DN article

​The Daily Nation is today exposing the insincerity, backtracking and outright arm-twisting that have been blamed for the long-drawn doctors’s strike that enters the second month this week.

In doing so, it hopes that the parties to the dispute — the doctors and the government — will come to their senses and end the suffering of hundreds of thousands of Kenyans who have gone without medical care since the beginning of December last year.

Our report is based on two things: a secret return-to-work formula drawn by the doctors’ union on January 28 this year, and which was to be signed between them and the national and county governments as a way to end the strike; and the negotiators’ inflexibility.

Dr Mailu, the soft-spoken geneticist who became CS Health in January last year, now finds himself fighting the biggest battle of his life yet. Apart from the loss of lives, a lot is at stake for his ministry, such as medical training that is hosted in referral hospitals, and collection of data for disease surveillance.

The four-page document, which we obtained from an official of the union, has glaring irregularities that were either honest mistakes or deliberately aimed at hoodwinking the government to pay more than was actually captured in the agreement.

The Ministry of Health late last month refused to sign the document, to the chagrin of the striking doctors.

To begin with, the 15-point agreement states that all medical practitioners, pharmacists, and dental officers, including specialists in the public service, shall be moved one job group higher effective July 2016.

A table in the appendix of this agreement quotes job group ‘M’ as earning a minimum basic salary of Sh54,532 and a maximum of Sh68,165. At this group, medical interns will also get a house allowance of Sh28,000, a doctor’s allowance of Sh72,000, a commuter allowance of Sh8,000, and a non-practice allowance of Sh19,000. The take-home package for interns in the pay structure proposed by the doctors’ union totals to about Sh221,000, inclusive of risk and extraneous allowances.

But the salary of job group ‘M’ as stipulated in government records is different from what the doctors are demanding. The minimum basic salary is fixed at Sh44,989 and a maximum of Sh56,236. The house allowance is Sh28,000, the doctors allowance is Sh66,000, a commuter allowance of Sh6,000, and a non-practice allowance of Sh12,000. When the risk and extraneous allowances are tallied, the intern’s take-home is Sh196,989.

These are consistent with what the Salaries and Remuneration Commission (SRC) provided on December 6, 2016 as the salary structure for public officers.

What the doctors are asking for, therefore, is Sh24,543 more than what is provided for, for job group ‘M’.


A close scrutiny of the document shows that the benefits of job group ‘M’ have been replaced with figures from ‘N’, and from there the inconsistencies cascade all the way to ‘T’.

Further scrutiny in the appendix shows that doctors have also created a new job group ‘T’ which does not exist in any available government pay structure.

Surprisingly, at this job group — which is the pay scale for specialists — doctors are asking for a minimum basic salary of Sh192,060 and a maximum of Sh302,980, a difference of Sh110,920, which is the highest margin across all job groups in the country.

What is even more suspicious is that a specialist junior, in job group ‘S’, will take home a minimum salary of Sh221,058, which is Sh28,998 more than their seniors.

And there is more. The agreement states that the entry level for medical interns shall be ‘C5’ effective July 1, 2017, despite earlier documents placing interns at ‘M’.

If interns are paid on ‘C5’ terms, their minimum salary will move from Sh54,532 to Sh64,919 and a maximum of Sh81,148, which are the SRC guidelines.

When asked to explain these inconsistencies, a source within the union was lost for words and offered to send us another document with “better edits”.

As a result of these inconsistencies, the Ministry of Health has started questioning the mandate of the negotiating team, asking whether it has the clout to reach any agreement on behalf of doctors.

Health Cabinet Secretary Cleopa Mailu, who was not available for comment on the new document, has previously said that the doctors have “constantly changed” their decisions, adding that “when a union agrees to a position and changes in the next minute, it becomes very difficult to negotiate and reach an agreement”.

But the doctors say they walked out of the last meeting because the government “gave them a new Collective Bargaining Agreement” and not what they had agreed to earlier.


As the back-and-forth game plays out, the strike — and all the passionate discussions around it — has taken a life of its own.

The abhorrence against it has moved from the plight of patients to political undertones, such as politicians waiting for an opportune time to play the God syndrome for campaign mileage.

So testy has the subject become that even those authorised to speak on behalf of those directly affected by the strike want anonymity when talking to the press as they claim to have insider information on who does not want the strike solved, and why.

Dr Mailu, the soft-spoken geneticist who became CS Health in January last year, now finds himself fighting the biggest battle of his life yet. Apart from the loss of lives, a lot is at stake for his ministry, such as medical training that is hosted in referral hospitals, and collection of data for disease surveillance.

Initially, at the centre of all the hubris was a document that the doctors wanted registered and the demands therein fulfilled: the collective bargaining agreement between them and the government, signed in 2013.

In it, doctors asked for, among many other things, salary increments that range from as low as 75 per cent to as high as 180 per cent, facilitation for post-graduate studies, better working conditions, and better relations with their employers.

And they have a reason to ask for better terms. Data from the Ministry of Health shows that there were only 9,734 registered doctors to attend to the 44-million-plus Kenyans as at 2015.

Not all of these practise, but assuming they do, that would mean every doctor takes care of about 4,500 people, against the WHO recommended ratio of 1:600. A Kenyan doctor, therefore, carries out the duties of eight professionals in countries that have met the recommended threshold.


Last week, the Senate complicated matters even more when it asked doctors to stop insisting on a salary agreement that has already been declared illegal by the courts.

The Senate Health Committee observed that the CBA the doctors are pushing for has been overtaken by events and will derail efforts to end the strike.

“They can’t hang on an illegal document,” said the committee chairman Dr Wilfred Machage. “Nobody has prevented doctors from coming up with another legal document.”

The Labour Relations Act requires that such agreements be registered with the Industrial Court, something that had not been done by either the government or the Kenya Medical Practitioners and Dentists Union (KMPDU) when they entered into the agreement in 2013.

And, in its strike notice to the Head of Public Service, Mr Joseph Kinyua, the union stated that it wanted the CBA “signed on June 27, 2013 registered and implemented”.

It is, however, an offence to implement a CBA before it is registered by the Industrial Court, but once registered it binds parties to comply with the commitments therein.

And so goes the story of Kenya’s worst industrial dispute in recent history. The doctors are hanging on the promises of a document that the Executive, the Legislature and the Judiciary say is illegal, but they insist that a promise is a promise, and it should be kept.

While there was hope at the start of the strike two months ago, there is none now. Only despair, death, and a growing thick skin.

Additional reporting by Verah Okeyo


That is what we can afford. But if you tell me that we pay doctors because they have gone on strike, and if we pay everyone who goes on strike what they demand, then we can’t go on living in this country. It is our duty to inform striking personnel that our economy can only afford this. Henry Rotich, Treasury Cabinet Secretary, on why striking doctors should accept the 40 per cent pay rise offered to them by government


We hope government agrees to mediation. We want the process to be open, in front of the press, so that the public can get to know what is happening. Dr Ouma Oluga, Kenya Medical Practictioners, Pharmacists and Dentists Union Secretary-General


When a union agrees to a position and changes in the next minute, it becomes very difficult to negotiate and reach an agreement and that is what we have been subjected to as a ministry… as a government… for the last 52 days. Health Cabinet Secretary Cleopa Mailu on why the doctors strike has dragged on for over 50 days.


The ongoing doctors’ strike is a very unfortunate occurrence. The government is prepared to sit with doctors to resolve the matter before the year’s (2016) end. Eric Kiraithe, Government Spokesman, adding that the union was offered a good package but refused it.


This is beyond the ability of any single ministry in the national or county government to handle effectively. How can the government import doctors if they cannot pay their own? Prof Lukoye Atwoli, Kenya Medical Association secretary, in an appeal to the World Health Organisation and the International Labour Organisation to help end strike.


Our striking doctors need to consider the package the government is offering them. Our neighbouring countries pay much less than the salaries our medics are currently receiving. Peter Munya, Council of Governors chairman, after asking county bosses to issue sacking letters to striking doctors if they fail to resume work.


A timeline of death, pain, and despair

November 2016

November 18: Doctors meet with Ministry of Health to avert looming strike, set for December 5, 2016.

Nov 30: CS Mailu urges doctors to drop strike threat, seeks dialogue, but doctors announce nationwide strike demanding the recognition, registration and implementation of the 2013 Collective Bargaining Agreement.


December 2016

Dec 2: Court stops doctors’, nurses’ strike following a case filed by the Council of Governors.

Dec 4: Doctors start strike in defiance of court order, colleagues from coast asked to travel to Nairobi for demos.

Dec 5: Poor patients suffer as health workers’ strike begins, affecting 2,700 public health facilities, forcing families to transfer ailing kin to private hospitals; polio vaccination drive postponed, CS Mailu urges medics to resume work as negotiations continue.

Strike enters fifth day, doctors’ strike gets worse as KNH consultants down tools.

Dec 9: KDF doctors step in to handle emergency cases at KNH, counties announce plans to hire temporary medical staff to alleviate suffering, leaders as government to revert health services to national management, State says it is displeased with protracted talks.

Dec 10: Governors fault government for signing 2013 CBA with doctors

Dec 11: Strike by nurses called off after the Ministry of Health and the union sign a Sh7 billion agreement as doctors union says it will evaluate government’s offer.

Dec 14: Nurses union officially calls off strike and signs pact with governors.

Dec 20: Medical associations call on international organisations to help end doctors’ strike, union officials found guilty of disobeying Labour Court order

Dec 22: As striking doctors fear the government might sack them to force them to resume work, resident doctors at Aga Khan Hospital show support for striking counterparts

Dec 27: Counties announce they will not pay the thousands of doctors their December salaries

Dec 28: National government challenged to take over the responsibility of paying salaries of the striking doctors from the counties, Bomet Governor Isaac Ruto, accompanied by a group of rowdy youth, storm a doctor’s union meeting at Fair Hill Hotel and allegedly rough up the officials, bringing the meeting to disarray.


January 2017

Jan 3: Seven counties withhold December salaries of more than 300 striking doctors

Jan 4: President Uhuru Kenyatta meets doctors in Mombasa over strike at State House, offers a 40 per cent pay rise.

Jan 6: Doctors meet to assess State’s pay deal but reject the offer and maintain they only want the 2013 CBA.

Jan 8: State House trashes CBA, calls doctors for negotiations even as the health sector crisis deepens, doctors and ministers exchange barbs.

Jan 10: Doctors warm up for a bruising legal battle with the government after a court orders arrest of union officials for contempt of court, Nairobi County government threatens to sack striking doctors if they do not return to work.

Jan 11: Police fail to arrest Kenya Medical Practitioners’, Pharmacists’ and Dentists’ Union officials as ordered by a court.


Jan 12: Council of Governors (CoG) chairman Peter Munya urges county bosses to issue sacking letters to striking doctors if they fail to resume work, the Employment and Labour Relations Court sentences six officials of the doctors’ union to a one-month suspended sentence on condition that they continue with negotiations with government to end strike.

Jan 13: Ministry of Health announces raft of measures to cushion desperate Kenyans from the impact of the doctors’ strike, including partnering with faith-based hospitals, Health CS Cleopa Mailu directs that medicines in public health facilities be redistributed to faith-based hospitals, government in a paid advert appears to revise its offer to doctors to end their strike by extending the time for resolving labour issues from 60 to 90 days.

Jan 14: Kenyans says they have resorted to nursing the sick at home as strike enters 42nd day.

Jan 15: Senators say President Uhuru Kenyatta and governors to blame for deaths due to doctors’ strike.


Jan 16: The Archbishop of the Anglican Church of Kenya, Jackson ole Sapit, calls on doctors to call off their strike to save the country from witnessing more deaths and agony.


Jan 17: The end of strike seems imminent following talks between the government and the medical practitioners’ union in Nairobi, clinical officers also demand a pay increase and issue a one-week strike notice.

Jan 19: Doctors take to Twitter in a bid to explain why they will not budge and why they refused a 40-per cent pay rise offer, medical students demonstrate and urge government to meet demands of doctors, medics talks continue as doctors’ strike enters 46th day.


Jan 22: As medics away from the hospital, clinical officers forced to take on extra work.

Jan 23: Government announces nearly 4,000 dismissal letters to be issued to striking doctors.

Jan 24: Doctors, through their union officials, move to the Employment and Labour Relations Court seeking an extension of the negotiation period with the Ministry of Health.

Jan 25: Fresh bid to end doctors’ strike collapses as CS Mailu accuses union leaders of indecision.

Jan 26: The Labour Court extends the suspension of a jail sentence it granted doctors’ union officials on the condition that they end their job boycott in five days, county governments begin the process of firing doctors who are on strike as Council of Governors Chairman Peter Munya explains that the termination process started as soon as the dismissal letters were issued to the doctors, nurses threaten to go on strike again on February 1 because their pay slips do not reflect the allowances their employers promised late last year.

Jan 29: Council of Governors Chairman Peter Munya tells nurses not to boycott work again as counties are processing their allowances.

Jan 30: Governors say they will henceforth hire doctors on three-year renewable contract as opposed to the current permanent work terms.

Jan 31: The National Assembly is prompted into joining the Executive and the Judiciary in seeking an end to the strike after the doctors’ union submits their petition to the House.


Medics take war to Twitter, share sad stories from in-the-red wards

By the time the doctors’ strike comes to an end, whether the doctors get their demands or not, their voices will remain etched in history.

Their voices and words, like digital footprints, will forever be etched on social networking sites, where in their numbers they have aired, shared and re-shared their grievances. They have in unison explained why they will not be going to work unless drastic changes are seen not only on their pay slips, but also in their work environments.

Their rallying call throughout the strike has been the hashtag #LipaKamaTender, through which they have kept asking the government to pay them as quickly and easily as a tender is handled in government projects.

But there have been more hashtags in the past two months, such as #MyBadDoctorExperience, through which medics recounted experiences of being forced to work without drugs, gloves or electricity, and under severe staff shortages that left many on the verge of collapse.

One Twitter user, a doctor identified as Anthony, told of how he had to light up the theatre after lights went out in the middle of a Caesarean section. “The back-up generator was out of fuel. We ended up using a Nokia phone flashlight (as the) torch available had expired batteries.”

“Waiting all day to perform an emergency surgery because there are few theatre rooms and multiple emergencies in wait,” said Joyce Omuok.

“Got pricked in casualty, patient HIV+, no post-exposure prophylaxis (PEP). Had to travel to Nairobi at 1am to get it,” narrated Nasirumbi Magero.

Then the stories got serious and ridiculous.

“Watching a patient die because the ambulance had been given to the MCA to pick his tomatoes from market,” wrote Jeff Kims.

“My bad doctor experience is transporting an intensive care unit (ICU) patient from Garissa to Kenyatta National Hospital (KNH) by road. They (sic) died at Thika,” tweeted one doctor, who only identified herself as Njeri.

“Consoling a mother who lost her baby because the only available anaesthetist was in main theatre with another patient,” wrote Wambugu Justus.

While Beldina Gikundi shared how she had to donate her own blood for a bleeding mother because there was no blood in the hospital’s blood bank.

Robert Simiyu could not administer an emergency drug to a patient because “syringes were out of stock.”

Wambui Munjua shared: “Watching the nutritionist mix cow milk with water as hospital could not afford formula for the babies in the nursery.”

“Losing an eight-year-old girl to leukemia because there was no blood or ambulance,” a user only identified as Munyoki tweeted.

But there have been divergent voices, counter-narratives, who questioned the doctors “calling”, hard stance to negotiate, why they are not bounded by the Hippocratic Oath, accept the government offer and go back to work.

But even then, the doctors have not backed down from their Twitter accounts.



Tinnitus is described as ringing in the ears. It is the perception of sound in the ears or head where no external source is present.This common problem is a symptom of an underlying medical condition such as circulatory system disorder, ear injury or  age-related hearing loss. Tinnitus can  get worse with age and better with treatment.


Objective tinnitus : This is the type your doctor can hear when he examines you. This type is rare and may be caused by a blood vessel problem an inner ear bone condition or muscle contractions.

Subjective tinnitus : This is the type only you can hear. It is the most common type and usually caused by outer, middle or inner ear problems. Problems with  the hearing (auditory) nerves or the part of your brain that interprets nerve signals as sound can also result in this type.


Tinnitus is not a disease. It is a symptom that there is something wrong with the auditory system. This includes the  ear, the auditory nerve that connects the inner ear to the brain and the parts of the brain that process sound. Some health conditions that may cause ringing in the ear includes :

  • ear and sinus infection
  • noise induced hearing loss
  • brain tumors
  • Meniere’s disease
  • hormonal changes in women
  • thyroid abnormalities
  • heart and blood vessel diseases
  • medications such as cancer medications, diuretics and antibiotics


Factors that can increase your risk for this condition includes :

  • exposure to louder voice
  • older age
  • being male
  • being a smoker
  • having cardiovascular problems such as high blood pressure and atherosclerosis


Symptoms of Tinnitus includes these types of phantom noises in your ears

  • ringing
  • hissing
  • clicking
  • roaring
  • buzzing

The pitch of these noises may range from high to low. It may happen in one or both ears.


The following test will help doctors diagnose this ear condition.

Hearing exam : This test will help rule out or identify possible causes of tinnitus. You will be asked to  sit in a sound proof room wearing earphones through which will be played specific sounds into one ear at a time. You will be asked to indicate when you hear a sound and results are compared with results considered normal for your age.

Movement : You will be asked to  move your eyes, clench your jaw or move your neck, arms and legs. Your doctor will then determine tinnitus changes or worsens.

Imaging tests :You may have a   CT scan and MRI  depending on the underlying cause of your condition.


The first treatment of tinnitus is to find out the underlying cause and treat it. These include

  • removal earwax
  • treating heart or blood vessel diseases
  • changing medications

You doctor may also recommend using an electronic noise suppression device. These include

  • hearing aid if you are having hearing problems
  • white noise machines which produce simulated environmental sounds such as falling rain or ocean waves
  • masking device which produce a continuous, low-level white noise that suppresses tinnitus symptoms
  • tinnitus restraining which is a device that  delivers individually programmed tonal music to mask the specific frequencies of the tinnitus you experience

Medication that may relieve symptoms of the ear condition includes

  • Tricyclic antidepressants, such as amitriptyline
  • Alprazolam (Niravam, Xanax)


Complications of tinnitus includes

  • memory loss
  • sleep problems
  • trouble concentrating
  • anxiety
  • stress
  • depression


Take these precautions to prevent ringing in the ears

Wear hearing protection.

Turn volume down.

Take care of any underlying cardiovascular disease.



“That stupid woman! She thinks she can embarrass me in front of the whole village like this? Pleli fuckin! She will know who I am today! They don’t call me Wero Pelion for nothing!”

Kipkiror  is furious. His eyes have turned into a shade of red I have never seen before. I don’t know if it’s the Chang’aa we just had, anger or a mixture of the two.  Anyway, I have never seen him this mad before. His whole body is shaking with rage you’d think he was a suswet in the wind. He grabs his walking stick and stomps out of the drinking den. I dash after him.

You see, all this would not have happened had it not been for that useless bastard Kipkor and his big mouth. Personally, I have never liked him. He is always picking up and spreading rumours here and there about everyone in the village. You’d be astonished at just how many fights he has caused. It is forgiveable when a woman is the one spreading rumours.. But this man here is an embarrassment to all circumcised men. You’d think he never went to Kaptorus with the rest of the men. Someone ought to beat some sense into him.

Kipkiror is walking so fast  I am finding it hard to keep up with his pace.  I am half running. The alcohol is not exactly doing me any justice. I feel a bit dizzy. I shake my head furiously hoping to clear the fuzziness. It doesn’t help much. But the fear of what my friend could do to his dear wife sobers me up a little. The can now see a bit clearly.

Where was I? Yes that idiot who calls himself Kipkor. You see we were busy sipping our Chang’aa outside Tecla’s house with a couple of other men when he joined in. That man can never keep quiet.  He found us talking about other things but suddenly makes the conversation all about him. How rude?

But being noble men, we just sat there and listened. The problem started when he was halfway through the kipsiling of the potent drink.

“Some of you call yourselves men! Yet, a simple task like  making a woman pregnant
defeats you. Ha! Such shame”

“What are you talking about?”

“All I am saying is that some of you are being called “father” by other men’s children. I Kipkor, son of Kabelo, can never accept to be taken for a fool like that”

“Stop with all this nonsense. If you are not telling us the whole story, be on your way”

“ Well, if you insist. So this morning, my wife told me that Philomena confided in her that the father of all her three children is not actually her husband. I always suspected something fishy about that woman. You see that first born, he has a pointed head that no one in the clan has. I always knew there was something cooking there”

Philomena is Kipkiror’s second wife, the one he brought home after the first ran away because she couldn’t bear him children.
I bet you now understand where all this is coming from


We are now entering the compound. Kipkiror heads straight to the pantry and comes back with a Panga. His wife is busy cooking in the kitchen unaware of what is happening.

“I will kill that chepkarta before she kills me!”

“Don’t do it kaborin , it’s not worth it!” I plead with him

“ She cannot do this to me and get away with it. I will skin both her and her useless lover alive!”

He bangs on the kitchen door “Woman, come out!”

Philomena is confused.  She emerges from the kitchen holding a cooking stick.

“What is going on? What’s with all the noise?”

Her expression suddenly changes once she sees the panga her husband is holding His fiery eyes are enough to tell her that something is not right.

“Who is he? Tell me now! Who is he?”

“I don’t know what you are talking about?”

“So now you want to pretend, eeh?”

He grabs her by the waist and lands a couple of blows on her face.

“Uwiiii! Don’t kill me Kipkemoi! Meketan ! “

“Tell me! Who is he?”

He is ruthlessly beating her now. She’s fallen to the ground and her lower lip is bleeding. I cant take it anymore.

“Stop it Kipkiror! You’re going to kill her”

I hold his hand to restrain him but he’s too strong.

“Why should I stop, eeh? Why?” He’s trying to shake off my hand so that he can punch her some more.

“Woman, tell me who is he? Who is the bastard?”

“Uwiii! Uwiii! I am dying! Help me!”

“ Kipkiror, I am the one….”

Dead Silence

Tell Kipkiror I have Gone


The sun today is too hot; but not as hot as my tempers.  I am boiling over with rage I can barely see the path. I cannot feel the weight of the “Tenja” on my back; the stones are hurting my feet. Fury is a bad thing.

By now you’re wondering why I’m in such a horrid mood.  I should never have gone to River Tot at this hour. Going there at this hour of the day is  an invite for trouble. Those idle village women always come to do the whole week’s laundry on Chumamos. It is never a good day to go to the river. The water is filthy.

You can tell the dirtiest woman by how they combine their stained babies’ clothes with those of their husbands in the same basin.  Diryy blankets reeking of dried urine are washed on Chemos. One would think they last saw water when the Pokot were still at large. These Kamogo women are Seretan, but let me not judge them. Atleast they have children to wash clothes for.

I set my jerrican at the door. The house is quiet.  Chumba must have gone out to play again; she’s the daughter of my brother in law; schools have closed so she came to stay with me till January. I pick up sikor to light the fire.  I should cook; perhaps after I eat I’ll stop being angry. That thing about an hungry man being an angry man.

Anyway, back to my story. You see, I have always avoided those village women. I have never been one to entertain gossip.  So ever since I got married, I have keep away from them them like plague. I fetch my water  at 6am when none of them is awake.  I till my Shamba on Sunday after Misa and in the middle of the week. I  wash my clothes  on Monday morning.  It has always worked for me. But today, I had to  go to Kabetwa  to visit my sister at the clinic. That’s the reason I was at the river at Midday.

Anyway, all would have been well had it not been for that Chesawil  of a woman;  Jelagat .  I have never liked her. She is always poking her nose into other people’s business.  Why cant she just mind her home and let people be?  She should feed and wash her children for starters. They are always going to people’s home at lunch time; waiting eagerly for an invite. Those children, they never get satisfied. You give them a whole plate of githeri and they will wolf it down and look at you as if they didn’t eat anything. Maybe they have minyoo.

Anyway, Jelagat ruined my day. I don’t call her Chesawil for no reason.

You see, it has been 3 years since I got married. I have never conceived.  To my people that is a curse; what good is a woman that cannot give birth?  Jelagat has always made it her duty to make me feel even worse than I already do.  I know she and and the other women have talked and talked about me from every single angle judging by the scornful eyes they give me whenever I pass them on the way.

“Iamune  Talaa? You didn’t tell us you got a co-wife? That skinny girl Chepng’eno; I hear Kipkiror is planning to take goats to her family. After all, she’s carrying his child. How far along is she now?”

“I am not so sure. We haven’t talked in a while. Anyway, I have to run home; I didn’t leave food for Chumba. Catch you later.”

Now you know why I am mad. Imagine finding out from a woman you detest that your husband is expecting a baby with another woman? And more so,  the fact that he was planning to make her officially his wife.

I was mad. Mad at the gods for denying me the fruit of the womb. Where had I gone wrong? Surely, I have been a good woman my whole life. Why did the spirits have to curse me like that?

I was mad at Kipkiror. How could he do this to me? Why did he have to insult me by doing this? I was mad at that other woman for getting pregnant. Why her? Why not me?

My ugali is now ready; there’s still some stew from last night. I step out to go look for  Chumba so that we can eat. She comes running towards me,  she must have seen me from far. “Aunty I was at Sakoma’s house” she explains herself.

How I loved that little girl, I always wished she were my own. “Come let’s eat”

“Why are you so sad Aunty? Your eyes are red”

“I have an headache my child”

“You should eat then rest a bit. I’ll wash the vyombo for you”

As we eat in silence, thoughts rush to my head. I am calm now.  My thinking is clear.

I had always been a proud woman. Much as I loved Kipkiror,I would never stand the public insult that he was about to make of me. I would not condone the humiliation . No,  I would save myself before it all happened. After all, my home was just on the other side of the valley.  It’s not like I had forgotten the way.

Suddenly, I felt suffocated. I could not stand another single minute in the house that had been my home.

After my meal, I grab a bag and stuff all the clothes I could come across. It was time to go.

Chumba stood there, staring at me as if I was deranged.

“Tell Kipkiror I have gone”

Adapted from Canduhlitta


Peptic ulcer is an open sore that develops in the lining of the esophagus,  stomach or duodenum ( upper part of the small intestines). The most common symptom is a burning stomach pain. Peptic ulcer may occur at three different locations.

Esophageal ulcer : It occurs inside the esophagus which is the hollow tube that carries food from your throat to your stomach.

Gastric ulcer : It occurs inside the stomach.

Duodenal ulcer : It occurs inside the duodenum which is the upper portion of the small intestines.


It occurs when acid in the digestive tract eats away the inner lining of the esophagus, stomach and duodenum. This results  in a painful open sore that may bleed. Excessive acid production is  caused by  imbalance between digestive fluids in the stomach and duodenum.

Infection with Helicobacter pylori (H. pylori) may also cause an ulcer.

Certain over the counter and prescription medications like  ibuprofen (Advil, Motrin IB, ), naproxen (Aleve, Anaprox, ) and aspirin can irritate the lining of the stomach and cause an ulcer.

Gastronomas , tumors of the acid producing cells of the stomach  increases acid output and causes ulcers.


You may be at increased risk of getting peptic ulcer if :

– you are a smoker 
– you are infected with the H. pylori bacterium
– you drink alcohol regularly
– you have a family history of the disease
– you are 50 years and older
– you have medical conditions such as kidney and liver disease
– regularly take pain medications such as aspirin, ibuprofen, or naproxen


Signs and symptoms of peptic ulcer includes the following :

– a burning pain in the middle or upper portions of the stomach. The pain may get worse when stomach is empty or at  night.  It  may disappear and return for a few days or weeks.
– Eating foods that buffer stomach acid or that reduce acid production may  provide temporary relief.
– nausea and vomiting
– bloating
– heartburn

In severe cases, patients may

– have bloody stools
– vomit blood
– experience weight loss


Doctors will diagnose peptic ulcer by asking  you about your symptoms. They may then perform  certain diagnostic test to confirm the disease. In the mean time your doctor may give you medications for heartburn to  improve symptoms.

Upper Endoscopy :  Your doctor will pass a  hollow tube equipped with a lens (endoscope) down your throat and into your esophagus, stomach and small intestine. This is done to check for ulcers

Test for for H. pylori : This is done to check if the bacterium is the cause of your symptoms. This test can be done using your blood, stool and breathe. The type used depends on your condition.


Peptic ulcer may get worse if not treated. Treatment includes medications to reduce stomach acids, antibiotics to kills the H. pylori bacterium, lifestyle change and in more severe cases surgery.


Proton pump inhibitors : They  reduce stomach acid by blocking the action of the parts of cells that produce acid. They include Prevacid, Aciphex, Protonix, Prilosec,  Nexium and Dexilant.

Acid blockers : They are also known as histamine (H-2) blockers. They act to reduce stomach acid released into your digestive tract thereby relieving pain associatd with peptic ulcer. They include medications ranitidine (Zantac), famotidine (Pepcid) and  cimetidine (Tagamet).

Antacids : They neutralize stomach acid and provide rapid pain relief.

Antibiotics : They are  used to kill  H. pylori infection.  You’ll likely need to take antibiotics for two weeks, as well as additional medications like Pepto – Bismol .

Upper endoscopy : Some bleeding problems associated with peptic ulcer are  treated through upper endoscopy.

Surgery : One may need surgery if serious bleeding is involved.


Peptic ulcer can present complications such as
– internal bleeding
– infection of the abdominal cavity
– scar tissues  that can block passage of food through the digestive tract.


Take these precautions to prevent peptic ulcer

Do not smoke.

Avoid alcohol.

Don’t overuse pain medications like aspirin and diclofenac



  • Alcoholic liver disease (ALD) encompasses a spectrum of injury, ranging from simple steatosis to frank cirrhosis.
  • Alcohol remains amajor cause of liver disease worldwide
  • It is common for patients with ALD to share risk factors for simultaneous injury from other liver insults (e.g., coexisting nonalcoholic fatty liver disease, or chronic viral hepatitis).
  • The spectrum of alcohol-related liver injury varies from simple steatosis to cirrhosis.
  • These are not necessarily distinct stages of evolution of the disease, but rather, multiple stages that maybe present simultaneously in a given individual.
  • These are oft en grouped into three histological stages of ALD, including
    • fatty liver or simple steatosis.
    • alcoholic hepatitis (AH).
    • chronic hepatitis with hepatic fibrosis or cirrhosis.
  • The latter stages may also be associated with a number of histological changes, including
    • Mallory’s hyaline
    • megamitochondria
    • perivenular and perisinusoidal fibrosis
  • Alcoholic hepatitis is a syndrome of progressive inflammatory liver injury associated with long-term heavy intake of ethanol.
  • Alcoholic hepatitis (AH) remains a common and life threatening cause of liver failure, especially when it is severe.
  • Although the term “acute” is frequently used to describe this form of liver injury, it is usually subacute and has been developing for weeks to months before it becomes clinically apparent.


  • Patients with this form of alcoholic liver disease usually have a history of drinking heavily for many years.
  • Observational studies have shown an increased risk of cirrhosis with ingestion of greater than
    • 10-20 g of alcohol per day in women and
    • more than 20-40 g/d in men.


  • A variety of genetic,environmental and gender-related factors appear to independently influence the development of alcoholic liver disease.
  • Age, female gender, excess body weight [body mass index (BMI) > 27 kg/m2 in men, BMI > 25 kg/m2 in women have been identified as independent risk factors for development of liver disease. (Bruguera 2014)
  • In addition to a smaller volume of distribution, women are at higher risk due to a relative deficiency of gastric alcohol dehydrogenase compared to men.
  • several women have developed AH after gastric bypass, in which the amount of gastric mucosa available to metabolize alcohol was reduced.
  • More severe forms of AH are associated with consumption of large amounts of alcohol or binge drinking.
  • Not surprisingly concomitant malnutrition and the presence of coexisting hepatitis C has also been linked to a poorer prognosis.(Leslie, Pawloski et al. 2014)
  • The combination of hepatitis C virus and alcohol predisposes to moreadvanced liver injury than alcohol alone,76,77 with disease at a younger age, more severe histological features, and a decreased survival.(Stimac, Bradaric et al. 2013)
  • The risk of developing cirrhosis increases with the ingestion of > 60-80 g/day of alcohol for 10 years or longer in men, and >20g/day in women.6,50 Yet, even drinking at these levels, only 6%-41% develop cirrhosis.


  • The true prevalence of alcoholic hepatitis, especially of its milder forms, is unknown, because patients may be asymptomatic and never seek medical attention.
  • In the United States alone, alcoholic liver disease affects more than 2 million people (ie, approximately 1% of the population).
  • Although the exact prevalence is unknown, approximately 7.4% of adult Americans were estimated to meet DSM-IV criteria for the diagnosis of alcohol abuse and/or alcohol dependence in 1994
  • More recent data suggest 4.65% meet criteria for alcohol abuse and 3.81% for alcohol dependence. In 2003, 44% of all deaths from liver disease were attributed to alcohol.
  • Racial differences in incidence – no genetic predilection is noted for any particular race
  • Alcoholic hepatitis can develop at any age. However, its prevalence parallels the prevalence of ethanol abuse in the population, with a peak incidence in individuals aged 20-60 years.
  • Sexual differences in incidence – Women develop alcoholic hepatitis after a shorter period and smaller amounts of alcohol abuse than men, and alcoholic hepatitis progresses more rapidly in women than in men.


Ethanol metabolism

  • Most tissues of the body, including the skeletal muscles, contain the necessary enzymes for the oxidative or nonoxidative metabolism of ethanol.
  • However, the major site of ethanol metabolism is the liver.
  • Within the liver, 3 enzyme systems metabolise ethanol—
  1. Cytosolic ADH uses nicotinamide adenine dinucleotide (NAD) as an oxidizing agent. ADH exists in numerous isoenzyme forms in the human liver and is encoded by 3 separate genes, designated as ADH1, ADH2, and ADH3. Variations in ADH isoforms may account for significant differences in ethanol elimination rates.
  2. The microsomal ethanol-oxidizing system (MEOS) uses nicotinamide adenine dinucleotide phosphate (NADPH) and molecular oxygen. The central enzyme of MEOS is cytochrome P-450 2E1 (CYP2E1).
  • Peroxisomal catalase uses hydrogen peroxide as an oxidizing agent.
  • The product of all 3 reactions is acetaldehyde, which is then further metabolized to acetate by acetaldehyde dehydrogenase (ALDH).
  • Acetaldehyde is a reactive metabolite that can produce injury in a variety of ways.
  1. Toxic effects on cell membranes
  • Ethanol and its metabolite, acetaldehyde damage liver cell membranes.
  • Ethanol can alter the fluidity of cell membranes, thereby altering the activity of membrane-bound enzymes and transport proteins.
  • Ethanol damage to mitochondrial membranes may be responsible for the giant mitochondria (megamitochondria) observed in patients with alcoholic hepatitis.
  • Acetaldehyde-modified proteins and lipids on the cell surface may behave as neoantigens and trigger immunologic injury.
  1. Hypermetabolic state of the hepatocyte
  • Hepatic injury in alcoholic hepatitis is most prominent in the perivenular area (zone 3) of the hepatic lobule.
  • This zone is known to be sensitive to hypoxic damage.
  • Ethanol induces a hypermetabolic state in the hepatocytes, partially because ethanol metabolism via MEOS does not result in energy capture via formation of ATP.
  • Rather, this pathway leads to loss of energy in the form of heat.
  • In some studies, antithyroid drugs, such as propylthiouracil (PTU), that reduce the basal metabolic rate of the liver have shown to be beneficial in the treatment of alcoholic hepatitis.
  1. Generation of free radicals and oxidative injury
  • Free radicals, superoxides and hydroperoxides, are generated as byproducts of ethanol metabolism via the microsomal and peroxisomal pathways.
  • In addition, acetaldehyde reacts with glutathione and depletes this key element of the hepatocytic defense against free radicals.
  • Other antioxidant defenses, including selenium, zinc, and vitamin E, are often reduced in individuals with alcoholism.
  • Peroxidation of membrane lipids accompanies alcoholic liver injury and may be involved in cell death and inflammation.
  1. Steatosis
  • Oxidation of ethanol requires conversion of NAD to the reduced form NADH.
  • Because NAD is required for the oxidation of fat, its depletion inhibits fatty acid oxidation, thus causing accumulation of fat within the hepatocytes (steatosis).
  • Some of the excess NADH may be reoxidized in the conversion of pyruvate to lactate.
  • Accumulation of fat in hepatocytes may occur within days of alcohol ingestion;
  • with abstinence from alcohol, the normal redox state is restored, the lipid is mobilized, and steatosis resolves.
  • Although steatosis has generally been considered a benign and reversible condition, rupture of lipid-laden hepatocytes may lead to focal inflammation, granuloma formation, and fibrosis, and it may contribute to progressive liver injury
  • Nonoxidative metabolism of ethanol may lead to the formation of fatty acid ethyl esters, which may also be implicated in the pathogenesis of alcohol-induced liver damage.
  1. Formation of acetaldehyde adducts
  • Acetaldehyde may be the principal mediator of alcoholic liver injury.
  • The deleterious effects of acetaldehyde include
    • impairment of the mitochondrial beta-oxidation of fatty acids,
    • formation of oxygen-derived free radicals,
    • depletion of mitochondrial glutathione.
  • In addition, acetaldehyde may bind covalently with several hepatic macromolecules, such as amines and thiols, in cell membranes, enzymes, and microtubules to form acetaldehyde adducts.
  • This binding may trigger an immune response through
    • formation of neoantigens,
    • impair function of intracellular transport through precipitation of intermediate filaments and other cytoskeletal elements,
    • stimulation of hepatic stellate cells to produce collagen.
  • ALDH is downregulated by long-term ethanol abuse, with resultant acetaldehyde accumulation.
  1. Role of the immune system
  • Active alcoholic hepatitis often persists for months after cessation of drinking.
  • Its severity may worsen during the first few weeks of abstinence.
  • This observation suggests that an immunologic mechanism may be responsible for perpetuation of the injury.
  • levels of serum immunoglobulins, especially the immunoglobulin A (IgA) class, are increased in persons with alcoholic hepatitis.
  • Antibodies directed against acetaldehyde-modified cytoskeletal proteins can be demonstrated in some individuals.
  • Autoantibodies, including antinuclear and anti–single-stranded or anti–double-stranded DNA antibodies, have also been detected in some patients with alcoholic liver disease.
  • B and T lymphocytes are noted in the portal and periportal areas, and natural killer lymphocytes are noted around hyalin-containing hepatocytes.
  • Peripheral lymphocyte counts are decreased with an associated increase in the ratio of helper cells to suppressor cells, signifying that lymphocytes are involved in a cell-mediated inflammatory process.
  • Lymphocyte activation upon exposure to liver extracts has been demonstrated in patients with alcoholic hepatitis.
  • Immunosuppressive therapy with glucocorticoids appears to improve survival and accelerate recovery in patients with severe alcoholic hepatitis.
  1. Cytokines
  • Tumor necrosis factor-alpha (TNF-alpha) can induce programmed cellular death (apoptosis) in liver cells. (Marra and Tacke 2014)
  • Several studies have demonstrated extremely high levels of TNF and several TNF-inducible cytokines, such as interleukin (IL)–1, IL-6, and IL-8, in the sera of patients with alcoholic hepatitis. (Leake 2014)
  • Inflammatory cytokines (TNF, IL-1, IL-8) and hepatic acute-phase cytokines (IL-6) have been postulated to play a significant role in modulating certain metabolic complications in alcoholic hepatitis, and they are probably instrumental in the liver injury of alcoholic hepatitis and cirrhosis
  1. Role of concomitant viral disease
  • Alcohol consumption may exacerbate injury caused by other pathogenic factors, including hepatitis viruses.
  • Extensive epidemiologic studies suggest that the risk of cirrhosis in patients with chronic hepatitis C infection is greatly exacerbated by heavy alcohol ingestion.
  • Possible mechanisms include the impairment of immune-mediated viral killing or enhanced virus gene expression due to the interaction of alcohol and hepatitis C virus.


Questions to ask patients with suspected alcoholic hepatitis

  1. When did you first start to drink alcohol?
  2. How many days per week do you usually drink?
  • How many years have you been drinking on a regular or daily basis?
  1. How many times have you been arrested for driving under the
  2. influence of alcohol?
  3. How many times have you been arrested for public intoxication?
  • What type of alcohol do you usually drink? Beer? Wine? Hard liquor?
  • How many drinks of each type of alcohol do you drink on an average
  1. day?
  2. Do you usually drink at home? Bars?
  3. Have you been through an alcohol rehabilitation program? What typeinpatient
  • or outpatient? How many times?
  • Have there been prolonged times when you drank no alcohol?
  • When was your last drink?


  • patients with AH have been drinking heavily for years and then report a dramatic increase in the amount of alcohol intake, usually relating to a major life stressor, such as death of a parent, loss of a job, divorce etc
  • patients have often stopped drinking alcohol days to weeks prior to presentation due to
    • Malaise,
    • Poor appetite,
    • The realization that their drinking finally“caught up” with them.
  • Most commonly patients present with nonspecific complaints such as
    • Anorexia (27-77%)
    • Nausea and vomiting (34-55%)
    • Abdominal pain (27-46%)
    • Weight loss (29-43%)


  • Physical Examination Findings
    • Hepatomegaly (71-81%)
    • Ascites (35%)
    • Encephalopathy (from asterixis to coma) (18-23%)
    • Gastrointestinal bleeding requiring transfusion (23%)
    • Jaundice (37-100%)
    • Malnutrition (56-90%)
    • Hepatic bruit


Laboratory findings in AH are often nonspecific, but can on occasion provide clues to the diagnosis. These include

Liver Function Test

  • Mild to moderately elevated transaminases,
  • Ast: alt ratio above 1.5 with
  • Ast greater than 45 u/l but < 300 u/l.
  • However, an unusual variant of AH, known as alcoholic foamy degeneration, can lead to an AST as high as 730 U/L.
  • A serum bilirubin >2 mg/dl is often required to make a diagnosis,
  • Alkaline phosphatase (ALP) level elevations are typically mild in persons with alcoholic hepatitis.
  • The gamma-glutamyl transpeptidase (GGT) level is elevated markedly by alcohol use. (Although a normal value helps to exclude alcohol as a cause of liver disease, an elevated level is of no value in distinguishing between simple alcoholism and alcoholic hepatitis.)
  • Total blood cholesterol levels < 100 mg/dl can predict poor outcome; the lower the cholesterol, the worse the prognosis.

CBC Count

  • A complete blood cell (CBC) count commonly reveals some degree of neutrophilic leukocytosis with bandemia.
  • Usually, this is moderate; however, rarely, it is severe enough to provide a leukemoid picture.
  • Moderate anemia may be observed.
  • Alcohol use characteristically produces a moderate increase in MCV
  • Thrombocytosis may be observed as part of the inflammatory response;
  • Conversely, myelosuppression or portal hypertension with splenic sequestration may produce thrombocytopenia.

Screening Blood Tests

  • Screening blood tests to exclude other conditions (appropriate in any patient with alcoholic hepatitis) may include the following:
    • Hepatitis B surface antigen (hbsag) detects hepatitis B
    • Anti–hepatitis C virus by enzyme-linked immunosorbent assay (ELISA) detects hepatitis C
    • Ferritin and transferrin saturation detect hemochromatosis
    • Marked elevation of aminotransferase levels should raise concern for viral hepatitis or drug hepatotoxicity; in particular, people who are alcoholics may develop severe liver necrosis from standard therapeutic doses of acetaminophen
    • Alpha-fetoprotein (AFP) levels – Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma (HCC)
    • Alkaline phosphatase (ALP) Jaundice with fever can be caused by gallstones producing cholangitis

Liver Biopsy

  • Liver biopsy is not always required in the evaluation of alcoholic hepatitis,
  • but it may be useful in establishing the diagnosis, in determining the presence or absence of cirrhosis, and in excluding other causes of liver disease.
  • The risk of performing the biopsy should be weighed against the risk associated with the probable course of therapy, or the possible risk of an investigational treatment.
  • Percutaneous liver biopsy – should be avoided in the presence of severe thrombocytopenia or coagulopathy because of the risk of serious (possibly fatal) hemorrhage.
  • Transjugular liver biopsy – the risk of hemorrhage should be reduced. It can determine the transhepatic venous pressure gradient.
  • In alcoholic hepatitis, injury is characteristically most prominent in centrilobular (perivenular) areas (zone 3 of Rappaport).
  • Hepatocytes exhibit ballooning with necrosis.
  • Focal accumulation of polymorphonuclear leukocytes is noted in areas of injury.
  • Lymphocytes may also be present, especially in portal tracts.
  • Ropy eosinophilic hyaline inclusions- Mallory bodies may be observed in the perinuclear cytoplasm.
  • With electron microscopy, Mallory bodies may be observed to be composed of fibril clumps that histochemically are identifiable as intermediate filaments.
  • Mallory bodies are characteristic of alcoholic hepatitis, but they are not always present in this disease, and, occasionally, they can be observed in a variety of other disorders.
  • Macrovesicular steatosis, perivenular fibrosis, and frank cirrhosis commonly coexist with alcoholic hepatitis.


  • provides a good evaluation of the liver and other viscera, and it permits guided liver biopsy.
  • the liver appears enlarged and diffusely hyperechoic.
  • Features suggestive of coexistent portal hypertension and/or cirrhosis include the presence of varices, splenomegaly, and ascites.
  • helpful in excluding gallstones, bile duct obstruction, and hepatic or biliary neoplasms.
  • if stones are found or fever persists, cholangiography may be necessary.
  • Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma, which can be tested for by ultrasonography, computed tomography [CT] scanning, magnetic resonance imaging [MRI]) of the liver.



  • Cessation of alcohol consumption is the single most important treatment; without this all other therapies are of limited value.
  • Abstinence is even effective at preventing progression of liver disease and death when cirrhosis is present.
  • Life-long abstinence is the best advice and is essential for those with more severe liver disease.
  • Treatment for complications of cirrhosis, such as variceal bleeding, encephalopathy and ascites, may also be needed. (Raff and Singal 2014)


  • Good nutrition is very important and enteral feeding via a fine-bore nasogastric tube may be needed in severely ill patients. (Koretz 2014)


  • Patients with pure severe AH in the absence of cirrhosishave relatively little problem with ascites.
  • They eat so little that they do not take in enough sodium to retain much fluid.
  • Maintenance intravenous fluids should be avoided to minimize fluid retention.
  • When cirrhosis is also present, they may have more problematic fluid retention. In this case, if blood urea nitrogen and creatinine are normal, spironolactone can be given.
  • This drug will increase urinary excretion of sodium and water, increase serum potassium, and decrease the need for potassium supplementation.
  • Once serum potassium is normal without supplementation, oral furosemide can be added, if needed.
  • If azotemia occurs, diuretics should be stopped and the patient should be evaluated for hepatorenal syndrome. (Israelsen, Gluud et al. 2014)
  • The first step is to give 1 g of 25% albumin/kg body weight (100 g maximum) intravenously daily for 2 d and to monitor creatinine.
  • If creatinine improves with albumin, the azotemia is probably diuretic-induced. If creatinine continues to rise, hepatorenal syndrome is probably present, as this commonly occurs in severe AH.


  • patients with pure severe AH in the absence of cirrhosis have relatively little problem with upper gut hemorrhage.
  • The relatively short duration of AH usually does not lead to formation of varices that are large enough to bleed.
  • However, patients with underlying cirrhosis can bleed from esophageal varices.
  • Urgent endoscopy with banding of varices is warranted when this occurs.
  • Patients with severe AH are very intolerant of hypotension and seldom survive shock superimposed on AH.(Li, Liu et al. 2013)


  • In severe alcoholic hepatitis corticosteroids improve survival at 28 days from 65% to 85% Sepsis is the main side-effect of steroids, and existing sepsis and variceal haemorrhage are the main contraindication to their use.
  • If the bilirubin has not fallen 7 days after starting steroids, they are unlikely to reduce mortality and should be stopped


  • In severe alcoholic hepatitis, oral pentoxifylline reduces inpatient mortality, particularly from hepatorenal failure, from 46% to 25% (Joshi, Manori et al. 2013)
  • Pentoxifylline, which has a weak anti-TNF action. It appears to reduce the incidence of hepatorenal failure and its use is not complicated by sepsis
  • Baclofen has recently been evaluated in terms of safety and efficacy in the setting of alcoholic cirrhosis.
  • Baclofen significantly reduced alcohol cravings and significantly lengthened time to relapse with no significant adverse effects noted after 12 wk of continuous use in a well run randomized, controlled trial
  • Discharge is considered as the bilirubi level approaches 10 mg/dL, and the clinician can use this to help plan initiation of baclofen


MADDREY’S SCORE(Forrest 2014)

  • Maddrey’s score, which enables the clinician to assess prognosis in alcoholic hepatitis
  • PT = prothrombin time. Serum bilirubin in μmol/l is divided by 17 to convert to mg/dl):

The Maddrey discriminant function (DF) = [4.6 × (prothrombin time (PT)  – control PT) + serum bilirubin (mg/dL)]

  • A cutoff value of 32 is used to identify patients with a mortality rate above 50% without pharmacologic therapy.


  • MELD uses the patient’s values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. It is calculated according to the following formula

MELD = 3.78×ln[serum bilirubin (mg/dL)] + 11.2×ln[INR] + 9.57×ln[serum creatinine (mg/dL)] + 6.43×aetiology(0: cholestatic or alcoholic, 1- otherwise)

  • If the patient has been dialyzed twice within the last 7 days, then the value for serum creatinine used should be 4.0
  • Any value less than one is given a value of 1 (i.e. if bilirubin is 0.8, a value of 1.0 is used)
  • In interpreting the MELD Score in hospitalized patients, the 3 month mortality is:
    • 40 or more — 71.3% mortality
    • 30–39 — 52.6% mortality
    • 20–29 — 19.6% mortality
    • 10–19 — 6.0% mortality
    • <9 — 1.9% mortality


  • used to assess the prognosis of chronic liver disease
Measure 1 point 2 points 3 points
Total bilirubin, μmol/l (mg/dl) <34 (<2) 34-50 (2-3) >50 (>3)
Serum albumin, g/dl >3.5 2.8-3.5 <2.8
PT INR <1.7 1.71-2.30 > 2.30
Ascites None Mild Moderate to Severe
Hepatic encephalopathy None Grade I-II (or suppressed with medication) Grade III-IV (or refractory)
Points Class One year survival Two year survival
5-6 A 100% 85%
7-9 B 81% 57%
10-15 C 45% 35%


Bruguera, M. (2014). “[Liver diseases in the elderly.].” Gastroenterol Hepatol.

Liver diseases in the elderly have aroused less interest than diseases of other organs, since the liver plays a limited role in aging. There are no specific liver diseases of old age, but age-related anatomical and functional modifications of the liver cause changes in the frequency and clinical behavior of some liver diseases compared with those in younger patients. This review discusses the most important features of liver function in the healthy elderly population, as well as the features of the most prevalent liver diseases in this age group, especially the diagnostic approach to the most common liver problems in the elderly: asymptomatic elevation of serum transaminases and jaundice.

Forrest, E. (2014). “Letter: Prognostic scores in alcoholic hepatitis.” Aliment Pharmacol Ther 39(11): 1340-1341.

Israelsen, M. E., et al. (2014). “Acute kidney injury and hepatorenal syndrome in cirrhosis.” J Gastroenterol Hepatol.

Cirrhosis is the eighth leading cause of “years of lost life” in the US and accounts for approximately 1 to 2% of all deaths in Europe. Patients with cirrhosis have a high risk of developing acute kidney injury. The clinical characteristics of HRS are similar to prerenal uraemia, but the condition does not respond to volume expansion. HRS type 1 is rapidly progressive whereas HRS type 2 has a slower course often associated with refractory ascites. A number of factors can precipitate HRS such as infections, alcoholic hepatitis and bleeding. The monitoring, prevention, early detection and treatment of HRS are essential. This paper reviews the value of early evaluation of renal function based on two new sets of diagnostic criteria. Interventions for HRS type 1 include terlipressin combined with albumin. In HRS type 2 transjugular intrahepatic portosystemic shunt (TIPS) should be considered. For both types of HRS patients should be evaluated for liver transplantation.

Joshi, P., et al. (2013). “Pentoxifylline in severe alcoholic hepatitis: a prospective, randomised trial.” J Assoc Physicians India 61(5): 354.

Koretz, R. L. (2014). “The evidence for the use of nutritional support in liver disease.” Curr Opin Gastroenterol 30(2): 208-214.

PURPOSE OF REVIEW: Although there is a well established association between malnutrition and poorer clinical outcomes in patients with liver disease, that fact alone does not prove that improving the malnutrition will improve outcome. The best way to determine if nutritional interventions are effective is to compare them to untreated control groups in well designed and executed randomized clinical trials. RECENT FINDINGS: A recent systematic review assessed 37 trials that compared parenteral nutrition, enteral nutrition, or nutritional supplements to no nutritional therapy in patients with a variety of liver diseases. Since the publication of that review, an additional three trials have become available. Whereas all but one of the trials did have methodologic shortcomings that may have allowed the introduction of bias (which usually results in an overestimation of benefit), the trials failed to show much, if any, benefit. In fact, the single trial at low risk of bias found that more deaths occurred in the recipients of the supplements. SUMMARY: Although malnutrition may be associated with a poor outcome, the current best evidence indicates that the provision of adjunctive nutritional support (parenteral or enteral nutrition, or nutritional supplements) to patients with a variety of liver diseases (alcoholic hepatitis, cirrhosis, hepatocellular carcinoma, liver surgery, liver transplantation, obstructive jaundice, hepatitis C antiviral treatment) does not improve clinical outcomes.

Leake, I. (2014). “Alcoholic hepatitis: potential role of cytokine CCL20 in alcoholic hepatitis.” Nat Rev Gastroenterol Hepatol 11(2): 76.

Leslie, T., et al. (2014). “Survey of health status, nutrition and geography of food selection of chronic liver disease patients.” Ann Hepatol 13(5): 533-540.

Background. Obesity, a complex disease determined both by genetic and environmental factors, is strongly associated with NAFLD, and has been demonstrated to have a negative impact on HCV and other chronic liver diseases (CLD). Rationale. This study assessed the association between type and location of food sources and chronic liver disease (CLD) using Geographic Information Systems (GIS). Results. CLD patients completed surveys [267 subjects, 56.5% female, age 55.8 +/- 12.0, type of CLD: 36.5% hepatitis C (HCV), 19.9% hepatitis B (HBV), 19.9% non-alcoholic fatty liver disease (NAFLD); primary food source (PFS): 80.8% grocery store, secondary: 26.2% bulk food store, tertiary: 20.5% restaurants; fresh food (FF): 83%, pre-packaged (PP) 8.7%, already prepared (AP) 8.3%]. FF consumers had significantly fewer UEH servings/month (p = 0.030) and lived further away from convenience stores (1.69 vs. 0.95 km, p = 0.0001). Stepwise regression reveals the lowest FF consumers were NAFLD patients, subjects with UEH or restaurants and ethnic food stores as their PFS (R = 0.557, p = 0.0001). Eating already-packaged foods and utilizing restaurants or ethnic food stores as the PFS positively correlated with NAFLD (R = 0.546, p = 0.0001). Conclusions. Environmental food source measures, including type and density, should be included when examining areas hyper-saturated with a variety of food options. In hyper-saturated food environments, NAFLD patients consume more prepared food and less FF. CLD patients with UEH also eat significantly more prepared food and frequent restaurants and ethnic food stores as their PFS.

Li, N., et al. (2013). “[A retrospective analysis of ectopic varices in gastrointestinal tract diagnosed by endoscopy].” Zhonghua Nei Ke Za Zhi 52(11): 936-939.

OBJECTIVE: To understand the incidence, causes, clinical manifestations and treatment of ectopic varices (EV) in gastrointestinal (GI) tract. METHODS: GI endoscopic examinations were carried out in 99 783 patients from January 2004 to October 2012 in General Hospital of PLA. Sixty-four cases of ectopic varices in GI tract were discovered. The clinical manifestations of EV patients and treatment were analyzed retrospectively. The literatures of EV were reviewed. RESULTS: The prevalence of EV in GI was 0.06% (64/99 783) in all patients undergoing endoscopic examinations, including 5 in the gastric antrum, 37 in the duodenum, 2 in the colon, 17 in the rectum, 1 in terminal ileum as well as whole colorectum, and 2 in the anastomotic stomas. The causes of EV included portal hypertension with cirrhosis in 52 cases (42 of hepatitis as dominant, 5 of alcoholic, 3 of biliary). Twenty-five cases had past history of endoscopic sclerotherapy, tissue adhesive injection or band ligation.Extrahepatic portal vein obstruction was seen in 4 cases (1 with pancreatic cancer, gastric cardia after surgery, pancreatic cancer after surgery, small intestine after partial hepatectomy respectively) and 8 cases uncertain. Nine cases accepted endoscopic tissue adhesive injection (no post-operative hemorrhage occurred in 9 cases and EV disappeared in 3 cases). Endoscopic band ligation was performed only for one patient. CONCLUSIONS: EV in GI tract is a rare condition, which occurs commonly in duodenum, colon, and rectum. Portal hypertension is the most common cause. Gastrointestinal hemorrhage is the main clinical manifestation. EV should be considered in GI bleeding, with gastroesophageal varices hemorrhage excluded. Endoscopic adhesive injection is an effective way to treat EV.

Marra, F. and F. Tacke (2014). “Roles for Chemokines in Liver Disease.” Gastroenterology 147(3): 577-594 e571.

Sustained hepatic inflammation is an important factor in progression of chronic liver diseases, including hepatitis C or non-alcoholic steatohepatitis. Liver inflammation is regulated by chemokines, which regulate the migration and activities of hepatocytes, Kupffer cells, hepatic stellate cells, endothelial cells, and circulating immune cells. However, the effects of the different chemokines and their receptors vary during pathogenesis of different liver diseases. During development of chronic viral hepatitis, CCL5 and CXCL10 regulate the cytopathic versus antiviral immune responses of T cells and natural killer cells. During development of nonalcoholic steatohepatitis, CCL2 and its receptor are up-regulated in the liver, where they promote macrophage accumulation, inflammation, fibrosis, and steatosis, as well as in adipose tissue. CCL2 signaling thereby links hepatic and systemic inflammation related to metabolic disorders and insulin resistance. Several chemokine signaling pathways also promote hepatic fibrosis. Recent studies have shown that other chemokines and immune cells have anti-inflammatory and antifibrotic activities. Chemokines and their receptors can also contribute to the pathogenesis of hepatocellular carcinoma, promoting proliferation of cancer cells, the inflammatory microenvironment of the tumor, evasion of the immune response, and angiogenesis. We review the roles of different chemokines in the pathogenesis of liver diseases and their potential use as biomarkers or therapeutic targets.

Raff, E. and A. K. Singal (2014). “Optimal management of alcoholic hepatitis.” Minerva Gastroenterol Dietol 60(1): 25-38.

Alcoholic hepatitis, a clinical syndrome among people with chronic and active alcohol abuse presents with with jaundice and liver failure with or without hepatic encephalopathy. In patients with severe episode, this condition has a potential for 40-50% mortality within a month of presentation. Corticosteroids and pentoxifylline, only available current treatment options provide only about 50% survival benefit. Response to corticosteroids can only be assessed at 1 week of initiation of these drugs using Lille score or documentation of improvement in bilirubin levels. Requirement of minimum 6 months abstinence for liver transplantation cannot be met for alcoholic hepatitis patients who fail to respond to steroids. Emerging data on the benefit of liver transplantation for select patients with first episode of severe AH with non-response to steroids are encouraging. There remains an unmet need for studies assessing newer therapeutic targets and drugs and for optimizing the currently available treatment options. In this regard, decision to promote clinical and translational research by the National Institute of Alcohol Abuse and Alcoholism will be helpful in improving survival of patients with alcoholic hepatitis.

Stimac, D., et al. (2013). “[Hepatitis C: who should be treated?].” Acta Med Croatica 67(4): 325-328.

Therapy is strongly recommended in patients with acute infection, patients with elevated ALT levels, patients with normal ALT level and F > or = 2 METAVIR score, in genotype 1 nonresponders and relapsers to antiviral therapy with triple therapy (pegylated interferon, ribavirin, bocaprevir or telaprevir), in patients with compensated cirrhosis and patients on hemodialysis. It is possible to treat patients with HBV and HIV co-infection, patients with severe HCV extrahepatic manifestations and patients with transplanted liver. Drug users and alcoholics can be treated after 6-month abstinence, but also with supportive therapy. This therapy is not recommended in patients with fulminant hepatitis, patients with persistent normal ALT levels and without fibrosis, in kidney transplant recipients and in pregnant women.



Kwashiorkor is a form of malnutrition. It occurs when you don’t have enough protein in your diet. It is the most common nutritional disorder in developing countries. Children with Kwashiorkor may not grow or develop properly. It may be life threatening if not treated .


It is caused by not having enough protein in your diet. It is common in children in Africa and Central America. It is also common in developing countries where there is

  • famine
  • limited food supply
  • low levels of eduction

It usually occurs during political unrest, natural disasters or drought. Thee conditions may lead to lack of food which in turn leads to malnutrition.

Kwashiorkor is very rare in the united states. If it does occur, it is usually a sign  of child abuse or severe neglect.


Symptoms of kwashiorkor includes the following :

  • large belly that sticks out
  • failure to grow or gain eight
  • fatigue
  • changes in skin pigment
  • diarrhea
  • hair changes
  • irritability
  • flaky rash
  • loss of muscle mass
  • swelling
  • lethargy
  • shock which occurs in the latter stages of kwashiorkor


A physical exam may reveal an enlarged liver and well as edema (swelling). Your doctor may also order the following tests.


Kwashiorkor can be corrected by including more protein and calories in your diet. This is helpful if treatment is started early. You will be given more calories in the form of carbohydrates, sugar and fats to give you energy. You will then be given protein rich foods. Giving of calories is done slowly because your body needs to adjust since you have been without food for a while.

Your doctor may also recommend vitamin and mineral supplements.


Possible complication of kwashiorkor includes

  • coma
  • permanent and physical disability
  • shock


You can prevent kwashiorkor by eating enough carbohydrates and protein rich foods. These  include fat (at least 10 percent of total calories) and protein (12 percent of total calories).


What is kwashiorkor. Healthline Networks.http://www.healthline.com/health/kwashiorkor#Causes.

Kwashiorkor. NHS choices.http://www.nhs.uk/conditions/kwashiorkor/Pages/Introduction.aspx

The American Heritage® Stedman’s Medical Dictionary. Retrieved April 2014 from Dictionary.com website.http://dictionary.reference.com.

The Difference Between Men And Women


Let’s say a guy named Fred is attracted to a woman named Martha. He asks her out to a movie; she accepts; they have a pretty good time. A few nights later he asks her out to dinner, and again they enjoy themselves. They continue to see each other regularly, and after a while neither one of them is seeing anybody else.

And then, one evening when they’re driving home, a thought occurs to Martha, and, without really thinking, she says it aloud: “Do you realize that, as of tonight, we’ve been seeing each other for exactly six months?”

And then, there is silence in the car.

To Martha, it seems like a very loud silence. She thinks to herself: I wonder if it bothers him that I said that. Maybe he’s been feeling confined by our relationship; maybe he thinks I’m trying to push him into some kind of obligation that he doesn’t want, or isn’t sure of.

And Fred is thinking: Gosh. Six months.

And Martha is thinking: But, hey, I’m not so sure I want this kind of relationship either. Sometimes I wish I had a little more space, so I’d have time to think about whether I really want us to keep going the way we are, moving steadily towards, I mean, where are we going? Are we just going to keep seeing each other at this level of intimacy? Are we heading toward marriage? Toward children? Toward a lifetime together? Am I ready for that level of commitment? Do I really even know this person?

And Fred is thinking: …so that means it was…let’s see…February when we started going out, which was right after I had the car at the dealer’s, which means…lemme check the odometer…Whoa! I am way overdue for an oil change here.

And Martha is thinking: He’s upset. I can see it on his face. Maybe I’m reading this completely wrong. Maybe he wants more from our relationship, more intimacy, more commitment; maybe he has sensed – even before I sensed it – that I was feeling some reservations. Yes, I bet that’s it. That’s why he’s so reluctant to say anything about his own feelings. He’s afraid of being rejected.

And Fred is thinking: And I’m gonna have them look at the transmission again. I don’t care what those morons say, it’s still not shifting right. And they better not try to blame it on the cold weather this time. What cold weather? It’s 87 degrees out, and this thing is shifting like a garbage truck, and I paid those incompetent thieves $600.

And Martha is thinking: He’s angry. And I don’t blame him. I’d be angry, too. I feel so guilty, putting him through this, but I can’t help the way I feel. I’m just not sure.

And Fred is thinking: They’ll probably say it’s only a 90-day warranty…scumballs.

And Martha is thinking: Maybe I’m just too idealistic, waiting for a knight to come riding up on his white horse, when I’m sitting right next to a perfectly good person, a person I enjoy being with, a person I truly do care about, a person who seems to truly care about me. A person who is in pain because of my self-centered, schoolgirl romantic fantasy.

And Fred is thinking: Warranty? They want a warranty? I’ll give them a warranty. I’ll take their warranty and stick it right up their…

“Fred,” Martha says aloud.

“What?” says Fred, startled.

“Please don’t torture yourself like this,” she says, her eyes beginning to brim with tears. “Maybe I should never have…oh dear, I feel so…”(She breaks down, sobbing.)

“What?” says Fred.

“I’m such a fool,” Martha sobs. “I mean, I know there’s no knight. I really know that. It’s silly. There’s no knight, and there’s no horse.”

“There’s no horse?” says Fred.

“You think I’m a fool, don’t you?” Martha says.

“No!” says Fred, glad to finally know the correct answer.

“It’s just that…it’s that I…I need some time,” Martha says.

(There is a 15-second pause while Fred, thinking as fast as he can, tries to come up with a safe response. Finally he comes up with one that he thinks might work.)

“Yes,” he says. (Martha, deeply moved, touches his hand.)

“Oh, Fred, do you really feel that way?” she says.

“What way?” says Fred.

“That way about time,” says Martha.

“Oh,” says Fred. “Yes.” (Martha turns to face him and gazes deeply into his eyes, causing him to become very nervous about what she might say next, especially if it involves a horse. At last she speaks.)

“Thank you, Fred,” she says.

“Thank you,” says Fred.

Then he takes her home, and she lies on her bed, a conflicted, tortured soul, and weeps until dawn, whereas when Fred gets back to his place, he opens a bag of Doritos, turns on the TV, and immediately becomes deeply involved in a rerun of a college basketball game between two South Dakota junior colleges that he has never heard of. A tiny voice in the far recesses of his mind tells him that something major was going on back there in the car, but he is pretty sure there is no way he would ever understand what, and so he figures it’s better if he doesn’t think about it.

The next day Martha will call her closest friend, or perhaps two of them, and they will talk about this situation for six straight hours. In painstaking detail, they will analyze everything she said and everything he said, going over it time and time again, exploring every word, expression, and gesture for nuances of meaning, considering every possible ramification.

They will continue to discuss this subject, off and on, for weeks, maybe months, never reaching any definite conclusions, but never getting bored with it either.

Meanwhile, Fred, while playing racquetball one day with a mutual friend of his and Martha’s, will pause just before serving, frown, and say: “Norm, did Martha ever own a horse?”

And that’s the difference between men and women.


Adapted from withalittlehelp

Nonalcoholic Fatty Liver Disease




Nonalcoholic fatty liver disease is fat accumulation in the liver of people who don’t drink or drink little alcohol. This disease is common and may cause no complications . A more serious form of nonalcoholic fatty liver disease is called nonalcoholic steatohepatitis (NASH). This can cause inflammation and scarring of liver and eventual death of liver tissue.


The exact cause of nonalcoholic fatty liver disease in not clear but it occurs as a result of failure of the liver to breakdown fat resulting in its accumulation  in the liver tissue.


Certain factors and conditions may increase your risk of getting nonalcoholic fatty liver disease. These include :

  • rapid weight loss
  • obesity
  • Wilson’s disease
  • certain medications
  • high levels of cholesterol and triglycerides
  • malnutrition
  • viral hepatitis
  • inherited or autoimmune liver disease
  • metabolic syndrome
  • type 2 diabetes


This disease is mostly asymptomatic especially in it’s early stages. As disease progressed however it may exhibit symptoms such as

  • weight loss
  • fatigue
  • nausea
  • weakness
  • pain in the upper right abdomen
  • impaired judgement
  • enlarged liver


Nonalcoholic fatty liver disease is usually diagnosed during a routine medical exam. Doctor may also suspect you have it  after asking for your medical history and doing a physical exam. Doctor may then perform these test to conform the disease.

Blood test : Liver function test is done to evaluate liver enzymes and help with diagnosis.

Imaging tests : Imaging tests such as abdominal ultrasound, computerized tomography (CT) scan and magnetic resonance imaging (MRI) are used to diagnose fatty liver disease.

Liver biopsy : This confirmatory test involves taking  a sample of liver tissue  to the lab  to look for signs of inflammation and scarring.


There is no specific treatment for Nonalcoholic fatty liver disease. Treatment  means taking care of underlying medical conditions such as diabetes and obesity . These include losing weight if you are obese, managing blood sugar level if you have diabetes and changing medications if it is the cause.


Takes these steps to prevent this disease.

Maintain a healthy weight.

Eat healthy such as including more fruits and vegetables in your diet.

Take medication for disease that can cause fatty liver disease such as diabetes and high cholesterol. You can also reduce your cholesterol using home remedies.


by Kemboi Kibet

Cirrhosis is a liver disease which involves irreversible scarring of the liver. Some of the common causes of cirrhosis includes alcohol abuse, hepatitis B and hepatitis C. Early treatment of cirrhosis can limit further damage to the liver. This disease can be life threatening.


This disease is caused by long-term liver damage as a result of liver diseases and other conditions. Diseases and conditions that can cause cirrhosis includes the following

alcohol abuse
chronic viral hepatitis
bile duct disease such as biliary atresia
cystic fibrosis
genetic diseases such as glycogen storage diseases, Alpha-1 antitrypsin deficiency, autoimmune hepatitis and Wilson’s disease
accumulation of fat in the liver


Cirrhosis can be asymptomatic but when symptoms do appear, they usually include the following

itching skin
loss of appetite
easy bruising and bleeding
weight loss
Fluid build up and painful swelling of the legs (edema) and abdomen (ascites)
abdominal pain


To diagnose cirrhosis, your doctor will do a physical exam. He may also ask you about your medical history. Other tests that will be done to confirm this diagnosis include :

Liver function test : This blood test is done to checked for excess bilirubin and certain enzymes that may indicate liver damage.

Imaging tests : These include MRI, CT scan and ultrasound to check for liver damage.

Biopsy :A sample liver tissue is taken and examined for the cause and severity of liver damage.


Treatment of cirrhosis depends on the cause and extent of damage to the liver. The goal of treatment is to prevent further damage and avoid complications.It is also important to treat any underlying cause of the disease such as losing weight, stop drinking and medications of hepatitis. Any associated complications will also be treated. In advanced stages when the liver loses it’s function,liver transplant is necessary.


Stop drinking alcohol.
Maintain a healthy weight
Limit salt intake to reduce fluid buildup
Avoid raw shellfish
Get vaccinated for hepatitis A and B, influenza, and pneumonia.
Ask your doctor before using any over the counter medications, vitamins or supplement.
Practice safe sex to avoid any infections.
Do not share needles, razors, toothbrushes or other personal items with others

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