When doctors are too busy to care...

I'm not much of a worked up person when it comes to others feelings. I used to say, I just don’t care about what my friends say or think about me as long as they don’t say it right on my face. But even I happen to get emotional sometimes when I see how neglectful we can be.

I met this retired gentleman in the ward who came with right leg swelling about two months ago. Had been treated for filariasis in another hospital even when the blood film was negative and it turned to be a vain attempt. Fair enough. Let’s say the clinician made a "clinical" diagnosis and trial of treatment is just another way of "diagnosing" things, even though you wouldn’t like this kinda treatment on yourself.

He sought further medical attention in our centre (I mean the place where we go to study: P). His drs did the right thing considering other diagnoses and decided to investigate further. With extensive investigations it was found that he had cellulitis of right leg due to lyphatic obstruction, a right psoas abcess, and finally mycosis fungoides. Further investigations proves that he had "some kinda" malignancy going on with multiple lymphatic obstruction, satellite lesions in liver, kidney and pulmonary effusion as well. So let’s consider "it’s an advanced disease"- That is just excellent they managed to solve at least half of the mystery. Investigations are still going on to find the exact location of the disease.

I saw him again a month later; rarely do I get to talk to patients without a second tongue, so I was happy to see him again. Asked him how he is feeling, “want to climb a chair and jump off the building” he replied. I was taken aback by caustic remark. What happened? Is he terminal? Going through severe depression? He used to be such a nice gentleman, somebody must have broken him- I thought to myself.

Another friend of mine and I sat there at his bedside for an hour, not taking history, but just listening to him. He had lots of complaints about staffs at the hospital. Doctors, nurses, students,-anyone who walk in and out, basically.

“Yeah, he is a retired civil servant, what else do expect from old people like that” – you may think.

But let’s listen to what he had to say. “It’s been two months. They had been doing this and that, poking here and there. They don’t know where it is, what it is..made me eat medicine for Filaria, then say it’s not filarial, then say cancer, then say something else” I could see frustration on his face as he spoke with explosive tone and sometimes he paused for a deep breath- a sigh of frustration. We tried to explain to him the rationale of the persistent poking. How difficult it is sometimes to reach a definitive diagnosis when patients present with atypical presentations.

“I could accept that, but then why not say so, why do you have to be so ignorant of our feelings. We are not dead yet”.

Yep, he is right, this not a car which has a punctured tire that you take to a mechanic and point a finger to the tire-the mechanic would just fix it without saying a word. What if you took your car to the mechanic and you said it got a problem and the mechanic just started hammering the engine from sideways and didn’t tell you what he is doing? Would you be mad? Old man is not a car! He is a living being with feelings like howmuch we do.


The old man had more complaints.

“the nurses: they are not here to care for patients. They are too busy writing..Patient is sleeping..Patient is awake..Patient is not well today like other day” he elaborated on his statement.

“Sometimes I feel like doctors are just here to get salary. Only few are really concerned about me. They come in a gang..Like a group of flies..expose me and look at..and talk to themselves..write so many things. And then just go away. They tell me nothing.”

“ I asked them what is my problem, when can I go home, they said; have to talk to dr x (an old consultant), he is not around..look at my leg its getting worse, I cant even walk now, its so painful.. Sometimes I wonder what will happen to me if dr x is not here, he is the only one who actually care” – old man had a dry throat. But so much he had to say.

Finally he asked me “ what do you think? Am I just whining or do I really have a point- you are from IIUM, is that how they teach you to treat your patients” – Glad he expected something better from IIUM. I bragged about our “bio-psycho-socio-spiritual” model of management. But he knows that’s just theoretical crap and in reality nobody works that way.

“Sometimes I do wonder if we, people in health "care" profession are missing a heart. You may have the skill, knowledge and attitude but what if you don’t have an empathetic heart. what’s the use?”-I asked myself.

It’s understood that a busy HO or MO don’t get time to sit by the patient and talk about patients feelings-unless you are in psychiatry ward, of cause. But are we that busy for us not to even greet the dying old man when we see him and ask him how he is doing? Are we that preoccupied with commitments that we can’t even explain to him what we are doing and why we are doing it? I believe this has to change.

“ I want to help sick and those in pain, I want to make the old and dying person feel better” -You will surely hear this fancy answer when you ask anybody in medical school why do they want to be a doctor. But are we really doing it? Being busy is just not an excuse. Simply because you don’t want to be taken care by such a busy doctor when you are on the sick bed counting your last days.

"Crabbit Old Woman"

What do you see, what do you see?
Are you thinking, when you look at me-
A crabbit old woman, not very wise,
Uncertain of habit, with far-away eyes,
Who dribbles her food and makes no reply
When you say in a loud voice,
I do wish you'd try.
Who seems not to notice the things that you do
And forever is loosing a stocking or shoe.
Who, unresisting or not; lets you do as you will
With bathing and feeding the long day is fill.

Is that what you're thinking,
Is that what you see?
Then open your eyes,
nurse, you're looking at me.
I'll tell you who I am as I sit here so still!
As I rise at your bidding, as I eat at your will.

I'm a small child of 10 with a father and mother,
Brothers and sisters, who loved one another-
A young girl of 16 with wings on her feet,
Dreaming that soon now a lover she'll meet,
A bride soon at 20- my heart gives a leap,
Remembering the vows that I promised to keep.
At 25 now I have young of my own
Who need me to build a secure happy home;
A woman of 30, my young now grow fast,
Bound to each other with ties that should last;
At 40, my young sons have grown and are gone,
But my man's beside me to see I don't mourn;
At 50 once more babies play around my knee,
Again we know children, my loved one and me.

Dark days are upon me, my husband is dead,
I look at the future, I shudder with dread,
For my young are all rearing young of their own.
And I think of the years and the love that I've known;
I'm an old woman now and nature is cruel-
Tis her jest to make old age look like a fool.
The body is crumbled, grace and vigor depart,
There is now a stone where I once had a heart,

But inside this old carcass, a young girl still dwells,
And now and again my battered heart swells,
I remember the joy, I remember the pain,
And I'm loving and living life over again.
I think of the years all too few- gone too fast.
And accept the stark fact that nothing can last-
So open your eyes, nurse, open and see,
Not a crabbit old woman, look closer-
See Me.

(The following poem was among the possessions of an aged lady who died in the geriatric ward of a hospital.)

A Nurse's reply "To the Crabbit Old Woman"

What do we see, you ask, what do we see?
Yes, we are thinking when looking at thee!
We may seem to be hard when we hurry and fuss,
But there's many of you, and too few of us.

We would like far more time to sit by you and talk,
To bath you and feed you and help you to walk.
To hear of your lives and the things you have done;
Your childhood, your husband, your daughter, your son.

But time is against us, there's too much to do -Patients too many, and nurses too few.

We grieve when we see you so sad and alone,
With nobody near you, no friends of your own.
We feel all your pain, and know of your fear
That nobody cares now your end is so near.
But nurses are people with feelings as well,
And when we're together you'll often hear tell
Of the dearest old Gran in the very end bed,
And the lovely old Dad, and the things that he said,
We speak with compassion and love, and feel sad
When we think of your lives and the joy that you've had,
When the time has arrived for you to depart,
You leave us behind with an ache in our heart.
When you sleep the long sleep, no more worry or care,

There are other old people, and we must be there.
So please understand if we hurry and fuss -
There are many of you, And so few of us.

The origin of HIV and AIDS

For over twenty years it has been a cause of countless arguments, with everything from a promiscuous flight attendant to a suspect vaccine program being blamed. What is the truth?

The first recognized cases of AIDS occurred in the USA in the early 1980s. A number of gay men in New York and California suddenly began to develop rare opportunistic infections and cancers that seemed stubbornly resistant to any treatment. At this time, AIDS did not yet have a name, but it quickly became obvious that all the men were suffering from a common syndrome.

What type of virus is HIV?

HIV is a lentivirus which attacks the immune system. The name 'lentivirus' literally means 'slow virus' because they takes heck of a long time to manifest as a disease. They have been found in a number of different animals, including cats, sheep, horses and cattle. But the most interesting lentivirus in terms of its relation to HIV is the Simian Immunodeficiency Virus (SIV).

So did HIV come from Chimps?

It is now generally accepted that HIV is a descendant of a SIV because certain strains of SIVs bear a very close resemblance to HIV-1 and HIV-2.

HIV-2 for example corresponds to SIVsm, a strain of the SIV found in the sooty mangabey (White-collared monkey)-indigenous to western Africa. Other closest counterpart of HIV that had been identified was SIVcpz-found in chimpanzees.

Scientists now believe that chimpanzees were the source of HIV-1, and that the virus had at some point crossed species from chimps to humans. It was then concluded that all three 'groups' of HIV-1 - namely Group M, N and O came from the SIV found in this particular Chimp (P. t. troglodytes), and that each group represented a separate crossover 'event' from chimps to humans.

How could HIV have crossed species?

It has been known for a long time that certain viruses can pass between species. As animals ourselves, we are just as susceptible. There are various theories about how this 'zoonosis' took place, and how SIV became HIV in humans:

The 'Hunter' Theory

In this scenario, SIVcpz was transferred to humans as a result of chimps being killed and eaten or their blood getting into cuts or wounds on the hunter. Initially the body would have fought off SIV, with time it adapted itself within human host and became HIV-1. The fact that there were several different early strains of HIV, each with a slightly different genetic make-up, would support this theory as every time it passed from a chimpanzee to a man, it would have developed in a slightly different way within his body, and thus produced a slightly different strain.

The Oral Polio Vaccine (OPV) theory

Some other rather controversial theories have contended that HIV was transferred iatrogenically. One particularly well-publicized idea is that polio vaccines played a role in the transfer.

An oral polio vaccine called “Chat” was tested on about a million people in the Belgian Congo, Ruanda and Urundi in the late 1950s. This theory suggests that “chat” was grown in kidney cells taken from infected chimps. This would have resulted in the contamination of the vaccine with chimp's SIV, and a large number of people subsequently becoming infected with HIV-1.

People have contested saying that local chimps were not infected with a strain of SIVcpz that is closely linked to HIV. Furthermore, the oral administration of the vaccine would seem insufficient to cause infection in most people as virus needs to get directly into the bloodstream to cause infection.

Later, Wistar Institute in Philadelphia (one of the original manufacturers of the Chat vaccine) announced the vaccine was analyzed and no trace had been found of either HIV or chimpanzee SIV.

The Contaminated Needle Theory

Even though the use of disposable plastic syringes became common around the world in 1950s, some parts of Africa might not have done so. It is therefore likely that one single syringe would have been used to inject multiple patients without any sterilization in between. This would rapidly have transferred any viral particles from one person to another, allowing virus to mutate and replicate.

The Colonialism Theory

During the colonial rule Africans were forced into labour camps with poor sanitation, scare food supply and physical demands were extreme. Prostitution was widespread and workers would have been treated with poor health ethics including non sterile needles. These factors alone would have been sufficient to create poor health in anyone, so SIV could easily have infiltrated the labour force and taken advantage of their weakened immune systems to become HIV.

The Conspiracy Theory

A a significant number of African Americans believe HIV was manufactured as part of a biological warfare program, designed to wipe out large numbers of black and homosexual people. Many say this was done under the auspices of the US federal 'Special Cancer Virus Program' (SCVP), possibly with the help of the CIA. Spread through smallpox inoculation programme, or to gay men through Hepatitis B vaccine trials.

reference: http://www.avert.org/origin-aids-hiv.htm

Neurocutaneous syndromes- always a big worry.

Neurofibromatosis (mostly familial)

T1: requires 2 of following for the dx
1)6 or more Café-au-lait spots (>5mm in pre, >15mm in post puberty
2)Axillary/inguinal freckling
3)2 or more Lish nodules (may need Slit lamp)
4)2 or more Neurofibroma ( 1 plexiform neurofibroma)
5)A distinctive osseous lesion (phenoid dysplasia, or cortical thinning of long bones)
6)Optic gliomas
7)A first-degree relative with NF-1
Assoc: Scoliosis, kyphosis, pseudoarthrosis, Gliomas, Mental retardation, seizures, neurofibrosarcoma, hypertension

T2: 10% of all NF,diagnosis needs 1 of…

1)Bilateral acoustic neuromas
2)First deg relative with NF-2 and either unilateral acoustic neuroma or any two of the following: neurofibroma, meningioma, glioma, schwannoma, or juvenile posterior subcapsular lenticular opacities.
Assoc: CNS tumours

Tuberous Sclerosis (Autosomal Dominant)

Features:
1)infantile spasms (hypsarrhythmic EEG pattern)
2)Ash leaf spots/ Amelanotic Navi (Wood ultraviolet lamp)
3)Adenoma sebacium (rare b4 2yr)
4)Shagreen paches
5)Subungual or gingival fibroma
6)Café-au-lait spots
7)retinal pharcoma
Assoc: Mental Retradation, developmental delay, palpable kidney (PCKD), epilepsy, cardiac rhabdomyomata, calcified tubers in the periventricular area (CT)

Mc_Cune Albright Syndrome (non familial)

Aka Polyostotic fibrous dysplasia. Features are…
1)Precauceous puberty (3-4yr, f>m)
2)Café-au-lait spots
3)Fractures/skeletal asymmetry
4)Assoc: Multiple endocrinopathy ( adrenal hyperplasia, thyroid, parathyroid and Growth Hormone abnormalities)

Sturge-Weber Syndrome (sporadic)

Features are…
1)Port wine stain at maxillary/ophthalmic division of trigeminal nerve
2)Ipsilateral: Oxophthamos, colobomata, glaucoma, buphthalmos.
3)Contralateral hemiparesis
4)Homonymous hemianopia
5)Taleniectasia of conjunctiva
6)Dark red fundus (retinal detachment)
Assoc: Epilepsy, mental retardation, cranial calcification (CT)

Von Hippel-Lindau Disease (Autosomal Dominant)

Features include:
1)Cerebellar hemangioblastomas (increase ICP)
2)Retinal angiomata (vision is unaffected until retinal detachment occurs)
3)Hemangioblastoma of the spinal cord (abnormalities of proprioception and disturbances of gait and bladder dysfunction)
4)CT scan typically shows a cystic cerebellar lesion.
5)Cystic lesions of the kidneys, pancreas, liver, and epididymis as well as pheochromocytoma, ranal carcinoma.

Child with Fever and Rash- a confusing condition?

Fever plus rash is a common combination seen in children. Often comes in out breaks. Most of the time diagnosis is made on clinical grounds and treated accordingly. Therefore it is important to know the differentials for a child with this problem.

Measles

I=7-10d, fever, coryza, cough, conjunctivitis, catarrh, Koplik’s spot.
Rash: 4th day, behind the ear to face and trunk (red, maculopapular)
Cplx: pneumonia, Otitis media, Encephalitis
Ix: raise in measles antibody titre, Immunoflourescence of Nasopharyngeal aspirate
Tx: symptomatic fluid and PCM, no antibiotics unless complicated

Rubella

I= 10-21d, URTI, catarrh, cervical/suboccipital lymphadenopathy
Rash: erythematous, mainly on trunk
Cplx: Arthralgia, encephalitis (rare in childhood)
Ix: virus culture from stool/nose, rubella antibody titre

Mumps (no rash)

I=4-28d, parotitis (other glands rarely involved)
Cplx: meningitis, pancreatitis, orchitis
Ix: virus isolation from saliva, lymphocytosis, rise of Mumps antibody titre

Varicella (chicken pox)

I=10-21d, fever, rash (itchy): evolves from papules to vesicles, pulstures and scabes
Cplx: conjunctival lesion, encephalitis
Ix: electron microscopy of fluid from vesicles and virus culture, monoclonal antibody


Scarlet fever

I= 1-7d, (URTI) tonsillitis, rash (diffuse, erythematous, mainly on trunk 24-48hr after onset, papular, erythematous on trunk and limbs-looks red, face spared, blances, 3-4 d later rash fade with desquamation on hands, feet.)
Cplx: otitis media, Rh fever, Acute Nephritis
Ix: Throat swab for grp A haemolytic streptococcus, raised ASOT
Tx: penicillin V (250 mg/dose bid–tid PO) for 10 days, or benzathine penicillin G (600,000 IU for ≤60 lb, 1.2 million IU for >60 lb, IM) for compliance. Erythromycin (erythromycin estolate 20–40 mg/kg/24 hr divided bid–qid PO, or erythromycin ethylsuccinate 40 mg/kg/ 24 hr divided bid–qid PO) for 10 days

Other Differential Diagnoses to be considered:

Kawasaki disease (fever, rash, red swollen moth/hand/foot)

Meningococcemia (N. Meningitidis)

Roseola infentum (herpes 6&7)

Erythema infectiosum (parvo virus)

Dengue fever (fever, rash, bleeding, joint pain)

Hand foot mouth disease (coxsacie A)

Ricketsial diseases: Rocky Mountain spotted fever, Mediterranean spotted fever (eschar), scrub typhus (eschar) Dx by immunohistologic demonstration of rickettsiae on skin biopsy. Dec plt and wbc

I(incubation peiod), Ix (investigations), Tx (treatment), Dx (diagnosis) Cplx (complications)

Lassa fever - African version of Leptospirosis?

An acute viral illness that is endemic in parts of West Africa (Guinea, Liberia, Sierra Leone and Nigeria). Caused by, Lassa Virus (family Arenaviridae), a single-stranded RNA virus and is zoonotic. The reservoir of Lassa virus is a rodent known as the "multimammate rat" of the genus Mastomys. Rodents shed the virus in urine and droppings.

Therefore, the virus can be transmitted through direct contact with these materials, through touching objects or eating food contaminated with these materials, or through cuts or sores. Also spread through person-to-person by contact with virus in the blood, tissue, secretions, or excretions of an individual infected with the Lassa virus.

In some areas of Sierra Leone and Liberia, it is known that 10%-16% of people admitted to hospitals have Lassa fever.

Signs and symptoms of Lassa fever typically occur 1-3 weeks after the patient comes into contact with the virus. These include fever, retrosternal pain, sore throat, back pain, cough, abdominal pain, vomiting, diarrhea, conjunctivitis, facial swelling, proteinuria, and mucosal bleeding. Neurological problems have also been described, including hearing loss, tremors, and encephalitis.

Diagnosis is by detecting IgM and IgG antibodies as well as Lassa antigen by ELISA. The virus itself may be cultured in 7 to 10 days. Immunohistochemistry performed on tissue specimens can be used to make a postmortem diagnosis. The virus can also be detected by RT-PCR

Ribavirin has been used with success in Lassa fever patients. (most effective in the early course of the illness). The most common complication of Lassa fever is deafness- and in many cases hearing loss is permanent.

Approximately 15%-20% of patients die, can be as high as 50% in sever cases. However, overall only about 1% of infections with Lassa virus result in death. The death rates are particularly high for women in the third trimester of pregnancy, and for fetuses, about 95% of which die in the uterus of infected pregnant mothers.

Reff: http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/lassaf.htm