CLIENT CARE STUDY OF MISS. R.

T WITH SYSTEMIC LUPUS

ERYTHEMATOSUS

CHAPTER ONE
1.0 INTRODUCTION

This is a care study of Miss. R.T a 22 year old woman transferred to Federal Medical Center,
Abeokuta (FMCA) on 7th February, 2023 at 2:00pm because of seizures and a lesion in the brain.
She is a native of Ekiti State but had lived most of her life in Ogun State. She lived with her
husband and was not employed because of her illness. Both of her parents had died of human
immunodeficiency virus (HIV) infection.

For several months, the patient had experienced intermittent numbness of her tongue and slurred
speech. Two weeks before admission, she was hospitalized elsewhere because of fever (peak
temperature, 39.4°C) and joint pain. A diagnosis of lupus flare was made, her symptoms
responded to dexamethasone, and she was discharged home.

Over the last 2 weeks, the patient’s fatigue worsened, and she began experiencing dyspnea on
exertion after 3 minutes of walking. She started feeling feverish every morning and was not
eating much due to loss of appetite. She called her physician who advised her to go to the
emergency department (ETR) for further evaluation. She was admitted from the ETR for further
workup of her symptoms.

On examination, the patient was not in acute distress and answered questions appropriately. The
vital signs read thus;

Temperature: 37.4°C

Pulse: 100 beats per minute

Blood pressure: 98/63 mm Hg

Respiration: 16 per minute

Oxygen saturation: 100%

She had oral thrush and a blistering lesion consistent with herpes on her lower lip. The remainder
of the general physical examination was normal. On neurologic examination, she was alert and
oriented, with normal attention and speech, short-term memory was mildly impaired. Laboratory
tests were done. The patient continued to have joint pain and severe headaches and required
narcotics for pain control.

She was placed on admission. She was admitted into the Female Medical Ward where she spent
30 days. After being afebrile, the patient was discharged home against doctor’s advice (DAMA)
with instructions to follow up with rheumatology and primary care to obtain the results of
pending studies and have any additional workup as an outpatient.

Three weeks after hospital discharge, the patient returned to the ETR with a 1-day history of left
arm, leg, and face weakness with a mild headache and nausea. She reported that earlier that
morning she had transient difficulty speaking. She had been compliant with all her medications
and had been feeling better until 1 day ago. Physical exam revealed left-sided facial droop,
decreased strength in the left upper and lower extremities, symmetric reflexes, and an unsteady,
wide-based gait.

Repeated MRI of the brain with T2-weighted and fluid-attenuated inversion recovery (FLAIR)
images the next day confirmed the presence of an area of hyper intensity involving the posterior
left frontal and parietal lobe white matter, with patchy enhancement at the superior margin of the
lesion. Our patient received a CT head that was normal.

She was readmitted. On the 10th hospital day, the patient had a headache and was lethargic. She
followed commands but did not speak. Strength in the right arm and leg and muscle tone in the
right arm were decreased. An MRI of the brain showed an increase in the size and number of
lesions and possible leptomeningeal involvement. A transesophageal echocardiogram obtained
the next day showed no vegetation. The patient became progressively more somnolent. A
magnetic resonance cerebral angiogram performed on the 43rd hospital day showed progression
of the lesions.

On the 22nd day of readmission, the patient was obtunded, with decorticate posturing and
increased respiratory effort, the trachea was intubated, and she was transferred to the neurologic
intensive care unit. 
On the 24th hospital day, the patient's pupils were fixed and dilated. CT scanning of the brain
showed new areas of hypo attenuation in the right hemisphere and transtentorial and uncal
herniation. An intracranial pressure monitor was placed, and the intracranial pressure on Licox
insertion was 50 mm H2O. Despite therapy with mannitol and induced hypertension, the patient's
intracranial pressure increased to 130 mm H2O, and the cerebral perfusion pressure was less than
10 mm Hg. She met clinical criteria for brain death by the evening of that day.

An autopsy was performed.

1.1 The Developmental Milestone (Birth history, Immunization status):

She was born through cesarean section with no complication at a private hospital. She has
completed all her immunization schedule.

1.2 Past Medical History

The patient had a history of depression. She had been treated for narcotic and alcohol
dependency in the past, but did not currently use either intravenous drugs or alcohol to excess.
She smoked one pack of cigarettes daily.  Both of her parents had died of human
immunodeficiency virus (HIV) infection. She was allergic to sulfa medications. In addition to
antibiotics and diphenylhydantoin, her medications included fluoxetine, pantoprazole,
prednisone (30 mg daily), lorazepam, a nicotine patch, and a fentanyl patch for the pain in her
arm.

1.3 Social History

She was an alcoholic in the past and smoked one pack of cigarettes daily. She was a party lover
and had a fun social life.

1.4 Family History

No family history of autoimmune disease. Both of her parents had died of human
immunodeficiency virus (HIV) infection.

1.5 Present Medical History

The patient is a 22-year-old female who has been admitted to the Federal Medical Center
Abeokuta with the diagnosis of systematic lupus erythematosus (SLE). She was transferred from
a hospital because of seizures and a lesion in the brain. A diagnosis of systemic lupus
erythematosus (SLE) had been made 6 years earlier, associated with polyarthritis, myalgia, malar
rash, facial swelling, photosensitivity, pancytopenia, fevers, Raynaud's syndrome, pericardial and
pleural effusion, membranous glomerulonephritis, and alopecia. She had been treated
continuously with corticosteroids, with the addition of methotrexate, azathioprine,
mycophenolate, leflunomide, and etanercept at various times, and dapsone prophylaxis. Her
compliance with her medication regimen had been poor, and she had stopped taking dapsone 6
months earlier.

For several months, the patient had experienced intermittent numbness of her tongue and slurred
speech. Two weeks before admission, she was hospitalized elsewhere because of fever (peak
temperature, 39.4°C) and joint pain. A diagnosis of lupus flare was made, her symptoms
responded to dexamethasone, and she was discharged home.

Six days before admission to this hospital, she had transient tingling and shaking of her right
arm. The next day, she had a generalized tonic–clonic seizure and was admitted to another
hospital in Sango Ota. Treatment was started, and no additional seizures occurred. Magnetic
resonance imaging (MRI) of the brain revealed a small ovoid lesion in the left parietal lobe. She

The tingling in her right arm continued, and pain and weakness developed. A repeated MRI scan
on the fourth hospital day showed enlargement of the lesion in the brain, with vasogenic edema
involving the subcortical white matter of the left frontal and parietal lobes. Treatment with
ceftriaxone and acyclovir was started. The patient was transferred to this hospital, Federal
Medical Center Abeokuta 6 days after admission to the other hospital.

She was admitted into Female Medical Ward for more care and observation.

1.6 Investigation and Results:

 Double-stranded DNA >400

 SSA (Ro) positive, SSB (La) negative
 Low C3, low C4
 Lupus anticoagulant positive

Complete Blood Count (CBC):

  White blood cell count (WBC): 2.8 x 103/µL*
 White count differential: 61% segmented neutrophils, 29% lymphocytes*, 8%
monocytes, no eosinophils
 Hemoglobin: 9.0 g/dL*
 Hematocrit: 25.7%*
 Mean cell volume: 86 fL
 Platelets: 210/µL

Comprehensive metabolic panel:

 Sodium: 133 mEq/L*

 Potassium: 4.2 mEq/L
 Chloride: 105 mEq/L
 Bicarbonate: 21 mEq/L
 Blood urea nitrogen: 17 mg/dL
 Creatinine: 0.7 mg/dL
 Total protein: 7.8 g/dL
 Albumin: 2.8 g/dL*
 Total bilirubin 0.6 mg/dL
 Aspartate aminotransferase: 32 U/L
 Alanine aminotransferase: 36 U/L
 Alkaline phosphatase: 50 U/L

Urinalysis:

 30 mg/dL protein*
 No blood
 WBC: 3+ hpf*
 Red blood cells: none

*Abnormal values

 Two-view chest X-ray: No cardiopulmonary process

  Electrocardiogram: Sinus tachycardia

1.7 Plan

Admit to Female medical ward

Hydroxychloroquine 400 mg daily

Diphenylhydantoin

Fluoxetine

Pantoprazole

Prednisone (30 mg daily)

Lorazepam

A nicotine patch

A fentanyl patch

Levetiracetam

Pyrimethamine

Leucovorin (folinic acid)

Dapsone

Ampicillin

1.8 OBJECTIVES OF THE STUDY

1. To have comprehensive knowledge and skills about the care of patients with Lupus
disease.
2. To provide information about patient’s condition, treatment and prognosis.
3. To give information to the patient and the family on the causes, treatment and prevention
of systematic lupus erythematosus.
4. To increase clients’ awareness on medication compliance and positive attitude to early
recovery.
 CHAPTER TWO

LITERATURE REVIEW

2.0 DEFINITION

Lupus is a long-term condition that can cause inflammation in the skin, organs, and in various
other places in the body.

It’s an autoimmune condition. The immune system, which normally protects us against infection
and illness, starts to attack the body’s own tissues instead.

Lupus can be difficult to diagnose because its signs and symptoms often mimic those of other
ailments. The most distinctive sign of lupus a facial rash that resembles the wings of a butterfly
unfolding across both cheeks occurs in many but not all cases of lupus (Murphy, Isenberg, 2013).

Some people are born with a tendency toward developing lupus, which may be triggered by
infections, certain drugs or even sunlight. While there's no cure for lupus, treatments can help
control symptoms (Jacobson K, et al., 2016).

There are several different types of lupus:

 Systemic lupus erythematosus (SLE): This can affect almost any organ or body system. It
mostly affects your skin and joints, but sometimes it can affect your heart, lungs, kidneys
or brain.

 Discoid lupus: This is a milder illness, with most people having only skin symptoms.

 Subacute cutaneous lupus: This is even milder and mostly causes rashes and joint pain.

 Drug induced lupus: This is a reaction to a medicine. It fades away after you stop taking
the medicine that triggered your lupus.

 Neonatal lupus: This can occur if lupus-causing antibodies (a type of protein in your
blood) transfer from the mother to the baby during pregnancy. They can cause a rash,
liver, blood and sometimes heart problems. Neonatal lupus usually resolves about 6 to 12
months after birth when the antibodies degrade.
Most people with lupus have mild symptoms. About 9 in 10 are female and the majority develop
the condition between 15 and 45 years of age (Okpechi, 2013).

2.1 HISTORY OF LUPUS

The history of lupus can be divided into three periods: classical, neoclassical, and modern.  In
each period, research and documentation advanced the understanding and diagnosis of
systematic lupus erythematosus, leading to its classification as an autoimmune disease in 1851,
and to the various diagnostic options and treatments now available to people with systematic
lupus erythematosus. The advances made by medical science in the diagnosis and treatment of
systematic lupus erythematosus have dramatically improved the life expectancy of a person
diagnosed with lupus (Davis, Reimold, 2017).

2.1.0 Etymology

There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for
"wolf", and in Medieval Latin was also used to refer to a disease of the skin, and "erythematosus"
is derived from ἐρύθημα, Ancient Greek for "redness of the skin". All explanations originate
with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose
and cheeks. The reason the term lupus was used to describe this disease comes from the mid-
19th century. Many diseases that caused ulceration or necrosis were given the term "lupus" due
to the wound being reminiscent of a wolf's bite. This is similar to the naming of lupus vulgaris or
chronic facial tuberculosis, where the lesions are ragged and punched out and are said to
resemble the bite of a wolf (Goldman, et al., 2019).

2.1.1 Lupus in the classical period (1230-1856)

The history of lupus during the classical period was reviewed by Smith and Cyr in 1988. Of note
are the derivation of the term lupus and the clinical descriptions of the cutaneous lesions of lupus
vulgaris, lupus profundus, discoid lupus, and the photosensitive nature of the malar or butterfly
rash (Ahearn, Joseph, 2014).

The word ‘lupus’ (Latin for ‘wolf’) is attributed to the thirteenth century physician Rogerius who
used it to describe erosive facial lesions that were reminiscent of a wolf's bite. Classical
descriptions of the various dermatologic features of lupus were made by Thomas Bateman, a
student of the British dermatologist Robert William, in the early nineteenth century; Cazenave, a
student of the French dermatologist Laurent Biett, in the mid-nineteenth century; and Moriz
Kaposi (born Moriz Kohn), student and son-in-law of the Austrian dermatologist Ferdinand von
Hebra, in the late nineteenth century ( Kim, et al., 2013).

The lesions now referred to as discoid lupus were described in 1833 by Cazenave under the term
“erythema centrifugum,” while the butterfly distribution of the facial rash was noted by von
Hebra in 1846. The first published illustrations of lupus erythematosus were included in von
Hebra's text, Atlas of Skin Diseases, published in 1856.

2.1.2 Lupus in the neoclassical period (1872- 1948)

The Neoclassical era of the history of lupus began in 1872 when Kaposi first described the
systemic nature of the disorder: “...experience has shown that lupus erythematosus ... may be
attended by altogether more severe pathological changes, and even dangerous
constitutional  symptoms may be intimately associated with the process in question, and that
death may result from conditions which must be considered to arise from the local malady.”

Kaposi proposed that there were two types of lupus erythematosus; the discoid form and a
disseminated (systemic) form (Calderaro, Ferreira, 2012).

Furthermore, he enumerated various signs and symptoms which characterized the systemic form,
including: 

 subcutaneous nodules

 arthritis with synovial hypertrophy of both small and large joints

 lymphadenopathy

 fever

 weight loss

 anemia

 central nervous system involvement

The existence of a systemic form of lupus was firmly established in 1904 by the work of Osler in
Baltimore and Jadassohn in Vienna. Over the next thirty years, pathologic studies documented
the existence of nonbacterial verrucous endocarditis (Libman-Sacks disease) and wire-loop
lesions in individuals with glomerulonephritis; such observations at the autopsy table led to the
construct of collagen disease proposed by Kemperer and colleagues in 1941. This terminology,
‘collagen vascular disease,’ persists in usage more than seventy years after its introduction
(Grossman, et al., 2016).

2.1.3 Lupus in the modern era (1948-present)

The sentinel event which heralded the modern era was the discovery of the LE cell by Hargraves
and colleagues in 1948. The investigators observed these cells in the bone marrow of individuals
with acute disseminated lupus erythematosus and postulated that the cell “...is the result
of...phagocytosis of free nuclear material with a resulting round vacuole containing this
partially digested and lysed nuclear material...”.

This discovery ushered in the present era of the application of immunology to the study of lupus
erythematosus; it also allowed the diagnosis of individuals with much milder forms of the
disease. This possibility, coupled with the discovery of cortisone as a treatment, changed the
natural history of lupus as it was known prior to that time (Gordon, et al., 2014).

Two other immunologic markers were recognized in the 1950s as being associated with lupus:
the biologic false-positive test for syphilis and the immunofluorescent test for antinuclear
antibodies. Moore, working in Baltimore, demonstrated that systemic lupus developed in 7
percent of 148 individuals with chronic false-positive tests for syphilis and that a further 30
percent had symptoms consistent with collagen disease. 

Friou applied the technique of indirect immunofluorescence to demonstrate the presence of

antinuclear antibodies in the blood of individuals with systemic lupus. Subsequently, there was
the recognition of antibodies to deoxyribonucleic acid (DNA) and the description of antibodies
to extractable nuclear antigens (nuclear ribonucleoprotein [nRNP], Sm, Ro, La), and
anticardiolipin antibodies; these autoantibodies are useful in describing clinical subsets and
understanding the etiopathogenesis of lupus (Atallah, 2013).
2.1.4 First animal model developed

Two other major advances in the modern era have been the development of animal models of
lupus and the recognition of the role of genetic predisposition to the development of lupus. The
first animal model of systemic lupus was the F1 hybrid New Zealand Black/New Zealand White
mouse. 

This murine (mouse) model has provided many insights into the immunopathogenesis of
autoantibody formation, mechanisms of immunologic tolerance, the development of
glomerulonephritis, the role of sex hormones in modulating the course of disease, and evaluation
of treatments including recently developed biologic agents such as anti-CD4, among others. 

Other animal models that have been used to study systemic lupus include the BXSB and
MRL/lpr mice, and the naturally occurring syndrome of lupus in dogs (Oguro, 2016).   

2.1.5 Genetic component recognized  

The familial occurrence of systemic lupus was first noted by Leonhardt in 1954 and later studies
by Arnett and Shulman at Johns Hopkins. Subsequently, familial aggregation of lupus, the
concordance of lupus in monozygotic twin pairs, and the association of genetic markers with
lupus have been described over the past twenty years. 

Molecular biology techniques have been applied to the study of human lymphocyte antigen
(HLA) Class II genes to determine specific amino acid sequences in these cell surface molecules
that are involved in antigen presentation to T-helper cells in individuals with lupus. These studies
have resulted in the identification of genetic-serologic subsets of systemic lupus that complement
the clinico-serologic subsets noted earlier. 

It is hoped by investigators working in this field that these studies will lead to the identification
of etiologic factors (e.g., viral antigens/proteins) in lupus (Nab, et al., 2021).

Over the last decade or so, we have witnessed significant advances in the understanding of the
genetic basis of lupus, and of the immunological derangements which lead to the clinical
manifestations of the disease. 

Advances have been made in the assessment of the impact of the disease in general, and in
minority population groups, in particular and efforts are being made towards defining lupus
biomarkers which may help both to predict disease outcome and to guide treatments (Khosravi,
2012).

2.1.6 Lupus therapies then and now 

Finally, no discussion of the history of lupus is complete without a review of the development of
therapy. Payne, in 1894, first reported the usefulness of quinine in the treatment of lupus. Four
years later, the use of salicylates in conjunction with quinine was also noted to be of benefit. 

Cortisone/corticosteroids were introduced for the treatment of lupus in the middle part of the
20th century by Hench. Presently, corticosteroids are the primary therapy for almost all
individuals with lupus.

Antimalarial, used in the past principally for lupus skin and joint involvement, are now
recognized to prevent the occurrence of flares, the accumulation of damage, and the occurrence
of early mortality ( Dammacco, 2018).

Cytotoxic/immunosuppressive drugs are used for glomerulonephritis, systemic vasculitis, and

other severe life-threatening manifestations of lupus. Newer biologic agents are now used, either
off-label or after approval by regulatory agencies in the U.S., Europe, and other countries. 

Other potential drug products are being investigated as new disease pathways are being
discovered.

2.2 SIGNS AND SYMPTOMS

Symptoms of lupus can include:

 Joint pain
 Muscle pain
 Rashes
 Fever
 Sensitivity to sunlight
 Hair loss
 Mouth sores
 Dry eyes
 Fatigue
  Chest pain
 Stomach pain
 Shortness of breath
 Swollen glands
 Headaches
 Confusion
 Depression
 Issues with the kidneys, heart or lungs
 Seizures
 Blood clots
 Anemia
 Raynaud’s phenomenon

2.2.1 What are the symptoms of lupus in women?

A majority of the people diagnosed with lupus are women. Women tend to experience the
general symptoms of lupus, but they can also have complications that impact various parts of the
body. These complications can include kidney problems (more commonly seen in African-
American and Hispanic women than other groups), osteoporosis and heart disease.

2.3 CAUSES OF LUPUS

It’s unclear why some people get lupus. It’s thought to be the result of a mix of genetic,
hormonal and environmental factors. For example, the immune system makes proteins called
antibodies that fight infection. In lupus, the body also makes autoantibodies that are similar, but
attack the body’s own tissues instead. We’re not sure why this happens. There are some factors
that probably make this more likely:

 An illness or infection

 Strong sunlight

 Hormonal changes, such as during puberty

 Smoking cigarettes
  Some medications – this is known as drug-induced lupus, and this usually gets better
when people come off the medication that caused it.

Lupus isn’t directly passed on from a parent to their children, but if you have a close relative
with lupus then you may be at increased risk of developing it. Lupus isn’t contagious, so you
can’t catch it from anyone else.

2.4 PATHOPHYSIOLOGY

Systemic lupus erythematosus is triggered by environmental factors that are unknown. In

systemic lupus erythematosus, the body's immune system produces antibodies against self-
protein, particularly against proteins in the cell nucleus. These antibody attacks are the
immediate cause of systemic lupus erythematosus (Rahman, Isenberg, 2008).

Systemic lupus erythematosus is a chronic inflammatory disease believed to be a type III

hypersensitivity response with potential type II involvement (Crow, 2008). Reticulate and
stellate acral pigmentation should be considered a possible manifestation of SLE and high titers
of anti-cardiolipin antibodies, or a consequence of therapy (Scheinfeld, et al., 2003).

People with Systemic lupus erythematosus have intense polyclonal B-cell activation, with a
population shift towards immature B cells. Memory B cells with increased CD27+/IgD—are less
susceptible to immunosuppression. CD27-/IgD- memory B cells are associated with increased
disease activity and renal lupus. T cells, which regulate B-cell responses and infiltrate target
tissues, have defects in signaling, adhesion, co-stimulation, gene transcription, and alternative
splicing. The cytokines B-lymphocyte stimulator (BLyS), also known as B-cell activating factor
(BAFF), interleukin 6, interleukin 17, interleukin 18, type I interferons, and tumor necrosis factor
α (TNFα) are involved in the inflammatory process and are potential therapeutic targets
(Lisnevskaia, et al., 2014).

Systemic lupus erythematosus is associated with low C3 levels in the complement system
(University of Rochester Medical Center, 2016).

Impaired clearance of dying cells is a potential pathway for the development of this
systemic autoimmune disease. This includes deficient phagocytic activity, impaired lysosomal
degradation, and scant serum components in addition to increased apoptosis.
Systemic lupus erythematosus is associated with defects in apoptotic clearance, and the
damaging effects caused by apoptotic debris. Early apoptotic cells express “eat-me” signals, of
cell-surface proteins such as phosphatidylserine, that prompt immune cells to engulf them.
Apoptotic cells also express find-me signals to attract macrophages and dendritic cells. When
apoptotic material is not removed correctly by phagocytes, they are captured instead by antigen-
presenting cells, which leads to the development of antinuclear antibodies (Lisnevskaia, et al.,
2014).

Recent research has found an association between certain people with lupus (especially those
with lupus nephritis) and an impairment in degrading neutrophil extracellular traps (NETs).
These were due to DNAse1 inhibiting factors, or NET protecting factors in people's serum,
rather than abnormalities in the DNAse1 itself (Hakkim, et al., 2010). DNAse1 mutations in
lupus have so far only been found in some Japanese cohorts (Yasutomo, et al., 2001).

Autoimmunity possibly results from the extended exposure to nuclear and intracellular

autoantigens derived from late apoptotic and secondary necrotic cells. B and T cell tolerance for
apoptotic cells is abrogated, and the lymphocytes get activated by these
autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A
clearance deficiency in the skin for apoptotic cells has also been observed in people with
cutaneous lupus erythematosus (CLE) (Gaipl, et al., 2007).

2.5 DIAGNOSIC INVESTIGATIONS

It can be difficult to make a diagnosis of lupus because it doesn’t affect any two people exactly
the same. There are also many other conditions it resembles.

However, the earlier someone is diagnosed with lupus and treatment is started, the better their
chances of keeping this condition under control.

A diagnosis of lupus is made based on symptoms, a physical examination and blood tests.

There are a number of tests that can help lead to a diagnosis of lupus or rule it out. These can
then be used to monitor how well treatments are working. Some of these tests are:
Anti-nuclear antibody (ANA) test

About 95% of people with lupus test strongly positive for anti-nuclear antibodies (ANA), but the
test can sometimes be positive in people who don’t have lupus, so it can’t confirm the diagnosis
(Ther Clin Risk Manag. 2011).

Anti-double-stranded DNA (anti-dsDNA) antibody test

About 70% of people with lupus have these antibodies. A positive test means that lupus is highly
likely as the test is hardly ever positive in people who don’t have lupus. Levels of this antibody
can go up as the lupus becomes more active and will go down if treatment is effective (Buyon, et
al., 2003).

Anti-Ro antibody test

If an individual test positive for this antibody he/she may be more likely to get skin rashes and
suffer from dry eyes or a dry mouth, known as Sjögren’s syndrome. Rarely, this antibody can
pass across the placenta during pregnancy this is the organ that passes food through from a
pregnant woman to her unborn baby. If she carry the anti-Ro antibody and decide to have a baby,
the pregnancy will be more closely monitored.

Antiphospholipid antibody test

A positive test for these antibodies may mean an increased risk of miscarriage and developing
blood clots. These antibodies can come and go so these tests can be repeated.

Kidney and liver function tests

These include blood and urine tests, which are carried out regularly so any problems caused by
the lupus or by drug treatment can be picked up and dealt with quickly.

A simple urine test can show if there’s protein or blood in the urine. This test can help doctors
recognize a problem in the kidneys at an early stage. Further tests may be carried out if
necessary.

Blood cell counts

Blood cell counts can help to show whether the bone marrow is affected, either by the condition
or the drugs.
Scans and x-rays

Different types of scans and x-rays can assess how well your heart, lungs, liver and spleen are
working.

2.6 PREVENTION

For people who have already received a diagnosis for lupus, there are a few preventative
measures one can take to reduce how often you experience a flare-up and the severity of the
symptoms (Kaul, et al. 2016).

Environmental Exposure

Certain environmental factors can affect the risk of developing lupus. Research has shown that
lupus is linked to:

 Using or being exposed to ultraviolet (UV) light 

 Current or past history of smoking cigarettes

 Exposure to silica dust commonly found in cleaning powders, soil, pottery materials, and
cement

To reduce environmental triggers, an individual may consider (American Academy of

Dermatology Association):

 Protecting your skin: Limit exposure to the sun and UV light. Seek shaded areas when
outdoors, wear sun-protective clothing (such as long-sleeved shirts, sunglasses, and wide-
brimmed hats), and wear sunscreen that blocks UV-A and UV-B with a sun protection
factor (SPF) greater than 55. Fluorescent, compact fluorescent, and halogen light bulbs
may also emit some UV light. Replace these bulbs with LED or incandescent bulbs.

 Quitting smoking: Smoking can trigger lupus flares. If one smokes cigarettes, try to quit
smoking or speak to healthcare provider about ways to reduce tobacco intake. 

 Limiting exposure to toxins: Look for household products that do not contain silica
dust. If you are around people who smoke, secondhand smoke can also trigger a flare-up.
Try your best to find environments that limit your exposure to secondhand smoke or
request your friends and family to not smoke in your home or car. 
Nutrition and Dietary Choices

Previous studies indicate that some nutrition and dietary factors may play a role in the
development of lupus. Some experts suggest that eating foods like fatty fish, olive oil, and
cooked vegetables can soothe symptoms of chronic conditions like lupus. Coffee has been shown
to decrease disease activity in lupus and even lower cytokine (proteins in the immune system that
are important to cell signaling) levels (Barbhaiya, et al., 2016).

There isn’t a special diet that people with lupus should eat. However, the Centers for Disease
Control and Prevention (CDC) explain that it’s important to maintain a well-balanced diet made
up of fruits, vegetables, and whole grains. It may also be helpful to eat moderate amounts of lean
protein like beans, fish, and chicken (Wallace, et al. 2022).

2.7 MANAGEMENT

There is no cure for lupus, but most people are able to manage their symptoms and enjoy a good
quality of life. This usually requires a combination of medicines and maintaining a healthy
lifestyle.

Treatment for lupus is very individual and depends on the severity of the disease and the organs
involved. You might need to try a few different medicines to see what works. The doctor may
refer you to a rheumatologist (a specialist in joint inflammation).

Medications

Medicines that can control symptoms of lupus include:

 Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications can help reduce

pain and swelling in joints and muscles.

 Corticosteroids: Corticosteroids, namely prednisone, can reduce swelling and pain and

calm the immune system.

 Antimalarial drugs: Studies found that taking antimalarial drugs, which are used to
treat malaria, can stop lupus flares. These drugs can treat joint pain, skin rashes, fatigue,
and lung inflammation.
  BLyS-specific inhibitors: These drugs limit abnormal immune cells found in those with
lupus, which can reduce symptoms.

 Chemotherapy/immunosuppressant: For severe cases of lupus that especially affect

major organs, these medicines may be used to suppress the immune system.

Lupus alternative treatments

Some people use complementary or alternative treatments to ease lupus symptoms. But there’s
no proof that any of them treat or cure the disease. Some herbal supplements can even interact
with prescription drugs or make your symptoms worse. Talk to your doctor before starting any
treatments.

Research has found some benefits with certain treatments, including:

 Vitamins and supplements. Vitamins C and D and antioxidants may help with

symptoms and boost your overall health. The omega-3 fatty acids in fish oil also might be
useful.

 Dehydroepiandrosterone (DHEA). This hormone may lessen symptom flare-ups but

can also have mild side effects like acne or hair growth.

 Acupuncture. Small studies show that acupuncture can lessen pain and fatigue.

 Mind-body therapy. Meditation and cognitive behavioral therapy could ease pain as

well as mental health issues like depression and anxiety.

Lifestyle Changes

Some daily changes can ease symptoms and improve your quality of life:

 Exercise: Low-impact exercises such as walking, swimming, and biking can help you
keep muscle and lower your chances of osteoporosis (thinning of the bones). It might also
boost your mood.
 Get enough rest: Pace yourself. Follow periods of activity with periods of rest.
 Eat well: Get a healthy, well-balanced diet.
 Avoid alcohol: Alcohol can interact with your medications to cause stomach or intestinal
problems, including ulcers.
  Don't smoke: Smoking can hurt blood flow and make lupus symptoms worse. Tobacco
smoke also harms your heart, lungs, and stomach.
 Play it safe in the sun: Limit your time in sunlight, especially between 10 a.m. and 2 p.m.
Wear sunglasses, a hat, and sunscreen when you’re outdoors.
 Treat fevers: Take care of high temperatures right away. A fever may be a sign of an
infection or a lupus flare-up.
 Be a partner in your care: Work toward an honest and open relationship with your doctor.
Be patient. It often takes time to find the medication and dosage that works best for you.
Follow your doctor's treatment plan, and don't be afraid to ask questions.
 Get to know your disease: Keep track of your lupus symptoms, which parts of your body
are affected, and any situations or activities that seem to trigger your symptoms.
 Ask for help: Don’t be afraid to ask for help. Consider joining a support group. It often
helps to talk to other people who have been through similar experiences.

2.8 EPIDEMIOLOGY

The global rates of Systemic lupus erythematosus are approximately 20–70 per 100,000 people.
In females, the rate is highest between 45 and 64 years of age. The lowest overall rate exists in
Iceland and Japan. The highest rates exist in the US and France. However, there is not sufficient
evidence to conclude why Systemic lupus erythematosus is less common in some countries
compared to others; it could be the environmental variability in these countries. For example,
different countries receive different levels of sunlight, and exposure to UV rays affects
dermatological symptoms of Systemic lupus erythematosus (Danchenko, et al., 2006).

Certain studies hypothesize that a genetic connection exists between race and lupus which affects
disease prevalence. If this is true, the racial composition of countries affects disease and will
cause the incidence in a country to change as the racial makeup changes. To understand if this is
true, countries with largely homogenous and racially stable populations should be studied to
better understand incidence (Danchenko, et al., 2006). Rates of disease in the developing world
are unclear (Tiffin, et al., 2013).

The rate of Systemic lupus erythematosus varies between countries, ethnicity, and sex, and
changes over time (Danchenko, et al., 2006). In the United States, one estimate of the rate of
Systemic lupus erythematosus is 53 per 100,000 (Danchenko, et al., 2006) another estimate
places the total affected population at 322,000 to over 1 million (98 to over 305 per 100,000). In
Northern Europe the rate is about 40 per 100,000 people (Rahman, et al. 2008). Systemic lupus
erythematosus occurs more frequently and with greater severity among those of non-European
descent. That rate has been found to be as high as 159 per 100,000 among those of Afro-
Caribbean descent (Danchenko, et al., 2006). Childhood-onset systemic lupus erythematosus
generally presents between the ages of 3 and 15 and is four times more common in girls (Borgia,
et al. 2015).

While the onset and persistence of Systemic lupus erythematosus can show disparities between
genders, socioeconomic status also plays a major role. Women with Systemic lupus
erythematosus and of lower socioeconomic status have been shown to have higher depression
scores, higher body mass index, and more restricted access to medical care than women of higher
socioeconomic statuses with the illness. People with Systemic lupus erythematosus had more
self-reported anxiety and depression scores if they were from a lower socioeconomic status.

2.9 PROGNOSIS

The prognosis of lupus is better today than ever before. With close follow-up and treatment, 80-
90% of people with lupus can expect to live a normal life span.

It is true that medical science has not yet developed a method for curing lupus, and some people
do die from the disease. However, for the majority of people living with the disease today, it will
not be fatal.

Lupus varies in intensity and degree. Some people have a mild case, others moderate and some
severe, which tends to be more difficult to treat and control. For people who have a severe flare-
up, there is a greater chance that their lupus may be life-threatening.

People with non-organ threatening aspects of lupus can look forward to a normal lifespan
if they:

 Follow the instructions of their physician

 Take their medication(s) as prescribed

 Know when to seek help for unexpected side effects of a medication or a new
manifestation of their lupus
Although some people with lupus have severe recurrent attacks that result in hospitalization,
most people with lupus rarely require hospitalization. Especially those who maintain a healthy
lifestyle.

New research brings unexpected findings each year. The progress made in treatment and
diagnosis during the last decade has been greater than that made over the past 100 years. It is
therefore a sensible idea to maintain control of a disease that tomorrow may be curable.

A common misperception about life expectancy

Some confusion about lupus life expectancy relates to the way research is communicated. 

Research that shows 80-90% of people with lupus live for more than 10 years is often
misinterpreted as giving people with lupus only 10 years to live. It is important to understand
that the "10 years" used in this context does not represent the number of years the person lived
after their diagnosis, but rather the number of years involved in the study. 

These studies followed patients with lupus from the time of diagnosis for a period of ten years.
At the end of this research period, researchers were able to conclude that 80-90% of the people
enrolled were still alive. 
 CHAPTER THREE

HOME VISISTS

3.0 1st VISIT

Date: 14th March, 2023

Objectives

1. To assess her home, environment and state of health.

2. To establish therapeutic rapport with my client and her family.

I got to her house at 3.15pm. I exchanged pleasantry with family members and I was well
received because they were aware of my visit. I requested humbly that I should be taken round
the house to have an in-depth assessment and obliged.

 Household description:

 Environment: The environment was neat, quiet, conducive and no stagnant water in their
surroundings.

 Type of construction: The house was built with blocks.

 Type of roofing: Corrugated iron sheet

 Number of rooms and sleeping arrangement: It is a 2bedroom flat with a sitting room.

 Sleeping arrangement: My client sleeps in the same room with her husband.

 Number of household in the building: Two members are living in the house.

 Source of water: Borehole

 Lighting: The house is adequate lighting.

 Condition of the floor: The floor is well tilled with non-slippery tiles.

 Kitchen facility: There is a well equipped kitchen with gas cooker and utensils and well
ventilated with a window and an escape door.

 Toilet facilities: Functional water closet system.

  Bathroom: One bathroom attached to each room.

 Refuse disposal: There is an environmental bucket which is being collected by

environmental officers on weekly basis.

 Relationship in the compound: She is friendly with her neighbors.

Observation

 The environment was neat.

 No slippery floor.

 Generally conducive with good interpersonal relationship.

Problem identified

Her health keeps deteriorating after she was discharged against doctor’s advice. She can’t really
talk well, she feels body weakness and loss of appetite. She looks pale and her body itches with
oral and nasal ulcers with lesions on the skin.

She was encouraged to visit the hospital but she was still adamant about hospital care and
management. Her husband tried to talk to her but she is keen on staying at home.

Vital Signs:

Temperature: 37.8 degree Celsius

Pulse: 86 beats per minutes

Respiration rate: 18 cycles per minutes

Blood Pressure: 90/60mmHg

I did tepid sponging to help reduce the high temperature.

Nursing Diagnosis

Impaired skin integrity related to exacerbation of the disease process evidenced by itching, oral
and nasal ulcers.
Objective

Patient will maintain optimal skin integrity as evidenced by an absence of rashes and skin lesions
within period of nursing care.

Nursing Intervention

1. Encourage adequate nutrition and hydration.

2. Instruct the client to clean, dry, and moisturize intact skin, use warm (not hot) water,
especially over bony prominences, use unscented lotion. Use mild shampoo.
3. Instruct the client to avoid contact with harsh chemicals and to wear appropriate
protective gloves, as needed.
4. Recommended prophylactic pressure-relieving devices e.g special mattress
5. Instruct the client to avoid spicy or citrusy foods.
6. Instruct the client to keep ulcerated skin clean and dry. Apply dressings as needed.

Rationale

1. These measures promote healthy skin and healing in the presence of wounds.
2. Scented lotions may contain alcohol, which dries the skin. Prescribed solutions reduce
dryness of the scalp and maintain skin integrity.
3. Chemicals aggravate this condition.
4. Skin is necessary to prevent infection and promote healing.

Evaluation

Patient maintained optimal skin integrity after nursing intervention.

3.1 2nd Visit

Date: 17th March, 2023

Objectives:

1. To review the client’s condition.

2. To assess the level of compliance to medication

3. To instruct client and family on side effects of drugs, contraindication and signs to report.
4. To identify nursing diagnosis

Activities/ Observations

I arrived the home of my client around 3.00pm. I met my client on the bed in her room. I greeted
her and I was welcomed. Miss. R.T however, did not complied with the medications and the
symptoms persisted. She is looking weak and she was strongly told to go back to the hospital.
She complained of pain and inability to eat. She has lost a lot of weight. She had high
temperature. First aid was done for her. She agreed to go to the clinic after much conviction. An
ambulance was called. The home visit was terminated as she was taken to the hospital’s
emergency unit where she was later transferred to the intensive care unit.

Vital Signs:

Temperature: 38.8 degree Celsius

Pulse: 76 beats per minutes

Respiration rate: 16 cycles per minutes

Blood Pressure: 80/55mmHg

Nursing Diagnosis

Acute pain related to inflammation associated with increased disease activity evidenced by facial
grimace.

Objective

Patient will report pain at a level of less than 3 to 4 on a scale of 0 to 10 within the period of
nursing intervention.

Nursing Intervention

1. Encourage the patient to assume an anatomically correct position with all joints.
2. Remind client to avoid prolonged periods of inactivity.
3. Encourage client to take 15 minutes warm shower.
4. Encourage use of nonpharmacological measures of pain control such as relaxation,
distraction.
 5. Instruct client to take anti-inflammatory medications as prescribed.

Rationale

1. Such measures assist in preventing the development of contractures.

2. Activity is required to prevent further stiffness and to prevent joints from freezing and
muscles from becoming atrophied.
3. Warmth reduces stiffness and relieves pain.
4. To diminish pain.

Evaluation

Patient reported pain of less than 3 of the pain scale after nursing intervention.
 CHAPTER FOUR

4.0 SUMMARY

This is a case study of Miss. R.T a 22 year old woman with systemic lupus erythematosus. She
was transferred from a hospital in Sango Ota to Federal Medical Center Abeokuta for further
investigations and treatment. She was admitted and stayed in the hospital for 30 days but was
later discharged against doctor’s advice. She was discharged home, her case worsened and she
was readmitted into the intensive care unit.

She used 24 days in readmission before she eventually gave up the ghost.

4.1 CONCLUSION

Systemic lupus erythematosus (SLE), commonly referred to simply as lupus, is a chronic

autoimmune disease that can cause swelling (inflammation) and pain throughout your body.
When you have an autoimmune disease, your body’s immune system fights itself. The immune
system is supposed to fight possible threats to the body infections, for example but, in this case,
it goes after healthy tissue.

If you have lupus, you might experience joint pain, skin sensitivities and rashes, and issues with
internal organs (brain, lungs, kidneys and heart). Many of your symptoms might come and go in
waves often called flare-ups. At times, symptoms of lupus might be mild or not noticeable
(meaning they’re in remission). Other times, you could experience severe symptoms of the
condition that heavily impact your daily life.

4.2 RECOMMENDATION

While lupus can affect your health, it doesn’t have to affect your quality of life. By focusing on
your medications and wellness, you can live as healthy a life as possible.

In addition to sticking to your treatment plan, some things that you can do at home to help focus
on your wellness include:

 staying active and getting plenty of exercise

 eating a healthy, balanced diet

 finding ways to manage stress

  being sure to get enough rest and not overwork yourself

Additionally, reading about other people’s lupus journeys may help you to learn more about
living with lupus. There are many lupus blogs available that you can dive into.

Sometimes, coping with a diagnosis of lupus may be challenging. It may help to share your
experience with others through in-person or online support groups.
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