HEAD INJURY: EXTRADURAL HEMATOMA

Extradural hematoma forms about 2% of all head injuries in England. There are no figures for Nigeria.
Mechanism of trauma
This is usually due to motor traffic accidents. Incidence may have dropped as a result of the uses of seat belts and air bags. There are two types.
1 Blunt or closed injuries : commonly
• Whiplash injury
• Crushing injury
2 Penetrating injuries , due to bullet or missile. Commoner in war situations
Types of injury
1 Scalp laceration, abrasion, or haematoma ( subcutaneous, subaponeurotic or subperiostea)
2 Skull fractures ( linear, basal or depressed. Always exclude csf leakages through the ear or nose
3 Brain injury localized as in contusion and laceration or generalized as in concussion
Concussion
Is a transient loss of function of transmission of physiological signals due to axonal damages as in a diffuse brain trauma. This is demonstrable through ct scan and mri. Repeated knocks on the head of boxers lead to permanent damage.
Extradural hematoma
This is a space occupying hematoma between the skull and the dura. It is due to the laceration of the middle meningeal vessels, usually located in the temporal region. Occasionally if bleeding is from the diploic and venous sinuses , then it is located in the frontal and occipital areas.
Clinical features
Injury is from mild to severe , usually blunt in type.it is commonly associated with skull fractures. This may be absent in children.
Features are initial loss of consciousness that is followed by a temporary recovery of consciousness . this phase is called the lucid phase and is ver significant clinically. There are drowsiness , headaches that is sometimes excruciating , ipsilateral dilatation of the pupils, rising of blood pressure, slowing of pulse rate and respiration. Contralateral signs of hemiparesis , hyperreflexia, increased muscle tone, ankle clonus and positive Babinski signs may develop within 24 hours of trauma.

Investigations
SKULL X- RAY A.P, LATERAL VIEWS
CT SCAN
MRI
CAROTID ANGIOGRAPHY
Of course, we also investigate any associated injuries.

Complications
Raised intracranial pressure may lead to coning or herniation of the brain stem through the foramen magnum.

Management
This is a dire emergency. Sometimes the patient is merely picked up unconscious without any history. There may be no witness to describe what made him unconscious . you need then to exclude other causes of loss of consciousness such as alcohol, epilepsy, cerebrovascular accident , hyperglycemia , hypoglycemia, ureamia, hepatic failure, etc.
Assess the posttraumatic amnesia PTA
Use the Glasgow scale of coma to determine the level of coma: response to eye opening: spontaneous(4) to speech (3), to pain (2), nil (1); best verbal response : orientated (5) confused ($) inappropriate words (3) incomprehensible words (2) nil (1); and best motor response : obeys command (6) localizes pain (5) flexes to pain, withdrawal (4) flexes to pain abnormal (3) extend to pain (2) nil (1).
Assess bleeding from the ears or nose ; assess leakages of CSF from the orifices
Observe for fixed dilatation of the pupil, a grave prognostic import indicative of downward descent of he midbrain and compression of the cerebral peduncle on the opposite tentorial rim and stretching of the third nerve ; indicative of ipsilateral intracranial pathology. Fixed pin points pupils is indicative of pontine or morphine ingestion.
Blood pressure rises whilst the pulse rate and respiratory rate decrease. Note that ntracranial bleeding is maximally about 200mls and is not a cause of any shock. If there is a circulatory collapse in ahead injured patient, look else where for the cause.
Esthablish lateralizing signs as mentioned above
In extradural hematoma, there may be severe headaches, confusion, restlessness, apathy.
The definitive treatment for extradural hematoma is burr holing . it is a diagnostic as well as a therapeutic process. It can be done under local anaesthesia or general anaesthesia and a light general anaesthesia . sometimes , if the patient is unconscious , we use local anaesthesia and a light general anaesthesia . by standards, the ptient is intubated to keep the intracranial pressure low. Decompression process is so dramatic that in a patient where only local anaesthesia is used, as soon as the clot is rmoved, the brain expands and the patient recovers consciousness on the table. The site of the first burr hole is midway between the eye and the ear, from the lower border of the zygomatic bone upwards and slightly backwards for about 8cm. the site of the burr hole is indicated by the abrasion. The fascia of the temporalis major is incised and the fibres are split to expose the bone just above and behind the midpoint of the zygomatic arch. Hudson’s brace and trephines are used serially to expose the dura. If there is an extradural hemorrhage , the clot will be seen; on the other hand the dura may be plum coloured but bulging due to subdural hemorrhage; if the dura is normal and not bulging the tap is considered negative.
If there is an extradural hemorrhage, you extend the wound to not only remove the clot but also to have access and diathermise the bleeding vessel. You may need to irrigate the wound with normal saline. If the venae commitantes are the source of the bleeding, you need to reach it and address the issue. If the source of the bleeding is the posterior branch of the middle meningeal vessels, you have to place a drain in the wound and close the wound.
If the burr hole yields nothing, repeat the process on the contralateral side.
Do we allow a non-surgeon to do burr holes?

Yes, we do allow . indeed, a burr hole is a dire emergency and must be done at the earliest possible time. It is within the precints of the general surgeon.
Postoperative treatment
Decompress with mannitol and dexamethasone
Maintain drain until dry
Results are usually excellent, if treatment is early.
Antonio Abayomi Jorge Ferreira

This paper was first presented at a specialist clinical meeting in lagos Nigeria in 2013
Ferreira is a retired surgeon of the Nigerian army

a story of a chorionic carcinoma

Story of chorocarcinoma. A 60 year old woman gravida 2 para 1+1 one alive who presented at xyz general hospital gynaecological emergencies with 1 week history of  heavy vaginal bleeding prior to presentation. Her last menstrual period was 3months ago. There was no significant haemodynamic changes in her cardiovascular status. Her last confinement was 12 years ago which resulted into pregnancy loss at 12 weeks of gestational age.

Gynaecological history: menarche not sure, nil pap smear and nil subscription to any form of familp planning method mode.

Obstetrics history: single spontaneous vaginal delivery 45 years ago.

Past medical history: nil hypertension, nil diabetes mellitus

Past surgical history: none

General examination: shows healthy and good looking elderly woman not pale anicteric acyanosed not in any form of respiratory difficulty nil pedal edema.

Clinical parameters: BP 120/90 mmhg, pr is 80b/m, rr is 14cpm pcv 30%

Abdomen: abdominal swelling noted which measures 13cm from the pubic symphysis upto lower abdomen

Initial impression was leiomyoma

Investigation and result: molar gestation or gestational trophoblastic diseases.

 

Refferal : the patient was sent to tertiary facility for a comprehensive review.

University of New Mexico Health Sciences Center, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, 2211 Lomas Boulevard NE, Albuquerque, NM 87131-5286, USA. Hsmith@salud.unm.edu

Abstract

Gestational trophoblastic disease (GTD) encompasses a unique group of uncommon but interrelated conditions derived from placental trophoblasts. For the purposes of discussion GTD is the appropriate collective name for hydatidiform mole, whereas the term gestational trophoblastic neoplasia (GTN) is reserved for cases with persistent human chorionic gonadotropin (hCG) titer elevation after evacuation of hydatidiform mole, metastatic disease, or choriocarcinoma. Although the pathology and clinical behavior of CM and PM are different, the initial management of both conditions is surgical evacuation by suction curettage, determination of the baseline, and follow-up with (hCG) titers. There are guidelines for risk-factor scoring and a staging system that classifies untreated patients into distinct prognostic categories so that treatment outcomes can be objectively compared. The rates of GTN and choriocarcinoma are decreasing and survival has dramatically improved

Choriocarcinoma is a malignant, trophoblastic[1] cancer, usually of the placenta. It is characterized by “early hematogenous spread” to the lungs. It belongs to the malignant end of the spectrum in gestational trophoblastic disease(GTD). It is also classified as a germ cell tumor and may arise in the testis or ovary.

signs and symptoms:

Aetiology:

Choriocarcinoma of the placenta during pregnancy is preceded by:

Rarely, choriocarcinoma occurs in primary locations other than the placenta; very rarely, it occurs in testicles. Although trophoblastic components are common components of mixed germ cell tumors, pure choriocarcinoma of the adult testis is rare. Pure choriocarcinoma of the testis represents the most aggressive pathologic variant of germ cell tumors in adults, characteristically with early hematogenous and lymphatic metastatic spread. Because of early spread and inherent resistance to anticancer drugs, patients have poor prognosis. Elements of choriocarcinoma in a mixed testicular tumor have no prognostic importance.[2][3]

Choriocarcinomas can also occur in the ovaries.[4][5]

Pathology:

Characteristic feature is the identification of intimately related syncytiotrophoblasts and cytotrophoblasts without formation of definite placental type villi. Since choriocarcinomas include syncytiotrophoblasts (beta-HCG producing cells), they cause elevated blood levels of beta-human chorionic gonadotropin.

Syncytiotrophoblasts are large multi-nucleated cells with eosinophilic cytoplasm. They often surround the cytotrophoblasts, reminiscent of their normal anatomical relationship inchorionic villi. Cytotrophoblasts are polyhedral, mononuclear cells with hyperchromatic nuclei and a clear or pale cytoplasm. Extensive hemorrhage is a common finding.

Treatment:

Since gestational choriocarcinoma (which arises from a hydatidiform mole) contains paternal DNA (and thus paternal antigens), it is exquisitely sensitive to chemotherapy. The cure rate, even for metastatic gestational choriocarcinoma, is around 90–95%.

At present,[when?] treatment with single-agent methotrexate is recommended for low-risk disease, while intense combination regimens including EMACO (etoposide, methotrexate,actinomycin D, cyclosphosphamide and vincristine (Oncovin) are recommended for intermediate or high-risk disease.[6][7]

Hysterectomy (surgical removal of the uterus) can also be offered[8] to patients > 40 years of age or those for whom sterilisation is not an obstacle. It may be required for those with severe infection and uncontrolled bleeding.

Choriocarcinoma arising in the testicle is rare, malignant and highly resistant to chemotherapy. The same is true of choriocarcinoma arising in the ovary. Testicular choriocarcinoma has the worst prognosis of all germ-cell cancers.[9]

 

 

References:

  1. choriocarcinoma” at Dorland’s Medical Dictionary
  2. ^ Rosenberg S, DePinho RA, Weinberg RE, DeVita VT, Lawrence TS (2008). DeVita, Hellman, and Rosenberg’s Cancer: Principles & Practice of Oncology. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7207-9. OCLC 192027662.
  3. ^ Kufe D (2000). Benedict RC, Holland JF, eds. Cancer medicine (5th ed.). Hamilton, Ont: B.C. Decker. ISBN 1-55009-113-1. OCLC 156944448.
  4. ^ Gerson RF, Lee EY, Gorman E (November 2007). “Primary extrauterine ovarian choriocarcinoma mistaken for ectopic pregnancy: sonographic imaging findings”. AJR Am J Roentgenol. 189 (5): W280–3. doi:10.2214/AJR.05.0814. PMID 17954626.
  5. ^ Ozdemir I, Demirci F, Yucel O, Demirci E, Alper M (May 2004). “Pure ovarian choriocarcinoma: a difficult diagnosis of an unusual tumor presenting with acute abdomen in a 13-year-old girl”. Acta Obstet Gynecol Scand. 83 (5): 504–5. doi:10.1111/j.0001-6349.2004.00092a.x. PMID 15059168.
  6. ^ Rustin GJ, Newlands ES, Begent RH, Dent J, Bagshawe KD (1989). “Weekly alternating etoposide, methotrexate, and actinomycin/vincristine and cyclophosphamide chemotherapy for the treatment of CNS metastases of choriocarcinoma”. J. Clin. Oncol. 7 (7): 900–3.PMID 2472471.
  7. ^ Katzung, Bertram G. (2006). “Cancer Chemotherapy”. Basic and clinical pharmacology(10th ed.). New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-145153-6.OCLC 157011367.
  8. ^ Lurain JR, Singh DK, Schink JC (2006). “Role of surgery in the management of high-risk gestational trophoblastic neoplasia”. The Journal of reproductive medicine. 51 (10): 773–6.PMID 17086805.
  9. ^ Verville, Kathleen M. (2009). Testicular Cancer. Infobase Publishing. p. 76.ISBN 9781604131666.

 

cervical cancer screening and awareness in ingawa general hospital katsina

facilitators:

  1. dr shuaib, federal medical center , katsina state, Nigeria
  2. dr samual, federal medical center, katsina state, Nigeria
  3. dr yakubu, GH ingawa, katsina state, Nigeria
  4. dr nura, GH ingawa, katsina state, Nigeria

Screening

Read about screening for cervical cancer.

What screening is

Screening means testing people for early stages of an illness before they have any symptoms. For screening to be useful the tests:

  • must be reliable at picking up the illness
  • must be simple and quick
  • overall must do more good than harm to people taking part

What is cervical cancer screening

Cancer screening involves testing apparently healthy people for signs that could show that a cancer is starting to develop.

Cervical screening is a way of preventing cancer by finding and treating early changes in the neck of the womb (cervix). These changes could lead to cancer if left untreated.

The screening uses a test called cytology, which many people know as the smear test. A nurse or doctor takes a sample of cells from the cervix with a small brush. They send the sample to a laboratory to be checked for abnormalities. In some cases, samples are also tested for a virus called human papilloma virus (HPV) that increases the risk of cervical cancer.

Who has cervical screening

The NHS cervical screening programme invites women from ages 25 to 64 for cervical screening. Women aged 25 to 49 are invited every 3 years. After that, women are invited every 5 years until the age of 64.

the screening in our hospital will however covers sexually active women as early as 16years due to early marriage, a cultural pattern in the community.

Why younger women don’t have screening

We know from research that cervical cancer is very rare in women younger than 25. But changes in the cervix are quite common in younger women. So, screening them leads to unnecessary treatment and worry. Scientists have worked out that screening younger women leads to more harms than benefits.

The cervical screening test

The screening test involves taking a sample of cells from the surface of the cervix. The test is called liquid based cytology (LBC).

To have the test you take off your underwear and lie on your back on a couch. You need to lie with your knees drawn up and spread apart. If this position is difficult for you, you can ask your nurse to take the cell sample when you are lying on your side with your knees drawn up.

To take the sample of cells, the doctor or nurse gently slides an instrument called a speculum into your vagina so that they can see the cervix clearly. Having the speculum put in may be a little uncomfortable, but it shouldn’t hurt. It can be more uncomfortable if you are very tense. Try to relax. Taking a few deep breaths can help.

The doctor or nurse gently scrapes the surface of your cervix with a small soft brush. This collects a sample of cells from the outer layer of the cervix. They put the sample into a pot of liquid and send it to the laboratory. Then they take out the speculum and the test is over. You can get down from the couch.

In the laboratory, a pathologist puts the sample under a microscope. They examine the cells and report any abnormal ones. They may also test to see whether the HPV virus is present in the sample.

HPV testing

In the future, primary HPV testing will be rolled out across England. This means that they will test the sample of cells for HPV first. If HPV is found, they will then test for cell changes.

After the cervical screening test

The laboratory sends the results of your test back to your GP surgery. They will write to you with the result, usually within 2 weeks of having the test.

What the results mean

There are several different results you can have after a screening test. Most women have a normal result. In this case you will be invited for screening again in 3 to 5 years depending on your age.

Problems with the result

Some results are due to problems with the test rather than because there are any abnormal cells. You may be told that you need a repeat test because yours could not be read properly. This is sometimes called having an inadequate sample. This could be because:

  • there were not enough cells in the sample
  • you have an infection and it wasn’t possible to see the cells clearly enough
  • you were having a period and there was too much blood to see the cells clearly
  • the cervix was inflamed and it wasn’t possible to see the cells clearly enough

In all these cases, the letter you get will ask you to go back and have another test. This is usually about 3 months later.

If you have an abnormal result

Around 1 in 20 women (5%) have an abnormal result after a cervical screening test. It means that there are some changes to the cells on the cervix. These changes are not cancer. The cells often go back to normal by themselves. But in some women, if not treated, these changes could develop into cancer in the future.

Abnormal results can be reported in 2 different ways. You are most likely to be told you have:

  • borderline or mild cell changes (also called low grade dyskaryosis)
  • moderate or severe cell changes (also called high grade dyskaryosis)

It is very rare for an abnormal result to show that a cancer has already developed, especially if you have been having regular screening. But this is possible.

If you have a cervical erosion

This has nothing to do with cervical cancer. Cervical erosion is a condition often picked up by cervical screening tests. You may hear it called an ectropion. It means that there are glandular cells on the surface of the cervix. Glandular cells are normally only seen inside the cervical canal. The cervix often looks a little inflamed in areas of erosion.

An erosion will not harm you. It is common in teenagers, in pregnancy, and in women on the pill. It can cause slight bleeding, especially after sex. Usually it goes away by itself without any treatment.

If you have mild cell changes

Currently, what happens if you have borderline or mild cell changes (low grade dyskaryosis) varies depending on where you live.

In England, Northern Ireland and Wales

If you have borderline or mild cell changes, the laboratory will test your sample for the human papilloma virus (HPV). HPV is a very common virus. Most women have it at some point in their lives, and in most cases your body will get rid of the virus without you ever knowing you had it.

It can be passed from person to person during intimate sexual contact. Certain types of HPV increase the risk of cervical cancer.

If no HPV is found in the sample, it is called HPV negative. In this situation the cell changes are very likely to go back to normal or stay the same. So it is safe for you to go back to the routine screening programme and have tests every 3 to 5 years, as normal.

If your sample shows a type of HPV that increases cervical cancer risk, you will get an invitation for a test called a colposcopy. Colposcopy means looking very closely at the cervix using a specialised magnifying instrument called a colposcope. This test can show whether you need treatment for the abnormal cells.

In Scotland

In Scotland, your doctor or nurse will either suggest a colposcopy or ask you to go back for another screening test (a repeat smear) in 6 months time. If your next test is normal you may have 2 further tests, 6 months apart, before going back to regular screening every 3 to 5 years.

If your repeat test shows abnormal cells, you will then have a colposcopy to check them more closely. You may then need some treatment.

If you have moderate or severe cell changes

If you have moderate or severe cell changes (high grade dyskaryosis), you will be referred for a colposcopy. The doctor or specialist nurse will take a sample of cells (a biopsy) from the abnormal area. They may ask you to go back for treatment depending on the result of the biopsy. Or in some clinics, they may offer you treatment at the same time as the colposcopy.

You usually only need treatment once. Then you have follow up tests to check that the treatment has worked.

If you have an abnormal test and have successful treatment you are very unlikely to get cervical cancer if you continue to have screening. If you don’t have treatment, you are at risk of getting cervical cancer in the future.

Benefits of cervical screening

Scientists and experts estimate that cervical screening saves around 4,500 lives each year in the UK.

Women screened between the ages of 35 to 64 are thought to have a 60 to 80% lower risk of being diagnosed with cervical cancer in the 5 years following the test compared to women who haven’t been screened. The benefit of screening increases with age.

Since cervical screening started in the 1980s in Great Britain, rates of cervical cancer have almost halved.

Possible harms of cervical screening

Cervical screening works very well but, like any screening test, it isn’t perfect. In a few cases, tests will seem to find abnormal changes that aren’t really there. This is called a false positive result. It leads to unnecessary worry for the woman and also the need for more tests.

There is also a risk that cell changes may be missed. This is called a false negative result. So it is important to go for screening every time you are invited.

Sometimes it is difficult to tell whether changes in the cervix will go back to normal or will develop into cancer after some years. So, some women will have treatment for changes to cervical cells that would not have caused any harm if they had been left alone. This is called overdiagnosis or overtreatment. For a few women, the treatments may cause problems such as bleeding afterwards or a small increase in future pregnancies of having the baby early.

It is hard to know exactly how often women are overdiagnosed or overtreated in this way. But in women from their early 20s to mid 60s, the benefits of preventing cervical cancers are very great.

HPV vaccination

Since 2008, girls aged 12 and 13 have been offered a vaccination against the human papillomavirus (HPV). The vaccine can prevent over 70% of cervical cancers.

It is important for girls to have the vaccination when it is offered at school. But there are many types of HPV linked to cervical cancer. Although the vaccine protects against the 2 types that cause most cases of cervical cancer, it doesn’t protect against all of them. This means that screening is still important for girls who have been vaccinated.

As well as attending for screening when you are invited, you still need to look out for any unusual changes to your body. Check for any abnormal bleeding, unpleasant discharge or pain after sex. If you notice anything unusual, make an appointment to see your doctor and get it checked out.

Smoking can increase the risk of cervical cancer. Cancer causing chemicals in cigarette smoke can go into the blood and travel around the body. These chemicals can damage the cells of the cervix.

 

credits:

cancer research center UK

NHS, uk

Meningitis: A Rising Epidemic in Northern Nigeria: Say Deja VU

definition: meningitis is simply inflamation of the meninges i.e the membrane covering of the brain and spinal cord.

aetiology and risk factors: primary infection to the brain or secondary infection from areas close to the brain like ear infection (otitis media), nasal infection( suppurative rhinitis). all ages can be affected particularly children under 5 ,senior citizens or elderly age group, compromised immune state like diabetes mellitus, tuberculosis and HIV infected individual.

Epidemiology:
”Between 26 January and 5 March 2015, the Nigeria Centre for Disease Control (NCDC) of the Federal Ministry of Health of Nigeria notified WHO of 652 suspected cases of meningococcal disease, including 50 deaths. Cases have been reported in 10 local government areas of 2 states, Kebbi and Sokoto. Laboratory tests have confirmed the predominance of Neisseria meningitidis serogroup C in the affected areas, with no other serogroups being identified.
In Zamfara state, there has been a recent emergence of suspected cases of meningococcal disease; however, an outbreak has not yet been confirmed.” GAR/WHO.

in 2017, the recurrence of meningitis was initially reported in abuja and sokoto state in march. So far the number of mortality recorded across the northern belt is astonishing.

management
a. good clinical history and sequeale

b. good clinical acumen, examination

c. investigate properly

d. treatment options

.commence antibiotics coverage 3rd generations cephalosporins and those that can permeate the blood brain barriers. where the problem lies here is compliance and affordability issues by the patients relative. if such exist kindly used penicillin inj provided patient will not react to it.
combine your medications with aminoglycosides and steroids if patient presented early.

My Msc thesis: Effect of hypothyroidism on prolongation of QT interval in female population and consideration for the phenomenon torsade des pointed.

nterval
Schematic representation of normal
ECG trace ( sinus rhythm ), with waves,
segments, and intervals labeled.
In cardiology , the QT interval is a measure of
the time between the start of the Q wave and
the end of the T wave in the heart’s electrical
cycle . The QT interval represents electrical
depolarization and repolarization of the
ventricles . A lengthened QT interval is a
marker for the potential of ventricular
tachyarrhythmias like torsades de pointes and
a risk factor for sudden death.
Correction for heart rate
Like the R-R interval, the QT interval is
dependent on the heart rate in an obvious way
(the faster the heart rate the shorter the R-R
Interval and QT interval) and may be adjusted
to improve the detection of patients at
increased risk of ventricular arrhythmia.
Modern computer-based ECG machines can
easily calculate a corrected QT (QTc), but this
correction may not aid in the detection of
patients at increased risk of arrhythmia. There
are a number of different correction formulas.
The standard clinical correction is to use
Bazett’s formula ,[1] named after physiologist
Bazett, calculating the heart rate-corrected QT
interval (QTcB). Please be ware that Bazett’s
formula is based on observations of only 12
patients in 1920 and does meet current
scientific quality standards. A more robust
method is the Frammingham correction based
on the Framingham Heart study, recent
longterm cohort data of over 5000 subjects.
Bazett’s formula is:
where QTcB is the QT interval corrected for
heart rate, and RR is the interval from the
onset of one QRS complex to the onset of the
next QRS complex, measured in seconds, often
derived from the heart rate (HR) as 60/HR
(here QT is measured in milliseconds).
However, this non-linear formula, obtained
from data in only 39 young men, is not
accurate, and over-corrects at high heart rates
and under-corrects at low heart rates. [2]
Fridericia [3] has published an alternative
correction formula using the cube-root of RR.
There are several other methods, such as
regression-analysis: [4]
Upper limit of normal QT interval, corrected for
heart rate according to Bazett’s formula , [1]
Fridericia’s formula [3] and subtracting 0.02 s
from QT for every 10 bpm increase in heart
rate. [5] Up to 0.42 s (≤420 ms) is chosen as
normal QTc of QT B and QT F in this diagram.
Definitions of normal QTc vary from being
equal to or less than 0.40 s (≤400 ms), [5]
0.41s (≤410ms), [6] 0.42s (≤420ms) [7] or
0.44s (≤440ms). [8] For risk of sudden cardiac
death , “borderline QTc” in males is 431-450
ms, and in females 451-470 ms. An
“abnormal” QTc in males is a QTc above 450
ms, and in females, above 470 ms. [9]
If there is not a very high or low heart rate,
the upper limits of QT can roughly be
estimated by taking QT=QTc at a heart rate of
60 beats per minute (bpm), and subtracting
0.02s from QT for every 10 bpm increase in
heart rate. For example, taking normal QTc ≤
0.42 s, QT would be expected to be 0.42 s or
less at a heart rate of 60 bpm. For a heart rate
of 70 bpm, QT would roughly be expected to
be equal to or below 0.40 s. Likewise, for
80 bpm, QT would roughly be expected to be
equal to or below 0.38 s. [5]
Measurement
The QT interval is most commonly measured
in lead II for evaluation of serial ECGs, with
leads I and V5 being comparable alternatives
to lead II. Leads III, aVL and V1 are generally
avoided for measurement of QT interval.
[10] The accurate measurement of the QT
interval is subjective [11] because the end of
the T wave is not always clearly defined and
usually merges gradually with the baseline. QT
interval in an ECG complex can be measured
manually by different methods such as the
threshold method, in which the end of the T
wave is determined by the point at which the
component of the T wave merges with the
isoelectric baseline or the tangent method, in
which the end of the T wave is determined by
the intersection of a tangent line extrapolated
from the T wave at the point of maximum
downslope to the isoelectric baseline. [12]
With the increased availability of digital ECGs
with simultaneous 12-channel recording, QT
measurement may also be done by the
‘superimposed median beat’ method. In the
superimposed median beat method, a median
ECG complex is constructed for each of the 12
leads. The 12 median beats are superimposed
on each other and the QT interval is measured
either from the earliest onset of the Q wave to
the latest offset of the T wave or from the
point of maximum convergence for the Q wave
onset to the T wave offset. [13]
Abnormal intervals
Prolonged QTc causes premature action
potentials during the late phases of
depolarization. This increases the risk of
developing ventricular arrhythmias or fatal
ventricular fibrillations. [14] Higher rates of
prolonged QTc are seen in females, older
patients, high systolic blood pressure or heart
rate, and short stature. [15] Prolonged QTc is
also associated with EKG findings called
Torsade de Pointes, which are known to
degenerate into ventricular fibrillation,
associated with higher mortality rates. There
are many causes of prolonged QT intervals,
acquired causes being more common than
genetic. [16]
Genetic causes
An abnormally prolonged QT interval could be
due to long QT syndrome , whereas an
abnormally shortened QT interval could be due
to short QT syndrome .
The QTc length is associated with variations in
NOS1AP gene. [17] The autosomal recessive
syndrome of Jervell and Lange-Nielsen is
characterized by a prolonged QTc interval in
conjunction with sensorineural hearing loss .
Due to adverse drug reactions
Prolongation of the QT interval may be due to
an adverse drug reaction. [18] Many drugs such
as haloperidol , [19] vemurafenib , ziprasidone ,
methadone[20] and sertindole [21] can prolong
the QT interval. Some antiarrhythmic drugs,
like amiodarone or sotalol work by getting a
pharmacological QT prolongation. Also, some
second-generation antihistamines, such as
astemizole, have this effect. In addition, high
blood-alcohol concentrations prolongs the QT
interval. [22] A possible interaction between
selective serotonin reuptake inhibitors and
thiazide diuretics is associated with QT
prolongation. [23] Macrolide antibiotics are also
suspected to prolong the QT interval, after it
was discovered recently that azithromycin was
associated with an increase in cardiovascular
death. [24]
Due to pathological conditions
Hypothyroidism , a condition of low function of
the thyroid gland, can cause QT prolongation
at the electrocardiogram . Acute hypocalcemia
causes prolongation of the QT interval, which
may lead to ventricular dysrhythmias.
A shortened QT can be associated with
hypercalcemia. [25]
Use in drug approval studies
Since 2005, the FDA and European regulators
have required that nearly all new molecular
entities be evaluated in a Thorough QT (TQT)
study to determine a drug’s effect on the QT
interval. [26] The TQT study serves to assess
the potential arrhythmia liability of a drug.
Traditionally, the QT interval has been
evaluated by having individual human reader
measure approximately nine cardiac beats per
clinical timepoint. However, a number of recent
drug approvals have used a highly automated
approach, blending automated software
algorithms with expert human readers
reviewing a portion of the cardiac beats, to
enable the assessment of significantly more
beats per timepoint in order to improve
precision and reduce cost. [27] As the
pharmaceutical industry has gained experience
in performing TQT studies, it has also become
evident that traditional QT correction formulas
such as QT F, QT B , and QT LC may not always
be suitable for evaluation of drugs impacting
autonomic tone. [28] Current efforts are
underway by industry and regulators to
consider alternative methods to help evaluate
QT liability in drugs affecting autonomic tone,
such as QT beat-to-beat and Holter-bin
methodologies. [29]
As a predictor of mortality
Electrocardiography is a safe and noninvasive
tool that can be used to identify those with a
higher risk of mortality. In the general
population, there has been no consistent
evidence that prolonged QTc interval in
isolation is associated with an increase in
mortality from cardiovascular disease. [30]
However, several studies[ which? ] have
examined prolonged QT interval as a predictor
of mortality for diseased subsets of the
population.
Rheumatoid arthritis
Rheumatoid arthritis is the most common
inflammatory arthritis. [31] Studies have linked
rheumatoid arthritis with increased death from
cardiovascular disease.[31] In a 2014 study,
[14] Panoulas et al. found a 50 ms increase in
QTc interval increased the odds of all-cause
mortality by 2.17 in patients with rheumatoid
arthritis. Patients with the highest QTc interval
(> 424 ms) had higher mortality than those
with a lower QTc interval. The association was
lost when calculations were adjusted for C-
reactive protein levels. The researchers
proposed that inflammation prolonged the QTc
interval and created arrhythmias that were
associated with higher mortality rates.
However, the mechanism by which C-reactive
protein is associated with the QTc interval is
still not understood.
Type 1 diabetes
Compared to the general population, type 1
diabetes may increase the risk of mortality, due
largely to an increased risk of cardiovascular
disease. [15][32] Almost half of patients with
type 1 diabetes have a prolonged QTc interval
(> 440 ms). [33] Diabetes with a prolonged QTc
interval was associated with a 29% mortality
over 10 years in comparison to 19% with a
normal QTc interval. [15] Anti-hypertensive
drugs increased the QTc interval, but were not
an independent predictor of mortality.[15]
Type 2 diabetes
QT interval dispersion (QTd) is the maximum
QT interval minus the minimum QT interval,
and is linked with ventricular repolarization.
[34] A QTd over 80 ms is considered
abnormally prolonged.[35] Increased QTd is
associated with mortality in type 2 diabetes.
[35] QTd is a better predictor of cardiovascular
death than QTc, which was unassocited with
mortality in type 2 diabetes. [35] QTd higher
than 80 ms had a relative risk of 1.26 of dying
from cardiovascular disease compared to a
normal QTd.
See also
Electrocardiogram
Comprehensive QTc Calculator with 5
formulas at TheCalculator.co
References
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Over? February 3, 2006
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Chakraborty S, Manohar D, Lokhandwala Y,
Kothari S. (2014). “Drug-induced QT
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Natekar M, Hingorani P, Kerkar V, Ramasamy
A, de Vries M, Zumbrunnen T, Kothari S, Narula
D (2011). “Comparison of 5 methods of QT
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14. ^ a b Panoulas VF, Toms TE, Douglas KM,
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51. doi : 10.1038/ng1790 . PMID 16648850 .
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19. ^ “Information for Healthcare
Professionals: Haloperidol (marketed as
Haldol, Haldol Decanoate and Haldol
Lactate)” . Archived from the original on
2007-10-11. Retrieved 2007-09-18.
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K (April 2007). “ECG changes in patients with
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24. ^ http://www.fda.gov/Drugs/Drugsafety/
ucm304372.htm [ full citation needed ]
25. ^ Hypercalcemia [full citation needed ]
26. ^ http://www.fda.gov/downloads/
RegulatoryInformation/Guidances/
UCM129357.pdf [full citation needed ]
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Thorough QT Study for a Leading
Pharmaceutical Company – Applied Clinical
Trials
28. ^ “Garnett” (PDF). Retrieved 6 June
2014.
29. ^ http://thew-project.org/document/FDA
%20CPI%20project.pdf [ full citation needed ]
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Lamas GA, Hennekens CH (May 2004).
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PMID 15136301 .
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T (August 1985). “The effect of proteinuria on
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et al. (March 2001). “Prolonged QTc interval
predicts mortality in patients with Type 1
diabetes mellitus” . Diabetic Medicine 18 (3):
199–205. doi: 10.1046/
j.1464-5491.2001.00446.x .
PMID 11318840 .
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Fabsitz RR, Lee ET, Welty TK (2000).
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population-based Casale Monferrato Study” .
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dc11-1397 . PMC 3322722 .
PMID 22301117 .

Torsades de pointes or torsade de pointes
( TdP or simply torsade(s) ) (French: [tɔʁsad də
pwɛ̃t] , translated as “twisting of the spikes”),
is a specific type of abnormal heart rhythm
that can potentially lead to sudden cardiac
death . It is a polymorphic ventricular
tachycardia that exhibits distinct
characteristics on the electrocardiogram
(ECG). It was described by Dessertenne in
1966. [1]
Signs and symptoms
Most episodes revert spontaneously to a
normal sinus rhythm. Other possible outcomes
include palpitations, dizziness, lightheadedness
(short episodes), fainting (longer episodes),
and sudden cardiac death .
Causes
Common causes for torsades de pointes
include diarrhea, low blood magnesium and
low blood potassium . It is commonly seen in
malnourished individuals and chronic
alcoholics . Certain combinations of drugs
resulting in drug interactions may contribute:
decreasing the metabolism of a medication
causing QT elongation such as clarithromycin
(Biaxin) , levofloxacin, or haloperidol (Haldol) ,
taken concomitantly with a specific cytochrome
P450 inhibitor like fluoxetine (Prozac) ,
cimetidine (Tagamet) ; foods like grapefruit will
result in higher than normal doses of the
medication responsible for the QT elongation.
Since these specific drugs worsen the
elongation of the QT wave in a dose-
dependent manner, inhibition of drug
metabolism raises the risks of developing a
malignant torsades de pointes arrhythmia.
Prescription drug interactions
TdP as a prescription drug side effect has been
a major liability and reason for withdrawal of
medications from the marketplace. [2]
Examples include amiodarone , methadone,
lithium , chloroquine , erythromycin ,
amphetamine , ephedrine, pseudoephedrine,
methylphenidate and phenothiazines. [3] It can
also be the side effect of some antiarrhythmic
medications such as sotalol , procainamide and
quinidine. The gastrokinetic drug cisapride
(Propulsid) was withdrawn from the US market
in 2000 after such interactions led to deaths
caused by long QT syndrome-induced
torsades de pointes. To correct the prolonged
QT interval, magnesium IV 2gm will help
effectively block calcium flow as well as
prevent recurrent Torsade de Pointes.
In September 2011 (subsequently updated in
March 2012 and February 2013), the FDA
issued a warning concerning increased
incidence of QT elongation with doses of the
antidepressant Celexa ( citalopram ) above
40 mg per day, which is considered the
maximum allowable dosage, increasing the risk
of Torsades. [4][5] However, the study,
“Evaluation of the FDA Warning Against
Prescribing Citalopram at Doses Exceeding 40
mg” reported no increased risk of abnormal
arrhythmias thus questioning the merit of FDA
warning. [6]
Risk factors
The following is a list of factors associated
with an increased tendency toward torsades de
pointes: [ medical citation needed ]
Lead II ECG showing torsades being shocked
by an implantable cardioverter-defibrillator
back to the patient’s baseline cardiac rhythm .
Hypokalemia (low blood potassium)
Hypomagnesemia (low blood magnesium)
Hypocalcemia (low blood calcium)
Bradycardia (slow heartbeat)
Heart failure
Left ventricular hypertrophy
Hypothermia
Subarachnoid hemorrhage
Hypothyroidism
The following is a list of drugs known to
induce Torsades de pointes, (possibly along
with QTc interval prolongation):
Ciprofloxacin (antibiotic)
AZD9291 (chemotherapy drug currently in
clinical trials; may be particularly dangerous in
combination with the above-cited
Ciprofloxacin)
Diagnosis
The ECG tracing in torsades demonstrates a
polymorphic ventricular tachycardia with a
characteristic illusion of a twisting of the QRS
complex around the isoelectric baseline (peaks
which are at first pointing up are seen to be
pointing down for subsequent “beats” when
looking at ECG traces of the “heartbeat”). It is
hemodynamically unstable and causes a
sudden drop in arterial blood pressure, leading
to dizziness and fainting . Depending on their
cause, most individual episodes of torsades de
pointes revert to normal sinus rhythm within a
few seconds, but may also persist and
possibly degenerate into ventricular fibrillation ,
which will lead to sudden death in the absence
of prompt medical intervention. Torsades de
pointes is associated with long QT syndrome ,
a condition whereby prolonged QT intervals are
visible on the ECG. Long QT intervals
predispose the patient to an R-on-T
phenomenon, where the R wave representing
ventricular depolarization occurs during the
relative refractory period at the end of
repolarization (represented by the latter half of
the T-wave). An R-on-T can initiate torsades.
Sometimes pathologic T-U waves may be seen
in the ECG before the initiation of torsades. [7]
A “short-coupled variant of torsade de
pointes”, which presents without long QT
syndrome, was also described in 1994. [8]
Drastic rotation of the heart’s electrical axis
Prolonged QT interval ( LQTS) – may not be
present in the short-coupled variant of torsade
de pointes
Preceded by long and short RR-intervals –
not present in the short-coupled variant of
torsade de pointes
Triggered by a premature ventricular
contraction (R-on-T PVC)
Treatment
Treatment is directed at withdrawal of the
offending agent, infusion of magnesium sulfate ,
[9][10] antiarrhythmic drugs , and electrical
therapy such as a temporary pacemaker as
needed.
Because of the polymorphic nature of torsades
de pointes, synchronized cardioversion may
not be possible, and the patient may require
an unsynchronized shock (or defibrillation ).
History
The phenomenon was originally described in a
French medical journal by Dessertenne in
1966, when he observed this cardiac rhythm
disorder in an 80-year-old female patient with
complete intermittent atrioventricular block . In
coining the term, he referred his colleagues to
the “Dictionnaire Le Robert,” a bilingual French
English dictionary, of which his wife had just
given him a copy. Here “torsade” is defined as
(a)a bundle of threads twisted in a helix or
spiral, for ornamental purposes, as in an Aran
sweater ; (b) long hair twisted together, or (c)
an ornamental motif as seen on architectural
columns.
The singular and plural forms ( torsade de
pointes and torsades de pointes) have both
often been used. The question of whether
either one is “correct” and the other “incorrect”
has repeatedly arisen. Among major medical
dictionaries, one enters only the plural form,
another enters the plural form as the
headword but lists the singular as a variant,
and another enters the singular form as the
headword and gives a usage comment saying
that the plural is not preferred. One group of
physicians suggests[11] that it would make
sense to use the singular form as the general
entity name (whether comprising a single or
repeated episodes) and that one might best
reserve the plural form for describing repeated
twistings during a single episode. Regarding
the natural language variation, they conclude
good-naturedly, “Wasn’t it the French who
coined the term ‘vive la difference?'” [11]
References
1. ^ Dessertenne, F. (1966). “La tachycardie
ventriculaire a deux foyers opposes variables”.
Archives des maladies du coeur et des
vaisseaux (in French) 59 (2): 263–272.
ISSN 0003-9683 . PMID 4956181 .
Prepaired by Rahel farhad
2. ^ Labant, MaryAnn (November 15, 2014).
“Weaving a Stronger Drug Safety Net”. Gen.
Eng. Biotechnol. News (paper) 34 (20). p. 1.
3. ^ “Drugs That Prolong the QT Interval or
Induce Torsades de Pointes” . Point of Care
Quick Reference . American Academy of
Pediatrics. March 11, 2010. Archived from the
original on March 7, 2014.

Case Report
A Case of QT Prolongation
Associated with Panhypopituitarism
Dilek Arpaci, Mustafa Volkan
Demir , Tayfun Garip, and Ali Tamer
Department of Internal Medicine,
Sakarya Education and Research
Hospital, 54290 Sakarya, Turkey
Received 10 March 2013; Accepted 17
April 2013
Academic Editors: H. Hattori, H. Ikeda,
and R. Murray
Copyright © 2013 Dilek Arpaci et al. This
is an open access article distributed
under the Creative Commons Attribution
License , which permits unrestricted use,
distribution, and reproduction in any
medium, provided the original work is
properly cited.
Abstract
We describe a 37-year-old patient with
panhypopituitarism who experienced
symptoms and signs of hormonal
insufficiency and QT prolongation on
electrocardiogram without electrolyte
disturbances. After hormonal (steroidal
and thyroid) replacement therapy
electrocardiographic findings were
normalized. Hormonal disorders should
be considered as a cause of long QT
intervals which may lead to torsade de
pointes, even if plasma electrolyte levels
are normal, because life-threatening
arrhythmia is treatable by
supplementation of the hormone that is
lacking.
1. Introduction
QT prolongation has various causes,
including drug toxicity, electrolyte
abnormality, myocarditis,
cerebrovascular disease, chromosomal
abnormalities of cardiac ion channels,
and hormonal disorders such as
hypopituitarism, hypothyroidism, and
adrenal insufficiency [1 –5 ]. It is well
known that QT prolongation can be
associated with polymorphic ventricular
tachycardia (VT), which is usually
resistant to antiarrhythmic drug
therapy.
We experienced a case of long QT
intervals associated with
panhypopituitarism that developed
idiopathically as a result of empty sella.
2. Case Report
A 37-year-old woman was admitted to
our hospital because of amenorrhea and
infertility. She also suffered from
fatigue, numbness, and swelling in
hands and foot. Her systolic blood
pressure was found to be <90 mmHg.
She had mild myxedema without
acromegalic phenotype. No galactorrhea
was described. Her past history was
remarkable. She had a traffic accident at
14 years of age. She had regular
menstrual cycles until 20 years of age.
After 20 years of age, no menstrual
bleedings have yet occurred nowadays.
She also complained from mild headache
around eyes. Polydipsia and polyuria
were not defined.
Laboratory tests include serum
biochemistry, and hormones revealed
glucose: 86 mg/dL (70–105 mg/dL), urea:
17.1 mg/dL (18–45 mg/dL), creatinine:
0.7 mg/dL (0.57–1.11 mg/dL), calcium:
8.8 mg/dL (8.4–10.2 mg/dL),
phosphorus: 3.3 mg/dL (2.5–4.5 mg/dL),
magnesium: 2.1 mg/dL (1.7–3.1 mg/dL)
Na: 141 mmol/L (136–145 mmol/L), K:
4.7 mmol/L (3.5–5.1 mmol/L), fT3: 2.12 
pmol/L (2.63–5.70 pmol/L), fT4: 5.81 
pmol/L (9.01–19.04 pmol/L), TSH: 1.28 
IU/mL (0.35–4.94 IU/mL), LH: 0.02 mIU/
mL, FSH: 0.06 mIU/mL, PRL: 1.81 ng/mL
(5.18–26.53 ng/mL), oestrogen: 24 pg/
mL, progesterone: 0.1 ng/mL, cortisol:
0.01 μg/dL (3–19 μg/dL), and ACTH:
10.9 pg/mL (22.5–95.3 pg/mL). She was
hypotensive without any electrolyte
imbalance. We administered stress-dose
steroid and then reduced to replacement
dose by titration. At followup,
hypotension was improved. Thyroid
function tests displayed lower fT3 and
fT4 and normal TSH levels which was
thought to be secondary hypothyroidism.
We gave her levothyroxine (LT4)
replacement. Urine-specific gravity was
1011 and fluid intake and urine output
were normal. She had no menstrual
bleedings for seventeen years, and also
serum progesterone level, was low so
called hypogonadism. She was consulted
with gynecologist and endometrial wall
thickness was lower, so she was offered
to take estrogen progesterone
replacement treatment. With all these
findings, we suspected
panhypopituitarism. Hypophyseal
magnetic resonance imaging (MRI) was
taken and was shown as hypophyseal
hypoplasia with dimensions of 4.6 mm
height and 8.5 mm width. And also
posterior pituitary bright spot was seen
on MRI. Twelve-lead electrocardiogram
was taken (Figure 1 ).
Figure 1: Twelve-lead
electrocardiogram on
admission shows long
QT intervals and
inverted T waves.
At cardiac auscultation murmur was
heard. Patient was consulted with a
cardiologist. A two-dimensional
transthoracic echocardiography was
taken it showed normal left ventricular
systolic function with 65% ejection
fraction, left atrium enlargement, and
mild mitral and tricuspid regurgitation.
A 24-hour rhythm holter
electrocardiography (ECG) was taken
(Figure 2 ); it showed that basic rhythm
was sinusal rhythm, minimal heart rate
was 44/min, mean heart rate was 62/
min, maximal heart rate was 107/min,
and no ventricular/supraventricular
tachycardia or pause was detected.
Maximal QT/QTc interval was 549 ms.
Figure 2: Some
significant ECG events
and minimal heart
rate ECG record
which were detected
at 24-hour rythm
holter ECG.
We considered that QT prolongation may
be caused by hypopituitarism. Steroid
replacement therapy was started on the
5th hospital day and thyroid
replacement therapy on the 11th hospital
day. Three weeks after starting steroid
replacement therapy, the levels of
cortisol and thyroid hormone were
normalized. Two-dimensional
echocardiography showed normal
cardiac wall and valve motions. Also, an
ECG showed QT normalization (Figure
3 ). QT/QTC interval was measured
364/392 ms.
Figure 3: Four weeks
after starting steroid
and thyroid
replacement therapy,
twelve-lead
electrocardiogram
demonstrates normal
QT intervals.
3. Discussion
We described a case of QT prolongation
associated with anterior hypopituitarism
without plasma electrolyte abnormality.
The cause of hypopituitarism could not
be defined in our patient. QT
prolongation may result from electrolyte
disturbances, the use of various
antiarrhythmic drugs, phenothiazines or
tricyclic antidepressants, liquid protein
diets, intracranial events,
bradyarrhythmias, and hormonal
disorders. In our patient, no drug use
was described what mentioned above.
But hormonal disorders
(hypocortisolemia and hypothyroidism)
were found in our patient.
QT prolongation may lead to torsade de
pointes a form of polymorphic
ventricular tachycardia which can cause
sudden cardiac death. In the literature,
there is only one report that described a
case of an association between torsade
pointes and hypopituitarism [6 ].
Electrocardiographic abnormalities
commonly associated with
hypopituitarism are low QRS voltage, ST-
segment depression, inverted T waves,
and a prolonged QT interval [7 , 8 ].
Although the mechanism remains
unclear, glucocorticoid deficiency, an
intracellular-extracellular electrolyte
imbalance of myocytes, and
histopathological changes in the
myocardium are thought to play a role in
this disorder. Recently, it was reported
that glucocorticoids upregulate Kv 1.5 K
channel gene expression in the rat
ventricle [9 ]. Iga et al. [10 ] suggested that
catecholamine release induced by
hypoglycemia might cause arrhythmia or
abnormal wall motion of the left
ventricle in patients with adrenal
insufficiency. In our patient, QT
prolongation without any arrhythmias
occurred in the absence of hypoglycemia
or plasma electrolyte abnormalities.
Some previous reports [4 , 11 ] have
suggested that hypomagnesemia induced
by adrenal insufficiency might cause
myocytic intracellular-extracellular
electrolytic imbalance, resulting in
shortening of the effective refractory
period and prolongation of the relative
refractory period. In our patient, serum
magnesium level was normal. Inverted T
waves and prolonged QT intervals seen
in our patient might be mediated by a
hormonal modulation of ion channels of
cardiac cells, which could contribute to
QT prolongation and lead to
polymorphic ventricular tachycardia
before plasma electrolyte abnormality.
But in our patient, polymorphic
ventricular tachycardia did not occur.
We found lower serum thyroid hormone
levels and plasma cortisol levels. After
steroid and thyroid hormone
replacement therapy, the QT interval
was normalized and no further VT
developed.
In conclusion, hormonal disorders must
be examined as a cause of polymorphic
ventricular tachycardia associated with
long QT intervals even if plasma
electrolyte levels are normal, because
supplementation of insufficient hormone
may permanently cure life-threatening
arrhythmia.
References
1. J. E. Hansen, “Paroxysmal
ventricular tachycardia associated
with myxedema a case report,”
American Heart Journal, vol. 61,
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A coffee over exchange blood transfusion

Objective : To determine the pattern and
determinants of blood transfusion in a Nigerian
neonatal unit.
Materials and Methods : Newborn babies who
required blood transfusions between January and
December, 2008, were studied. The sex, age, and
weight at the first transfusion, clinical conditions,
indications for transfusion, and the outcome were
analyzed with bivariate and multivariate methods.
Results : A total of 402 neonates were
hospitalized and 112 (27.9%) had blood
transfusion; 61.9% had exchange transfusion,
66.1% had red cell transfusion, and 8% had
plasma transfusion. There were 251 transfusions
with a rate of 4.8 transfusions per week. Blood
transfusions were done for severe jaundice
(55.4%), severe anemia (40.2%), and bleeding
disorders (4.4%). Weight < 2.5 kg, outside
delivery, and jaundice were independent
determinants of neonatal transfusion.
Conclusion : The blood transfusion rate in this
facility was remarkably high. Improved standard
of newborn care and infrastructural support are
required to reduce the transfusion rate.
Keywords: Bleeding, exchange transfusion,
hemolysis, neonatal jaundice, plasma transfusion
How to cite this article:
Ogunlesi T A, Ogunfowora O B. Pattern and
determinants of blood transfusion in a Nigerian
neonatal unit. Niger J Clin Pract 2011;14:354-8
How to cite this URL:
Ogunlesi T A, Ogunfowora O B. Pattern and
determinants of blood transfusion in a Nigerian
neonatal unit. Niger J Clin Pract [serial online]
2011 [cited 2015 Nov 22];14:354-8. Available
from: http://www.njcponline.com/text.asp?
2011/14/3/354/86783
Introduction
Blood transfusion is an essential form of medical
treatment, particularly in pediatric practice, where
common illnesses are usually related to blood
destruction or blood loss. [1] The procedure
replaces the volume and the specific constituents
of blood, which play specific roles in oxygen
carriage, immunity, and clotting. Therefore, blood
transfusion is required to maintain life, by
increasing the cardiac output and oxygen delivery
to tissues, and removing toxins like bilirubin from
the body. [2]
The need for transfusion in the neonate may
occur due to physiological or pathological causes.
Anemia of prematurity is a physiological
phenomenon, which is related to the inadequate
maternofetal transfer of iron and poor postnatal
production of endogenous erythropoietin in
infants. Although, replacement therapy with
synthetic erythropoietin is a common practice in
the developed world, [3] blood transfusion is
commonly used in parts of the developing world,
where recombinant erythropoietin is unavailable.
The leading causes of neonatal morbidities and
mortality in the developing world include
mechanical and chemical birth injuries, infections,
and jaundice. [4] These conditions may be
associated with hemolysis, disorders of
coagulation or accumulation of potential toxins.
Bleeding disorders in neonates often require blood
transfusion. [5] In such instances, blood
transfusion is required to prevent death from
acute circulatory collapse or severe hypoxemia.
Top-up transfusion with red cells is done for
anemic cases, while exchange blood transfusion
(EBT) is recommended for hyperbilirubinemia. In
some cases of severe hyperbilirubinemia, EBT is
required to rapidly remove the excess bilirubin
from the blood, to prevent irreversible brain
damage known as bilirubin encephalopathy.
Interestingly, recent studies have shown that
while the newborn exchange blood transfusion
rate in some health facilities in the developing
world like Nigeria remains very high, the
procedure has become very rare in most parts of
the developed world. [6]
Despite the huge requirement for the use of blood
and its products in neonatal care, the practice in
most parts of the developing world is fraught with
the problem of an inefficient blood banking
system. [7] In addition, facilities for the extensive
screening of blood prior to use are highly limited,
hence, the risk of transmission of infections like
hepatitis, cytomegalovirus, syphilis, and HIV is
high.
Yet, neonatologists in this part of the world are
confronted with the clinical need to transfuse a
large number of critically ill babies with blood, in
spite of the inefficient blood banking system.
This makes strict adherence to universal
guidelines on the use of blood and its products
difficult in the developing parts of the world.
Therefore, as a step toward improving the safety
and efficiency of blood transfusion therapies in
under-resourced settings, it is essential to
generate data on the prevailing situation of the
pattern of use of transfusion among newborn
babies. These data can then be used to devise
measures useful for improving transfusion
services in Nigeria and other poor-resource
settings. The present study is the first report from
this Nigerian Newborn Unit, which was
established more than two decades ago. The
objective of the study is to examine the pattern
and clinical determinants of blood transfusion
among Nigerian newborn infants.
Materials and Methods
This study was retrospectively carried out over
the period of January to December, 2008, at the
Neonatal Unit of the Olabisi Onabanjo University
Teaching Hospital, Sagamu, Nigeria.
This is a tertiary hospital located in the Ogun
State, southwest Nigeria, and provides general
and specialized neonatal care services to babies
delivered in the Maternity Unit of the hospital as
well as babies referred from other parts of the
Ogun, Lagos, and Ondo States of Nigeria.
The subjects were consecutive admissions who
required transfusion with blood and any blood
product. Babies who required blood transfusion at
the point of admission as well as babies who
required transfusion days after admission were
included in the study. The referred babies who
had been transfused from places of referral were
excluded.
The following data were obtained: age and weight
at first transfusion, indication for transfusion, and
specific clinical disorders like seizure, apnea,
dyspnea, jaundice or obvious bleeding. Others
included type of blood component and type of
transfusion done. The babies were clinically
classified into preterm, term or post-term.
In our unit, decisions to transfuse babies are
usually taken by the resident physicians and the
consultants in the unit. Generally, the indications
for blood use in our unit include severe anemia,
severe hemorrhage, severe hyperbilirubinemia,
overwhelming sepsis, severe thrombocytopenia,
and patent ductus arteriosus. Whole blood is
transfused at 20 ml / kg in cases of bleeding.
Double volume exchange transfusion with 160
ml / kg is done for severe hyperbilirubinemia or
overwhelming sepsis, while single volume
exchange transfusion with 80 ml / kg is done for
severe anemia within the first week of life. Due to
lack of facilities for packing red cells, we
transfuse 15 ml / kg of partially packed cells for
cases of severe anemia after the first week of life.
Severe anemia is defined, in our unit, as Packed
Cell Volume (PCV) 10 mg / dl /
kg for babies weighing 18 mg / dl for
babies weighing > 2 kg. Early clinical features of
bilirubin encephalopathy are also indications for
exchange transfusion. Fresh plasma is serially
transfused at 10 ml / kg / day in the presence of
sepsis or when double volume exchange
transfusion for severe hyperbilirubinaemia is
impossible. Grouping and cross-matching
according to standard principles precede all
transfusions, although we lack facilities for
irradiation. In addition to transfusion, other
important therapies like medications, fluid
therapies or respiratory supports with oxygen are
also used during the treatment.
Data were managed with SPSS 15.0 software
using descriptive statistics. The means were
compared with Student’s t-test, while the
proportions were compared using the Chi-Square
(c 2 ) test and Odds Ratio (OR). Bivariate analysis
was used to compare babies who required or did
not require transfusions for specific clinical
parameters. Variables having a significant
association with blood transfusion by bivariate
analysis were subjected to multivariate analysis
using a binary logistic method, to determine
independent relationships with the requirement for
blood transfusion.
Statistical significance was established when P
values were < 0.05 or 90% Confidence Interval
(CI) excluded unity.
Results
A total of 402 babies were admitted over a period
of one year and 112 (27.9%) of these had blood
transfusion. Overall, 251 transfusions were done
and the overall rate of transfusion was 4.8 per
week or 20.9 per month. The subjects comprised
of 80 (71.4%) males and 32 (28.6%) females, with
a male-to-female ratio of 2.5 : 1. The mean
weight of the subjects on admission was 2.0 ±
0.9 kg, while the babies who did not require
transfusion had a mean weight of 2.7 ± 0.9 kg.
The difference was statistically significant (t =
6.99; P < 0.0001). Sixty-three babies (56.2%) had
transfusions at the point of admission, while the
remaining 49 (43.8%) required blood after
admission.
Seventeen (15.2%) babies who had transfusion
were in-born, while the remaining 97 (84.8%)
were referred. The reasons for blood transfusion
included jaundice in 62 (55.4%), severe anemia in
42 (37.5%), PDA with anemia in three (2.7%), and
bleeding disorders in five (4.4%) babies.
Types of blood transfusion
Overall, 75 (66.7%) babies had EBT, 74 (66.1%)
had top-up transfusion, and six (8.0%) had fresh
plasma transfusion. Some babies had more than
one type of transfusion. Sixty-three (56.2%)
babies actually had multiple transfusions, while
49 (43.8%) had only one transfusion. Of the 75
EBT, 13 (17.3) were single volume procedures,
while 62 (82.7%) were double volume procedures.
All the double volume EBTs were done for severe
jaundice; none was done for severe sepsis. Thirty-
eight (33.9%) had only EBT, 37 (33.0%) had only
top-up transfusion, 31 (27.7%) had EBT with top-
up transfusion, and the remaining six (5.4%) had
EBT, top-up transfusion, and plasma transfusion.
The EBT rate was 1.4 per week or 6.2 per month.
Thirty-seven (49.3%) of the 75 babies who had
EBT subsequently developed anemia requiring
top-up transfusion.
[Table 1] describes the age of the babies at the
first transfusion. The peak age for blood
transfusion was between 97 and 168 hours of life.
Most babies had EBT between 97 and 168 hours
of life, while most babies had top-up transfusion
after the tenth day of life. These observations
were statistically significant in each case ( P
0.0001 and < 0.0001, respectively).
Table 1: Age of subjects at the first transfusion
Click here to view
In [Table 2] , a significantly higher proportion of
term infants had only one top-up transfusion,
while a significantly higher proportion of preterm
babies had three sessions of top-up transfusions.
Table 2: Number of transfusions distributed
according to maturity of subjects
Click here to view
Although a higher proportion of preterm babies
also had two sessions of EBT, the difference was
not significant.
Factors related to the use of blood transfusion
[Table 3] shows that significantly higher
proportions of male babies ( P < 0.0001), preterm
babies ( P = 0.001), and referred babies ( P
0.0001) had blood transfusion. Similarly, higher
proportions of babies with jaundice ( P < 0.0001),
apnea ( P = 0.001), and seizure ( P = 0.001) had
blood transfusion. However, there was no
significant difference in the proportion of babies
with and without respiratory distress or babies
with and without bacterial isolates on blood
culture, who also had blood transfusion. A
multivariate analysis [Table 4] showed that male
sex ( P < 0.0001), preterm birth ( P = 0.001),
referred status ( P < 0.0001), and presence of
jaundice ( P < 0.0001) were independent
determinants of blood transfusion requirement in
this cohort of babies. On the other hand, the
presence of apnea and seizures was not
independently associated with blood transfusion
use.
Table 3: Bivariate analysis of factors related to
blood transfusion requirement
Click here to view
Table 4: Multivariate analysis of possible
determinants of blood transfusion
Click here to view
Outcome
Twenty-nine (34.1%) of the 85 babies who died
during the hospitalization had blood transfusion,
as compared to 72 (25.7%) of the 280 babies
who were discharged home in good condition.
The difference was statistically insignificant (c 2 =
2.301; P = 0.129). Eight of the 75 (10.7%) babies
who had EBT died within 24 hours of the
procedure compared to six of the 37 (16.2%)
babies who had only top-up transfusion. The
difference was not statistically significant (c 2 =
0.698; P = 0.404).
Discussion
The findings in the present study showed that
most transfusions in our unit involved the use of
whole blood, partially packed cells, and plasma,
as we presently lack facilities to administer
concentrates of leucocytes or platelets. The
implication of this is that we are constrained to
use whole blood in situations where cell
concentrates would have been most ideal. This
should form a basis for advocacies to get health
planners and policy makers make provision for
such facilities in designated centers.
About one out of every four babies admitted to
our newborn unit required at least one
transfusion. This was relatively higher than the
rate of one out of every six, reported earlier from
Jos, Nigeria. [8] Similarly, the rate of 4.8
transfusions per week observed in the present
study was high indicating a great utilization of
blood and transfusion services in our unit. The
transfusion rate in our unit was also double the
rate of 2.4 transfusions per week previously
reported from Jos, Nigeria. [8] It is not certain
why we recorded double the rate of Jos at our
center, but we speculate that it might be due to
the fact that most of the babies studied in our
center were referred. Previous studies had shown
that referred babies were at a higher risk for
morbidities. [9] In the absence of regular training,
Traditional Birth Attendants are likely to lack the
appropriate, but simple skills, which could prevent
bleeding during delivery of babies.
Half of the transfusions in our unit took place
during the first week of life, thus, indicating the
role of perinatal events in the conditions
warranting transfusion. In the same vein, EBT was
most commonly carried out toward the end of the
first week of life. Thus, jaundice was obviously
the most prominent indication for transfusion in
this study. This implied that aggressive
prevention of severe hyperbilirubinemia using
effective phototherapy would prevent the bulk of
EBT. [6] Half of the babies who had EBT in the
present study subsequently had anemia, requiring
top-up transfusion. This is most likely related to
the ongoing hemolysis from the primary causes of
jaundice such as blood group incompatibilities.
Invasive bacterial infection following umbilical
cannulation during EBT may also predispose a
baby to hemolysis. It is also plausible that poor
mixing of blood used for the procedure may cause
sedimentation of cells, as also part transfusion of
plasma instead of whole blood. Some
practitioners routinely commence prophylactic
antibiotics following EBT, to prevent secondary
invasive bacterial infection, but this practice
remains controversial. [10] Therefore, aside from
adequate mixing of blood during EBT, there may
be very little that can be done to prevent post-
EBT anemia, especially when it is due to ongoing
hemolysis.
More than half of the babies studied in the
present report had multiple transfusions, unlike
29% previously reported from Jos, Nigeria. [8]
Further to this is the observation that preterm
babies often require multiple transfusions
compared to term babies. This might be related
to the greater physiological predisposition of
preterm babies to anemia compared to term
babies. [11] However, repeated transfusions of
preterm infants depresses endogenous
erythropoietin production and further suppresses
the bone marrow. [12]
Unfortunately, the scarcity of recombinant
erythropoietin in our part of the world leaves
practitioners with no other option apart from
multiple transfusions and the persistence of
anemia, among these babies. The higher number
of transfusions in the present study might also be
due to our practice of transfusing anemic babies
serially, usually in two or three stages, depending
on the PCV at the outset. This is far from the
ideal, but we are constrained to do this because
of the hindrances we encounter in getting blood
from the blood bank every time we need it.
Therefore, it is important to suggest a review or
modification of the existing guidelines on neonatal
transfusion, in consonance with the peculiarities
of the under-resourced parts of the world.
Bivariate analysis shows that the presence of
jaundice, apnea, and seizures are significantly
associated with the need to transfuse blood. The
relationship between seizures, apnea, and
transfusion may be explained in terms of their
characteristics as possible manifestations of
systemic hypoxemia. As a matter of fact,
transfusion would increase the partial pressure of
oxygen, and in turn, oxygen delivery to the
tissues, in such dire emergencies. Therefore,
attention should be focused on the prevention of
common clinical conditions associated with
newborn seizures [13] and apnea, as a way of
minimizing the need for transfusion. In addition, in
the present study, the independent contribution of
the presence of jaundice to the need for neonatal
transfusion agrees with the earlier submission
that jaundice is the leading indication for
transfusion. This may also be related to the role
of male sex, as severe hyperbilirubinemia has
been reported to be more common among males,
in our center. [14]
Conclusions
The transfusion rate in our newborn unit was high
and most transfusions take place within the first
week of life. In addition, we only transfuse whole
blood, partially packed cells, and plasma, but
more blood products would be used as laboratory
facilities improve with time. Efforts are required to
prevent severe hyperbilirubinemia as well as
conditions that may cause seizures and apnea, so
as to reduce the requirement for transfusions in
newborn units. The retrospective nature of this
study is acknowledged as a limitation. Therefore,
larger prospective studies are definitely desirable.
This study has formed a basis for conducting an
audit of blood use in newborn units in the
developed world.
References
1. Gorst DW. Haemorrhagic disorders and the use of
blood products. In: Hendrickse RG, Barr DG,
Matthews TS, editors. Paediatrics in the Tropics.
1st ed, Oxford: Blackwell Scientific Publications;
1991. p. 360-72.
2. Strauss RG. Transfusion therapy in neonates. Am
J Dis Child 1991;145: 904.
[ PUBMED]
3. Shannon K. Anaemia of prematurity: Progress and
prospects. Am J Pediatr HaematolOncol
1990;12:14.
4. Ogunlesi TA, Ogunfowora OB, Adekanmbi AF,
Fetuga MB, Runsewe-Abiodun TI, Ogundeyi MM.
Neonatal mortality at Olabisi Onabanjo University
Teaching Hospital, Sagamu. Niger J Paediatr
2006;33:40-6.
5. Ogundeyi MM, Ogunlesi TA. Approach to the
bleeding neonate. Niger J Med
2009;18:238-43.
[ PUBMED]
6. Owa JA, Ogunlesi TA. Why we are still doing so
many exchange blood transfusions for neonatal
jaundice in Nigeria. World J Paediatr
2009;5:51-5.
7. Enosolease ME, Imarengiaye CO, Awodu OA.
Donor blood procurement and utilization at the
University of Benin Teaching Hospital, Benin City.
Afr J Reprod Health 2004;8:59-63.
[ PUBMED]
8. Pam S, Bode-Thomas F, Joseph DE, Akor F,
Ejeliogu E. Which babies get blood in Jos,
Nigeria? Paediatr Haematol Oncol
2004;21:669-76.
9. Owa JA, Osinaike AI. Neonatal morbidity and
mortality in Nigeria. Indian J Pediatr
1998;65:441-9.
[ PUBMED]
10. Jackson JC. Adverse events associated with
exchange transfusion in healthy and ill newborns.
Pediatrics 1997;99:5.
11. Strauss G. Anemia of prematurity:
Pathophysiology and treatment. Blood Rev
2010;24:
12. Brown M, Berman E, Luckey D. Prediction of the
need for transfusion during anemia of prematurity.
J Paediatr 1990;116:773.
13. Ogunlesi TA, Adekanmbi AF, Fetuga MB,
Ogunfowora OB, Ogundeyi MM. Risk factors for
mortality in neonatal seizure in a Nigerian
Newborn Unit. South Afr J Child Health
2007;1:64-7.
14. Ogunlesi TA, Ogunfowora OB. Predictors of acute
bilirubin encephalopathy among term Nigerian
infants with moderate-to-severe
hyperbilirubinaemia. J Trop Pediatr
2011;57:80-6

Credit: TA Ogunlesi , OB Ogunfowora
Department of Pediatrics, Olabisi Onabanjo
University Teaching Hospital, Sagamu, Nigeria

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Clinical case of the week

A 14 years old gentleman walk into my consulting room with 2 month history of weight loss. All parameters conferred a healthy status as demonstrated by his father. The young man was in college grade 5 with previous hospital visit of 102kg now 76kg. Nil hx of chest disease to pin in tuberculosis. Nil exposure to HIV.

Patient was sent to do the following investigations which include FBC*FBS*Urinalysis*Retroviral screening.

Result
FBS was 560mg/ DL
Urinalysis was massive ketonuria with traces for protein and glucose.
RVS negative.

Further history prove nil family hx of diabetes. Patient was subsequently admitted and treated as a case of Type 1 DM with DKA.
Had rehydration with 0.9%saline and a shot of soluble insulin. The following day FBS was 148mg/dl.
He was counselled on diet modification and life style before discharge.

Dr yakubu

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Stroke made simple

Stroke is a brain disease. I can as well call it a cerebrovascular disease; we are still saying the same thing. For the clinician and health givers you can identify a sufferer of stroke by applying the FAST instrumentology.
F stand for facial muscle. The face has muscles 20 in numbers with good innervation both sensory and motor supplied by trigeminal nerve and facial nerve respectively. Here just look out for mouth deviation. Drooling of saliva.
A stand for arm. Damage to corticospinal tract can result into lower motor or upper motor neuron lessions. Here look for hypotonia ie flaccid appearance of the arm or hypertonia ie rigid appearance of the arm.
S stand speech. Various types of speech defects can arise eg aphasia which can be motor or sensory.
T talk to your doctor as soon as possible. To identify if this stroke is non hemorrhagic or hemorrhagic.

Dr yakubu.

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Homni: The new superorganism taking over Earth

This myth is closely related to my Yoruba mythology of Obantala.

Wandering Gaia

In Ancient Greek mythology, the Earth Goddess Gaia had nine titan sons, who attempted to control not just the Earth, but the entire Universe. I’d like to introduce another. It’s a new creature who emerged only in recent decades. But it’s a creature who is already as influential over life on the planet as the phytoplankton or forests that regulate global temperature, the weather and the air we breathe.

That new creature is us, or more precisely, what humanity is becoming. The entirety of our species, Homo sapiens, is evolving into a superorganism; I’ll call this new life force Homo omnis, or ‘Homni’.

We have now become the dominant force shaping our planet. Some say that because of our actions we have entered a new geological epoch: the Anthropocene, or the age of man. Homni is a product of this age, a product of human industrialisation, population…

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