them the importance of education and keeping their own kids healthy. This is how we will break the cycle of failure, of truancy and of illness.