before i gave in

we discussed the difficulties of this is in therapy

and

i talked a lot about the strongest force

pulling me towards self harm.

blood

i’ve always known that blood was a huge part of self harm for me

but

a new dimension has been growing

and

i’ve been scared to give voice to it

i am not comfortable with the transfusion blood

i want it out

i feel there is too much blood flowing through my veins

the numbers scare me

i find the idea of a healthy haemoglobin

unnatural

i am terrified to discover the results of my next blood test

all these days going by

with no blood loss

makes me feel sick

all those strong new blood cells

will

be generating more

it is horrifying

i need to get it out

i need to maintain levels

that won’t cause me constant worry

i do not fully understand why i feel this way

but

it’s compelling

i can’t leave my body to it’s own devices

i must take charge

and

expell this oxygenated intruder.

there are so many aspects of this

too many competing voices

i can’t appease them all

there will be unpleasantness whichever side i choose

the only solution

is to

remove the blood

&

release myself.

I was high in White Blood Cell Count, low in Haemoglobin, Haematocrit, Red Blood Cell. See below:

So the low areas are give sort of the same story that I’ve had since first trimester: I was slightly anemic and lacked iron. I knew this before and the problem is still there. It’s due to pregnancy.

However, why did I have low white blood cell count? White blood cell count happens when you have an infection, trauma, stress, allergy, tissue damage from burns, etc. It’s all the bad stuff. I instantly got worried. The OB never mentioned I had an infection which was the most likely cause and I haven’t gotten a cold at that time so I was worried. I wasn’t sure if the 2.3 I was over was really high or slightly high, etc. So I looked into this and found that white blood cell comes in different forms and that’s where the automated differential section on the bottom gave more information. I was high in neutrophil.

It is normal for neutrophil to be increasing your normal white blood cell counts during “pregnancy” from 7-15  X 10^9/L.

I hope this helps! Of course, it could also have been an infection I was fighting off (like allergies) or not getting enough fluids or the stress of flying on an airplane 3 days before. Everyone should ask their doctors to make sure it’s nothing more serious. It’s a common thing I think some women ignore or ob deem not important but it’s ultimately “you” who takes care of yourself and you should take a note of your blood reports in case your ob missed something (since they’re all so busy).

Anaemia is one of those things you’ll encounter all the time on the wards and in primary care. There are a ridiculous number of causes but I’ve classified them into microcytic, normocytic and macrocytic to make it easier to understand. Nine times out of ten your patient will have iron/B12/folate deficiency or will be anaemic due to chronic disease. I’ve also briefly covered the different causes of haemolysis (which is something I don’t ever remember being taught, but it seems quite important) and aplastic anaemia.

Click here to download notes on anaemia.

I DO NOT have the weight of the world on my shoulders and need to remember that!

(Note: This blog was written about my recent tummy tuck and arm lift surgery and the recovery process)

Monday 20th Feb – The pain is not too bad today  – I finally got out of my room and walked with one of the funnier nurses, i’ll call her Ye. She is an absolute cracker (this means she is extremely funny in Aussie slang for my American friends) and makes me laugh…  We walk up and down the ward a few times, and that is it – back to bed, wiped out again..but at least my hemoglobin levels are rising…  Mum came in after work and we went down to the cafe for a latte… It is the simple pleasures.

Tuesday 21st Feb – Had one drain tube removed today! One down 4 to go! I also went outside for the first time since admission and had coffee in the court yard! – Lovely day and I feel the last of summer slipping away as i am still stuck in here. Today was supposed to be the day I would get out… But given the complication of blood loss and still having tube in I will be here for a bit longer, House is not even talking release dates yet

Wednesday 22nd Feb – Two more drains out today – Still get light headed easily and resting a lot. Went for a couple of small walks off the ward today. My Dad came in on his way past which was a good distraction. Not a lot to report, my pain levels increased a little tonight managing this has been a little hard, but pain means your healing right?

Thursday 23rd Feb – Well I awoke today in pain, big pain and I was also upset on top of that, I suppose being my 10th day in here was getting to me a little. For some reason I am feeling the pain in my arms and abdomen more, it is a burning aching feeling.. I struggled with pain management all day.

Thursday night turned into a bit of a farce.. I asked my nurse at 7:30pm for pain relief she never came back with it. I am not one to keep buzzing and annoy them and thought that she must be caught with another patient. But at 7:50pm the pain became worse, a lot worse. So I buzz again and 5 minutes later she comes in – sees the tears rolling down my face because of the pain ( I don’t like to cry by the way) and exclaims “Oh I forgot about your pain meds” scurries off and then comes back in (sheepishly) and gives them to me, and seeing that I am clearly upset, quickly leaves.

The problem is that the pain was full force now, and took ages to get back under control… The key with pain management after major surgery is to keep it at bay and take the meds on time otherwise if can become excruciating… A point lost on this nurse today.

I do want to add that although I have been harsh here, I have massive respect for Nurses. Two of my best friends are ICU nurses, my house mate is also a nurse, plus the nursing staff here have been amazing, most going above and beyond the call. For me the issue was the nurses attitude to me today, which was short and abrupt all day and then she snuck away after giving me my medication, not a great look really – but you get poor performers in every industry!

Friday 24th Feb – Day 11 Going a bit stir crazy, but got another tube out – Only one to go…House said that I can hopefully have the last one out tomorrow and be released! YAY – but it depends on how much fluid collects… I am literally willing it to stop… Power of positive thought can’t hurt, can it! The pain is a little better today. Have been very grateful for all my visitors and friends / family calling. On a bad note though I found out that my Grandpa fell over, tripping on a step and has fractured his pelvis! -He is currently in hospital too! – My parents have really hit the jackpot with both of us in!

Saturday 25th Feb – Day 12 I didn’t sleep well last night – I awoke to House and a Nurse coming into my room, House was on his early morning rounds, and, at 8:10am I got the news that I wasn’t going home. Still draining too much and the tube can’t come out; House explained that while sometimes they let people go home with one or two drains still in, he won’t release me today given the extreme heat and my continued low hemoglobin levels, he said he wants re-assess the drain tomorrow and hopefully I can go home then.

It takes all my energy not to cry when they are in the room. I fully understand his reasoning and know that it is made in my best interests… But I just want to go home, sleep in my own  bed, sit on my couch…

I call my friend Janelle who was going to pick me up and take home. She listens to me cry and assures me that I can continue to hold out. She comes to visit later together with her partner – they make me laugh and cheer me up. I have continued to receive many supportive texts and calls from friends and family, thanks guys – these are so very welcome.

One of the things that has surprised me is that I tire so easily, I still have to rest regularly after 12 days. I really didn’t think of that prior to surgery, I thought that I would be sore and tender, but the fatigue really does hit me hard a few times each day. I just spoke to one of my nurses who just dropped in to say hello.  She asked what I was doing and I explained about my blog and that I was writing about the fatigue.. She explained that it has hit me harder because of the lower hemoglobin levels and that my body may continue like this for a few more weeks. This means that I will need to reassess my plans for when I return home, building in short walks and naps over the course of the day.                                     But that’s OK because at least I will be home.

So, being excited about going home tomorrow may have been premature. It is 10:00pm now, and I was just about to post this when I decided to check the drainage bottle, it is already at 100ml, so I think that it is now unlikely that it will come out tomorrow, my nurse agreed… I am worn out, sad, I can’t get my hopes up anymore that being said I should be more grateful for the good care I get here!

Will keep you updated in the next installment.

Till then, Lin xox

The SNP (single nucleotide polymorphism – the most common type of genetic variation among people) in question has a confirmed affinity with sickle cell anaemia, which affects the production of haemoglobin. Haemoglobin is found in the red blood cells, or erythrocytes, and is responsible for the transport of oxygen from where it is taken up at the lungs to where it is needed at respiring cells. In people with sickle cell anaemia, haemoglobin is produced slightly differently so that it has a tendency to clump together into long chains, called aggregates, which ultimately distort the shape of the erythrocyte from the usual flexible biconcave disk into one reminiscent of a crescent-moon or a farming sickle, which is where the condition gets its name. The problem is that these sickled cells are not able to pass through the smallest blood vessels as easily as ordinary cells and this leads to small clots, inhibiting the supply of oxygen to certain parts of the body. This can have results varying from periods of excruciating pain, called crises, to permanent damage to organs such as the brain which can lead to strokes and in some cases death.

It is difficult to see why, then, this SNP has not been eradicated from the human gene pool, nonetheless statistics suggest that that the SNP has been present for several generations at least. In the United States, one in every five hundred African-American births is affected by sickle cell anaemia and around two million Americans are carriers of the Sickle cell trait. The frequency of this SNP in people with recent African, Indian, the Mediterranean of the Middle East proposes the possibility that it provides some form of benefit to people living in these regions. Researchers have now confirmed that the benefit of being a carrier of the sickle cell trait is an inherent resistance to one of the world’s most dangerous diseases – malaria.

Malaria is a disease that, like sickle cell anaemia, involves the erythrocytes, it is caused by a parasitic organism transferred by mosquitoes that inhabits the erythrocytes where it multiplies with potentially fatal consequences for it’s host. The reason that malaria is only prominent in the regions mentioned above is that it is these regions where the mosquitoes that carry the parasite thrive. While it may not seem much consolation to be resistant to malaria if you are already suffering from sickle cell anaemia, not all of those whose genome contains the SNP in question actually develop sickled cells. This is because the allele (a characteristic of genetic information responsible for the determination of characteristics) for sickle cell anaemia is recessive, which means that a person’s DNA must contain two copies of the allele for the characteristic to be present, if only one copy is inherited then they will have no symptoms; in reality most of the people who this allele affects have only one copy of it and so do not suffer any of the symptoms of sickle cell anaemia outlined above, but still benefit from their natural resistance to malaria. This type of genetic asset is called “heterozygote advantage”.

People living in regions where malaria is widespread would certainly benefit from having this heterozygote advantage, in fact it is estimated that they have one tenth the risk of dying from malarial infection compared with a person who does not carry the trait, of course the downside is that some of the children of carriers of this trait will be born with sickle cell anaemia but since there is only a 25% chance of this when two carriers reproduce it could be argued that the pros outweigh the cons. In either case this topic encapsulates the beautiful complexity of the genome perfectly; that such a minute variation can have such huge ramifications for those involved, perhaps the difference between life and death, is awe-inspiring.

the three leaves

And what are these three leaves?

Simple.

They are kele ka patta, karipatta and palak patta!!

My son, Aniruddh, woke up this morning to go to school and the first thing he said to me was, “Daa-ad’, I am going to be a vegetarian tonight, okay!” (this wasn’t a question, it was a statement).

“That’s fine,” I replied, “but why tell me?”

“Because” he answered, packing his school bag with last-minute items, “I want you to cook me dinner with vegetables only, no chillies, I don’t want it to be too spicy, and no curry. Okaay!”

My son is one of the few people in my household allowed to get away with using the term ‘curry’.

“Yes son.” I replied, quickly thinking what vegetarian dish I could serve him that fitted his urgent requirements.

Monday is the one day when I get to cook what I want, how I want, and not what someone else wants me to, even if he is next to the almighty!! However, this is my son asking, so I must do it!!

Once he’s headed off to school, I head off into the kitchen to cook for my son.

So, what will it be?

Is it going to be potatoes, or cauliflower, or cabbage, or mushrooms, or . . . ? The list is endless and my mind is working overtime.

One thing I know, for sure, is that he will eat anything I cook as long as it fits into the ‘all vegetable, no chillies and not too spicy’ category.

So, I make my decision.

It will be slow-cooked mung lentils or moong dal,  with chopped, or puréed, spinach, tempered with black mustard seeds and kari leaf.

I will serve this dal palak with plain boiled rice.

As I can’t help myself, and so that it looks good, it will be served on a banana leaf.

the most beautiful, natural serving plate

I choose mung lentils because it is, now folks get ready for this, considered to be the Queen of all beans and lentils.

Moong dal, or mung lentils as they are called in the West, are a great source of potassium, which helps prevent blood pressure. One cup of cooked mung lentils is equivalent to eating two bananas a day (my son will be very happy to learn this as he bemoans having to take a banana to school for recess as he says it gets squashed!).

Mung lentils also contain iron and copper, magnesium and zinc. Iron, as we all know, is extremely good for the blood; copper, on the other hand, helps produce haemoglobin and magnesium helps keep you calm whilst zinc helps us smell and taste the food!

Mung beans are also known to prevent heart attacks, but if you’ve already had one, I’m sorry, but it’s too late to prevent one.

Sprouted mung beans in Chinese cuisine are considered to be cooling for the body and are eaten during the summer months.

My mother would make a moong dal called moogache varan during the summer months when we lived in New Delhi briefly in the 70s.

Mung lentils are also an excellent source of protein and contain more nutrition than eggs, fish and red meat. More importantly, the lentils are easy to digest and cause no flatulence, or far…ng, just what my son needs!

So, in order to prepare this queen of lentils dish for the little king this is what I do. Please follow me.

First off, I cook about 2 cups of mung lentils in plenty of cold water with a pinch of turmeric, so that they retain their colour.

mung lentils cooking

Once the water comes to the boil, I reduce the heat and slow cook the lentils until they start to break down.

At this stage your spinach leaves, which have been washed in cold running water, are finely puréed (you can chop them beforehand, if you want) in a blender and are immediately added to the lentils.

make sure the mung lentils are cooked

An aside, if you don’t mind my interrupting my cooking process, on spinach.

spinach leaves

The spinach leaf is an ancient leaf that has its origins in Southwest Asia. It has been used in this area for a long time, even before it was known in the western world. As we all know nowadays, it is rich in iron and a great source of antioxidants as well as containing the vitamins C, A and B.

So, let’s get back to our lentils and spinach.

Add the puréed spinach to the lentils

Once the spinach is added the salt goes in (I only use iodised salt a.k.a cooking salt), and then you fold the mixture once or twice.

Fold the spinach into the mung lentils

and it is now ready to have some flavours added to it, known as tempering!

Well, at this point I have to be careful as my son has warned me not to make it too spicy and he doesn’t want any chilli either!

So, a good spice that can do the job of both without being overpowering is a spice you’ll all know called mustard seed!

Mustard seeds come in two forms: either black or brown and yellow.

For this particular dish I am using the black seeds.

black mustard seeds aren't just black!

They have a slight pungency and bitterness and they are also called a pickling spice as they are often used to do this job. Excellent news! as the ‘pickling’ element will help preserve the dal, and in fact make it taste better the next day, if there are any leftovers!!

Mustard is also a source of Omega-3 and Omega-6 which reduces the risk of arthritis as we get older, which I’m afraid is something none of us can escape. It is also great for the immune system!

By the way, another aside whilst I’m getting on with my dish, did you know that Australia produces one of the best mustard oils in the world? This oil hails from the region of Yandilla in Queensland and the oil is sold by that name.

However, for my dish we are not using the oil just the spice.

Mustard leaves are very popular in India and are eaten by women going through the menopause.

The leaf, called sarson, is rich in folic acid and magnesium. The first is good for preventing osteoporosis and the second for reducing stress and restoring sleep patterns. It is also a rich source of vitamin E which helps reduce the occurrence of hot flushes!!

So, I need a medium for tempering.

Ghee is good and is very cooling. But, as most of you will know if you read my blogs regularly, I have never understood this medium of cooking, hence I prefer to use polyunsaturated vegetable oil, which is neutral.

Adding polyunsaturated oil to a hot pan

So, into the pan goes the oil. Just as it starts to smoke I remove it from the heat and add the black, or brown, mustard seeds.

adding the mustard seeds to the hot oil

Then I let them pop.

A close-up of the popping mustard seeds

The hot infusion is now ready to be placed on top of the cooked dal-with-spinach-purée.

But hold on a moment!!

Have I forgotten something?

Yes, I’ve forgotten the second leaf called kari leaf or karipatta.

kari leaves

This leaf will give the dal its unique aroma which will permeate through the dal if added to the hot oil.

I personally prefer to place the leaves on top of the dal.

Place the kari leaves on top of the dal

I then pour the hot oil onto the leaves.

Tempering - pouring sizzling mustard seeds and oil onto the kari leaves to 'snap fry' them

This makes the leaves ‘snap fried’ bringing out the volatile oils to the surface!

Curry leaf, as it is erroneously called, is good in helping  prevent  diabetes (we have known about this aspect of the kari leaf for a few years, actually a few thousand years but who’s counting?!).

The leaf is used as a mild laxative and as a coolant to the internal organs. It can also be used a mild antidote for small insect and spider bites.

We have two curryleaf  plants on our balcony and in the summer months they prevent mozzies from coming into the house.

The leaf has yet even more uses in its prevention  of bad breath as its essential oils are antibacterial!

Finally, the rice is cooked (boiled or steamed), and at the moment I am using a polished grain called Sona Masoori, this is a polished grain that comes from the region of Andhra Pradesh.

The grain of this particular rice is slightly thicker than Basmati but is easy to cook and half the price! Also, if you cook your rice using the absorption method you simply use 3 cups of hot water to 1 cup of rice for a superb accompaniment. Nothing could be finer!

So, we’re nearly there. My son has come home from school, he’s doing his homework in his bedroom (so I’m led to believe) and is waiting for his dinner.

I’ve nearly finished too but I’ve one last part to do.

The presentation.

My son likes to eat with his eyes first, just as all of us like to eat with our eyes first!!

If it doesn’t look good, and doesn’t smell good, it can’t taste good, that’s his philosophy!! I agree.

I place the boiled rice on a banana leaf and put the dal palak in a separate bowl, sprinkled with the juice of a quarter of a lemon.

(As you’ll all mostly know, the banana plant is very auspicious to Hindus and is a representation of the Goddess Durga!! The leaf is the purest form of a dinner plate and food served on the leaf has a positive effect on the human body besides bringing out the true colors of the food. The fruit and the flower of the banana plant are also very nutritious and . . . well, I don’t have the time now to go into that description as my son is waiting for his dinner.)

the banana leaf

So, I serve the meal, call him to come and get it and wait for his reaction as eagerly as any mother/grandmother/parent!!

He comes back for seconds in no time.

Mission accomplished for this evening!

“Daa-ad,” he asks eagerly, “what are we having tomorrow….?!”

Anah daata sukhi bhava!!

If you want to make this dal palak recipe at home and don’t want to have to read through the blog yet again, please click dal palak recipe for it in user-friendly form!

According to the doctor all babies have low hemoglobin levels at the age of 2 months – this is normal.  However because of Oliver’s medical history we needed to make sure his levels weren’t dangerously low.  The blood tests shows that Oliver’s hemoglobin levels are low.  Not too low, but low enough to want to keep an eye on things, so the plan is to continue with the iron supplements and examen his blood again in 2 weeks.

Good health for babies, come in baby steps..

P.S.  We have been having fun with Photo Booth :)

I am thankful that when the doctor told me to phone him on Monday to ask for the results I (a) already knew it takes a maximum of 2 hours for the lab to release the results.  And (b) am impatient enough to want to know sooner rather than later.

The ladies at Lancet already know Oliver by name from his previous hospital stay and when they gave us the blood results they recommended that we walk past the Doctor’s room first.  We knew blood would be given.  We had the feeling the doctor had been expecting this results, however when he saw just how low it was, he was clearly just as shaken as we were.

It has been a long day of waiting and we are still waiting for the blood to arrive.  Tomorrow will mean a little more waiting and hoping and praying that the blood does the trick!

P.S.  I’m really getting to experience a lot this hospital has to offer.  We started with the labour ward 2 weeks before Oli was born, followed by the maternity ward, neo natal ICU and now pediatrics.  Fantastic hospital and I really will recommend it to anyone.  But my honest preference I will be to stop these little visiting experiences.

P.S.S.  Oli’s body is breaking down the Bilirubine and the conjugated Billi very nicely, the levels have dropped so much and we are so thankful!

Cuddling after our first feed

During the second day in hospital, we were told that little Oliver had a bit of jaundice and would be placed under the lights for some phototherapy.  It was only the following morning when he was taken to Neo Natal ICU when the severity of the whole experience hit us.  And in many ways we were still completely unaware what the real issue was.  To the normal eye, he looked (even if a bit yellow) like a healthy 3.6kg baby.

Over the course of the weekend, Kobus and I learn a whole lot of new words, statistical counts and information we never knew we needed to know.  All this still meant very little, every bit of information was linked to a whole lot of other factors and no timeframe/ limit could be set to anything.  By the Monday we were finished, we needed answers and recommendations.  We needed to know that “A” is what we hope for, if “A” doesn’t happen we will proceed with “B” and if that doesn’t work we have “C, D and E” to look into.

Oliver was under the phototherapy lights, on the billi-blanket.  (which finally gave in due to overuse)

IV Drip to my arm, tanning away.

Diagnosis – ABO Incompatibility and Hyperbilirubinemia

• Bilirubin (BilliT – unconjugated and C – conjugated bilirubin)  - fantastic reference to the meaning of it all
• Haemoglobin

Timeline:

22 Sept @ 11h31 – Oliver Mackenzie Born

23 Sept @ 08h50 – BilliT 219 / C 73 / HB 12.3 – Phototherapy in the Maternity ward baby room

24 Sept @ 07h50 – BillT 332 / C 151 – Oli admitted to NICU, Fluid given via IV drip.

@14h00 – BilliT 345 / C 172 / HB 11.1

@17h30 – BilliT 362 / C 174 – Oli given a second drip with antibiotics to assist liver to process Billirubin.  Urine sample sent for testing reveals no abnormalities with liver and no infections.  Billirubin count peaks

@22h00 – BilliT 350 / C 179 / HB 9.3 – Billirubin coming down, Kobus and I get very excited.

25 Sept @ 07h50 – BilliT 351 / C200 - Conjugated Billirubin count introduced to K and I, as the count after the blood has passed through the liver for processing.  This count shows great concern due to the fact that it keeps increasing unlike the Billirubin count which seems to slowly start coming down.

Paed requests a sonar of Oli’s liver, gallbladder, pancreas and kidneys.  Although the liver is bigger than it should be at Oli’s age, this is normal due to the fact that it is working so hard at processing the Billirubin, other that this all the organs are normal.

@15h41 – BilliT 336 / C 184 - Conjugated count comes down – great excitement.  Blood sent to the blood bank to be analysed.

26 Sept @ 05h15 – BilliT 342 / C 215 / HB 8.8 – Conjugated count shoots up.  Followed by introduction of HB (haemoglobin) as the oxygen carrying property in the blood.  Complete meltdown, followed by “demand to know answers” session in the Pediatrician’s offices.  Blood is order from the blood bank and was given to Oli the same evening.

Pediatrician also orders a torch screen to rule out a bunch of other things that could determine whether there are any other complication that may have an effect on Oli’s recovery.

The nurse assisting Oli for the day mentions Lactose free formula in hope that this will help with the digestive process, Pediatrician gives the go ahead.

Kobus and I hold our baby for the first time in 3 days.

27 Sept @ 08h00 – BilliT 253 / C 146 / HB 11.6 – Improvement thank goodness.  Blood given to Oli makes a huge difference.  Kobus and I start assisting with bottle feeding (under the lights), bathing and nappy changing like “normal parents”.

Burping a baby under the lights

28 Sept @ 10h00 – BilliT 242 / C 141 / HB 12.5 – Torch Screen results brings good news.  Kobus and I are being taught a hard lesson in being patient and allowing the little body to recover at his own pace.

29 Sept @ 09h00 – BilliT 180 / C 110 / HB 10.4 – Great excitement as we stop the phototherapy and antibiotics.  Inevitably this means more cuddles with our baby and holding him when we give him his bottle.

No More Lights

30 Sept – BilliT 172 / HB 11.4 – Good news – IV drip removed and Oliver is allowed to drink breast milk again (all my hard work expressing milk finally paying off).  Bad news, his saturation levels have dropped and he requires some oxygen to assist him in breathing.

01 Oct – BilliT 150 / C 82 / HB 10.8 – Little Master Swart is doing so well fighting the Billi all on his own – no meds, no lights, no fluids.  But we can see he is very tired and for the first time since he has been in NICU we can see that he is a sick baby.  Our baby is fed his milk through a nose pipe to the tummy.

Forehead in great need of some intensive moisturizing TLC

02 Oct – Sunday. Day of rest.  No blood tests.  Incubator heaters switched off, littlest is dressed in clothing (for the second time in his little life) and maintains his own body temperature.

03 Oct – Oli is still getting oxygen when he needs it, the nurses are trying to wean him from the oxygen.  We breast feed from the breast for the first time since he has been admitted to NICU.  So proud of my little monster.

04 Oct – BillliT 141 / HB 10.4 – Pediatrician prescribed some iron drops to help Oli’s body create haemoglobin.  He thinks Oli needs time to recover and that no more blood/ additional medication is needed.

05 Oct – As I arrive at the hospital the nurses tell me that the pediatrician has been in to see Oli and that if everything remains as is, he can go home the following day :)

06 Oct – After 13 long days in NICU and two weeks after he was born, Oliver is discharged from hospital.

First day at home and taking in my surroundings

Early morning cuddles with my big brother

Ready for my first outing

I had been feeling exhausted for quite some time – The kind of exhaustion that would knock me out for hours because my body was too useless to do anything other than sleep. It didn’t affect life so much because my lectures started at 2pm so an early morning nap was a luxury I willingly took. Unfortunately, now that exams are just around the corner, I can no longer afford to take leisurely snoozes whenever I like. The tiredness really hampered my study routine so I decided some medical intervention was needed.

I went to the school nurse who did a finger-prick test which revealed my low haemoglobin count (1.5 mg lower than the minimum threshold for an adult female to be exact). Basically, I lack sufficient “iron-containing protein attached to red blood cells that transports oxygen from the lungs to the rest of the body”. Apparently anaemia is common among females and a healthy dose of vitamin B12 is all that’s needed.

Now, I’ve been told horror stories about the vitamin B injection. Even the nurse warned me how she’d seen grown men squirm before the needle. Well, frankly, I didn’t see what all the fuss was about. The injection itself wasn’t painful at all, and sure, the vitamin B burned a little but it was hardly something worth moaning about. Pfft.

Oh, and I got some cortisone cream for my elbows and they seem to be working (yay!).

Figure 1. Synthesis and breakdown of haemoglobin

Haemoglobin is made up of heme, an iron containing porphyrin and globin, a protein. Normally the erythrocyte lives about 120 days. Ageing or damaged erythrocytes are destroyed by the macrophages of the reticuloendothelial system of the spleen. Other sites notably the, liver and the bone marrow, are also capable of destroying erythrocytes. As the life span of erythrocytes is not increased in splenectomized patients, these sites can completely take over the function in the absence of the spleen. The spleen, unlike other reticuloendothelial sites, is sensitive to subtle damage to the erythrocytes.

Heme splits into globin and hemin and globin. The amino acids released from the catabolism of globin chain are reused for protein synthesis. Hemin is acted upon by heme oxygenase to give biliverdin and iron. The iron is reused for haemoglobin synthesis. Biliverdin, released from the catabolism of protoporphyrin, is finally excreted as conjugated bilirubin in the bile (Figure 1).

Biliverdin is converted to bilirubin by biliverdin reductase. Bilirubin is water insoluble and needs to be conjugated with glycuronic acid in the liver to make it water soluble and make excretion in bile possible. Unconjugated bilirubin binds to albumin and is carried to the liver. The hepatocyte takes up the unconjugated bilirubin by both simple and facilitated diffusion and converts it to bilirubin diglucuronide in two steps. Some bilirubin monoglucuronide is also formed. The enzyme uridine diphophate glucuronyl transferase (UDPGT) facilitated bilirubin conjugation.

Bilirubin is secreted into bile against a concentration gradient. MRP-2 (multidrug resistance like protein 2) is one of the proteins involved in bilirubin secretion.

In the intestine bilirubin is converted to urobilinogen, a colourless compound, by the intestinal flora. Urobilinogen is converted to a pigment responsible for the colour of faeces, urobilin. Some urobilinogen is absorbed and excreted in urine.

Bilirubin metabolism is affected in conjugation defects, secretion defects and in states of increased haemoglobin catabolism.

1. Bilirubin conjugation defects: Mutations in the UDGPT result in three syndromes. These are, in decreasing severity, Crigler-Najjar Syndrome I (CN-I), Crigler-Najjar Syndrome II (CN-II) and Gilbert’s syndromes. While CN-I is fatal except in those who undergo liver transplantation, Gilbert’s syndrome causes no symptoms otherthan jaundice. Patients with all three diseases have unconjugated hyperbilirubinemia which may range from usually >20mg/dL in CN-I, usually <20mg/dL in CN-II and <4mg/dL in Gilbert’s syndrome. Gilbert’s syndrome can mimic haemolysis. The absence of other evidence of red cell destruction, viz. increase in the LDH and decrease in the haptoglobin, and the absence reticulocytosis differentiates it from haemolysis.
2. Bilirubin secretion defects: Defects in secretion of conjugated bilirubin include Dubin-Johnson syndrome, Rotor syndrome, benign recurrent intrahepatic cholestasis (types 1 and 2) and progressive familial intrahepatic cholestasis (types 1, 2 and 3). (links take you to the OMIM page for the disease)

Increased haemoglobin catabolism: Increased haemoglobin catabolism, seen in patients with haemolytic anaemia and states associated with ineffective erythropoiesis, increases bilirubin production and overwhelms the hepatic uptake/conjugation capacity. This increases the unconjugated bilirubin. Increased bilirubin production in patients with haemolytic anaemia is a result of increased erythrocyte destruction by the spleen. Typically, hyperbilirubinemia is associated with extravascular haemolysis. Splenomegaly may accompany unconjugated hyperbilirubinemia due to haemolysis because of the increased workload. Patients of haemolytic anaemia show elevated LDH levels and reticulocytosis. Patients with ineffective erythropoiesis, e.g. megaloblastic anaemia due to folate/B12 deficiency, have increased haemoglobin catabolism due to destruction of haemoglobinized precursors in the bone marrow. There is reticulocytopenia, the increase in LDH is more pronounced than haemolytic anaemia, there is no splenomegaly. Haemolysis and ineffective erythropoiesis may co-exist in megaloblastic crises of haemolytic anaemia. Unconjugated hyperbilirubinemia due to increased bilirubin production is associated with increased urinary urobilinogen, a features not seen in inherited syndromes of bilirubin conjugation (CN-I, CN-II and Gilbert’s syndrome). It is unusual for the bilirubin to increase beyond 4mg/dL only from increased haemoglobin breakdown. When higher values are encountered other reasons for an increased bilirubin must be sought. All patients with increased haemoglobin breakdown do not show hyperbilirubinemia.

Image from http://i-heart-cupcakes.blogspot.com/2010/04/put-down-spoon-and-walk-slowly-away.html

Last Thursday when I visited the diabetic nurse she took loads of blood for the various tests.  These are Kidney function, Liver and blood count; Cholesterol and the HbA1C test.

The HbA1C test indicates what your average blood sugar levels have been over the past two or three months.  It measures how much glucose has become attached to the protein haemoglobin, an oxygen-carrying component of red blood cells.  The results used to be expressed as a percentage from 4 – 13.  Diabetes UK recommends keeping levels below 7%.  Nowadays as we are part of the European Union everything is being standardised as these levels are now expressed as a number (IFCC)

Back to my test results.

Kidney and Liver functions – normal

Blood count – normal

Cholesterol – 4.4  (I’m really pleased with this as the last time it was measured it was 6.1)

HbA1C = 60 (which equates to 7.5%)

I was really pleased with the results as these will be a base to improve upon.  I was expecting both the Cholesterol and the HbA1C to be a lot higher but they are really good.

The tests will be run again next time I visit in September so I am aiming to lower both the Cholesterol and HbA1C results along with my blood pressure (which was 130/80).

But for the time being, all is well