SYSTEMIC LUPUS ERTHYMATOSUS ERTHYMATOSUS (SLE)
1
A CASE STUDY REPORT OF A 33-YEAR-OLD FEMALE WITH SYSTEMIC LUPUS ERYTHEMATOSUS
A Case Study Repot Pese!ted to t"e Co##e$e o% Ats a!d S&'e!&es Caa$a State U!'es'ty
Po% Ade#'ta *a+'#a To#edo To#edo Ad'se
May Co#ee! L D'a!$o
O&to,e ./0 2
A CASE STUDY REPORT OF A 33-YEAR-OLD FEMALE WITH SYSTEMIC LUPUS ERYTHEMATOSUS
A Case Study Repot Pese!ted to t"e Co##e$e o% Ats a!d S&'e!&es Caa$a State U!'es'ty
Po% Ade#'ta *a+'#a To#edo To#edo Ad'se
May Co#ee! L D'a!$o
O&to,e ./0 2
AC1*OWLED2EME*T
Special thanks to Dr. Licayan for giving us such opportunity to access the medical records of some patients with autoimmune diseases in the city hospital (Butuan Medical Center, Butuan City. ! would like to e"tend my sincerest thanks to Madeline Logro#o for the financial support and to Mateo Diango for the guidance to the said area or vicinity of the patient. $nd also, for the cooperation of Mr. %llan Mantasa for giving significant information a&out her spouse illness or disease. 'hanks to the medical staff of Manuel . Santos )ospital (Butuan City for the medical information of Ms. 'iempo. 'o Mrs. Condrada *alagar 'iempo+ mother of oann 'iempo and Leah Mae 'iempo (sister for authoriing me to access her daughter-s medical records in M.. Santos )ospital. 'o my sister sister Lorrai Lorraine ne Diane Diane Diango Diango ./, ./, who patient patiently ly e"plai e"plained ned the medica medicall terms terms and processes. 'his 'his paper paper will will not not &e made made possi possi&l &lee with without out the the pres presen ence ce of ment mentio ione ned d references in the paper. p aper. 'o 'o the organiation and authors, thank you.
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TALE OF CO*TE*TS
Client-s Client -s 0rofile
1
)ospitaliation )istory
2
Literature of !llness
3
!. !!. !!!. !!!. !6. 6. 6 !. 6!!. 6!! 6!!!. !:.
3 3 15 11 17 18 13 13 19 1;
)istory $natomy and 0hysiology Signs Signs and Symp Sympto toms ms44 Clin Clinic ical al Mani Manife fest stat atio ion n 0athop hophys hysiology4 gy4Cause uses Diagnostic 'ests Mana anageme ement and 'reatment ent 0rognosis %pide pidem miol iology ogy 0ictures
Drug Study
25
Discussion and $nalysis
2;
Conclusion
7<
Summary
7;
$ppendices
85
!. !!. !!!. !!!. !6. !6.
Clie Client nt--s 0ict 0ictur uree and and Docu Docum menta entati tion on 0ict 0ictur uree Client-s $uth uthoriation Letter Clie Client nt--s Dis Dischar charge ge Summ ummary ary Clie Client nt--s La&o La&ora rato tory ry 'est esu esult ltss
85 82 87 88
eference
8=
Student-s Studen t-s Curriculum Curricu lum 6itae
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CLIE*T4S PROFILE
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Client-s /ame> Ms. o $nn *alagar 'iempo $ge> 77 years old Date of Birth> $pril 28, 1;<5 0lace of Birth> Santa Cru, Butuan City Blood 'ype> B? @ork> @ork> /one, )ousewife eligion> oman Catholic $ddress> 0+1 Manila de Buga&os, Butuan City 0arents> Mr. $natalio 'iempo Mrs. Condrada *alagar Spouse> %llan Mantasa /um&er of Children> $live> $live> 2 Dead> 1 Date of Death> May 2<, 2517 0lace of Death> Manuel . Santos, ==8 Montilla Boulevard, Butuan City
Hosp'ta#'5at'o! H'stoy Hosp'ta# Ad6'tted7 Butuan Medical Center, Butuan City
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Chief Complaints>
• •
$dmitting Diagnosis> Bipedal %dema Ainal Diagnosis> Chronic idney Disease due to Lupus /ephritis Connective 'issue Disease Lupus Systemic %rythematosus
Client-s )istory> $s per noted 0ulmonary 'u&erculosis Convulsion )istory Miscarriage (2512 $dmission Date> $pril 75, 2517 $dmission 'ime> =>55 pm Discharge Date> May <, 2517 Discharge 'ime> 8>75 pm $ttending 0hysician> Dr. De 6era, Arancisco Co4Mngt> Dr. Limcangco, 0onciano Dr. Lagrito Dr. De Castro adiologist> onathan M. 'ahud, M.D., D0B 0athologist> 0onciano S. Limcangco, M.D., Hosp'ta# Ad6'tted7 Manuel . Santos, Montilla Boulevard, Butuan City
Chief Complaints>
•
$dmitting Diagnosis> Difficulty in Breathing 6
•
Ainal Diagnosis>
/ausea %nd Stage enal Disease
Client-s )istory> /ote progress> Aacial and Bipedal edema, 0allor, SEB, /ausea, 6omiting, Aever, $llergy $dmission Date> May 2=, 2517 $dmission 'ime> /$ Discharge Date> /$ Discharge 'ime> /$ $ttending 0hysician> Dr. Sy, afael B. Surgeon> Dr. )ipol !!!, odrigo adiologist> *erardo 'an emanda&an, M.D., D0B 0athologist> %dgardo B. $&adino M.D., A0S0
oann *alagar 'iempo, a 77+year old lady lived in 0+1 Manila de Buga&us together with her spouse %llan Mantasa, she was &orn on $pril 28, 1;<5 at Santa Cru, Butuan City. 'heir way of living is through farming. She was admitted at Butuan Medical Center on $pril 75, 2517 under admitting physician, Dr. de 6era. 0rior to admission her spouse says that the patient complains a&out her discomfort, itchiness and difficulty in urination. $m&ulatory &rought &y her first degree cousin in the hospital due to her yellowish discoloration (Faundice of the skin with chief complaints of discomfort due to
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&ack itchiness, &ipedal edema, shortness of &reathing and a&dominal pain. 'he patient e"perienced episode of discomfort and pain for the past one year. Ene month prior to her hospitaliation or admission, noticed itchiness and redness of the face. 'he final diagnoses for the patient-s case are Chronic idney Disease related to Lupus /ephritis, Connective 'issue Disease namely Systemic Lupus %rythematosus and $nemia (su&Fect for &lood transfusion. $ccording to her spouse, the patient e"perienced convulsion in her younger age and also lung pro&lem in her teenage years during her stay in Eami City, indeed her medical history states that she has 0ulmonary 'u&erculosis and has a history of miscarriage. During her admission, she was seen and e"amined &y Dr. de 6era, orders and medicines were prescri&ed with some test like CBC, B'. @hile Creatinine test, %S and chest "+ray were reGuested and her vital signs was monitored. She was given some medication such as ranitidine =5 mg and = mg prednisone, on her first day of admission. En the second day furosemide was given after transfusion, /a)CE7 3=5mg, CaCE7 =55mg, ciproflo"acin =55 mg and were advised for dialysis. En the third day, she was given amlodipine 15 mg4ta&, the following dayH more &lood transfusion was followed up. En the fifth day, she was advised to wear masked all the time and the day after, permitted to go home per reGuest, prescri&ed with folic acid ? AeSE8, /a)CE7 3=5 mg, CaCE7, and prednisone = mg. 0atient was then admitted in Manuel . Santos )ospital, after the local election in May 2=, 2517 when she e"perienced &urning and intensive pain in the a&dominal region and lower &ack (lum&ar region (source> %llan Mantasa. 'he patient-s admission complaints were nausea and difficulty of urination. )er history noted the progressive 8
facial and &ipedal edema, pallor, shortness of &reathing, nausea, vomiting and allergy. 'he initial vital signs of the patient wasH temperature> 7< IC , B0> 1954 155 with noted swollen right leg and decrease of &reath sounds. Aurther intervention was done like she was prescri&ed or advised to catheteriation and dialysis.
LITERATURE OF ILL*ESS
!.
)!S'EJ
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'he term Klupus- (Latin for Kwolf- was first used during the Middle $ges to descri&e erosive skin lesions evocative of a Kwolf-s &ite-. !n 1<83 the 6iennese physician Aerdinand von )e&ra (1<131<<5 introduced the &utterfly metaphor to descri&e the malar rash. )e also used the term Klupus erythematosus- and pu&lished the first illustrations in his $tlas of Skin Diseases in 1<=3. Lupus was first recognied as a systemic disease with visceral manifestations &y Mori aposi (1<791;52. 'he systemic form was further esta&lished &y Esler in Baltimore and adassohn in 6ienna. Ether important milestones include the description of the false positive test for syphilis in SL% &y einhart and )auck from *ermany (1;5;H the description of the endocarditis lesions in SL% &y Li&man and Sacks in /ew Jork (1;27H the description of the glomerular changes &y Baehr (1;7=, and the use of the term Kdiffuse connective tissue disease- &y lemperer, 0ollack and Baehr (1;81. 'he &eginning of the modern era in SL% was the discovery of the KL%- cell &y )argraves, ichmond and Morton at the Mayo Clinic in 1;8<. (Bertsias et al., 2512
!!.
$/$'EMJ 0)JS!ELE*J Systemic Lupus %rythematosus (SL% is a chronic, inflammatory autoimmune
collagen disease resulting from distur&ed immune regulation that causes an e"aggerated production of autoanti&odies (ohnson et al., 255<. Systemic lupus erythematosus (SL% is a chronic disease that causes inflammation in connective tissues, such as cartilage and the lining of &lood vessels, which provide strength and fle"i&ility to structures throughout the &ody. 'he signs and symptoms of SL% vary among affected individuals, and can
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involve many organs and systems, including the skin, Foints, kidneys, lungs, central nervous system, and &lood+forming (hematopoietic system. SL% is one of a large group of conditions called autoimmune disorders that occur when the immune system attacks the &odys own tissues and organs (*enetics )ome eference, une 2518. Lupus is a chronic (long+term disease that causes inflammation N pain and swelling. Most patients feel fatigue and have rashes, arthritis (painful and swollen Foints and fever. 'he immune system is the &ody-s defense system. @hen healthy, it protects the &ody &y making anti&odies (&lood proteins that attack foreign germs and cancers. @ith lupus, the immune system misfires. !nstead of producing protective anti&odies, an autoimmune disease &egins and makes Oautoanti&odies,P which attack the patient-s own tissues. Doctors sometimes refer to this as a Oloss of self+tolerance.P $s the attack goes on, other immune cells Foin the fight. 'his leads to inflammation and a&normal &lood vessels (vasculitis. 'hese anti&odies then end up in cells in organs, where they damage those tissues.
$ Lupus complication includes kidney failure. Jour two kidneys are part of your renal system, which also includes two ureters, the &ladder, and the urethra. $s the primary organs of the renal system, your kidneys are responsi&le for>
•
Maintaining the correct amount and type of &ody fluids
•
emoving waste products and to"ic su&stances
•
egulating the hormones (chemical messengers that help control &lood pressure and &lood volume
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Lupus /ephritis
!nflammation of the nephrons, the structures within the kidneys that filter the &lood, is called glomerulonephritis, or nephritis. Lupus nephritis is the term used when lupus causes inflammation in your kidneys, making them una&le to properly remove waste from your &lood or control the amount of fluids in your &ody. $&normal levels of waste can &uild up in the &lood, and edema (swelling can develop. Left untreated, nephritis can lead to scarring and permanent damage to the kidneys and possi&ly end+ stage renal disease (%SD. 0eople with %SD need regular filtering of their &ody-s waste done &y a machine (dialysis or a kidney transplant so that at least one kidney is working properly.
Lupus nephritis most often develops within the first five years after the symptoms of lupus start. !t usually affects people &etween 25 and 85. !n the early stages of lupus nephritis, there are very few signs that anything is wrong. Eften the first symptoms of lupus nephritis are weight gain and puffiness in your feet, ankles, legs, hands, and4or eyelids. 'his swelling often &ecomes worse throughout the day. $lso, your urine may &e foamy or frothy, or have a red color. 'he first signs of lupus nephritis often show up in clinical la&oratory tests on the urine.
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Aig.1. $natomy of kidney affected with SL%+ Lupus /ephritis
Aig. 2> Comparison> $. /ormal /ephron and *lomeruli structure, B. SL%+Lupus /ephritis affected kidney (/ephron and *lomeruli
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!!!.
CL!/!C$L M$/!A%S'$'!E/ Enset is insidious or acute. SL% can go undiagnosed for many years. 'he clinical
course is one of the e"acer&ations and remissions. Multisystem features include nephritis, cardiopulmonary disease, rashes and more indirect evidence of systemic inflammation. $ccording to the genetics home reference of QS /ational Li&rary of Medicine, SL% may first appear as e"treme tiredness (fatigue, a vague feeling of discomfort or illness (malaise, fever, and weight loss. 'here are manifestations in different systems of the &ody. !n musculoskeletal system> arthralgias and arthritis (synovitis are common presenting features. oint swelling, tenderness, and pain on movement are common, accompanied &y morning stiffness. !n integumentary system> several different types are seen (e.g, RSCL% su&acte cutaneous lupus erythematosus + causes sores after &eing out in the sun, RDL% discoid lupus erythematosus+ causes a rash that doesnt go away (Medline 0lus, $ugust 2518. $ &utterfly rash across the &ridge of the nose and cheeks occurs in fewer than half of the patients and may &e a precursor to systemic involvement. Lesions worsen during e"acer&ations (flares and may &e provoked &y sunlight or artificial ultraviolet light. Eral ulcers may involve &uccal mucosa or hard palate. !n cardiovascular system> 0ericarditis is the most common clinical cardiac manifestation. 0opular, erythematosus and pulpuric lesions may occur on the fingertips, el&ows, toes and may progress e"tensor surfaces of forearms or lateral sides of hands and may progress to necrosis. Ether systemic manifestations> 0leuritis or pleural effusions may occur, lymphadenopathy occurs in half of all SL% patients and renal involvement (glomeruli may lead to systemic hypertension. SL% has varied and freGuent neuropsychiatric
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presentations, generally demonstrated &y su&tle changes in &ehavior or cognitive a&ility. Depression and psychosis are common (ohnson et al., 255<. Some people with lupus often have features that are not specific to lupus. 'hese include fever, fatigue, weight loss, &lood clots and hair loss in spots or around the hairline. 'hey may also have heart&urn, stomach pain, and poor circulation to the fingers and toes. 0regnant women can have miscarriages (E'!S, 2515. enal malfunction may occur as a result of systemic complication (Lupus /ephritis.
Symptoms of Lupus Nephritis are the following
Sudden and une"plained swelling, especially in the e"tremities (feet, ankles, legs,
•
fingers, arms or the eyes •
Blood in the urine
•
%levated &lood pressure
•
Aoamy appearance in urine
•
!ncreased urination, especially at night
!6.
0$')E0)JS!ELE*J4C$QS%S 'his distur&ance is &rought &y some com&ination of genetic, hormonal (as
evidence &y the usual onset during the child&earing years, and environmental factors (sunlight, thermal &urns. Certain medications, such as hydralaine ($presoline,
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procinamide
(0ronestyl,
isoniaid,
chlorpromaine
('horaine,
and
some
anticonvulsant, have &een implicated in chemical+or drug induced SL%. !n SL%, the increase in autoanti&ody production is thought to result from a&normal suppressor '+cell function, leading to immune comple" deposition and tissue damage. !nflammation stimulates antigens, which in turn stimulate additional anti&odies, and the cycle repeats (remissions and e"acer&ations (ohnson et al., 255<.
/ormal variations (polymorphisms in many genes can affect the risk of developing SL%, and in most cases multiple genetic factors are thought to &e involved. !n rare cases, SL% is caused &y mutations in single genes. Most of the genes associated with SL% are involved in immune system function, and variations in these genes likely affect proper targeting and control of the immune response. Se" hormones and a variety of environmental factors including viral infections, diet, stress, chemical e"posures, and sunlight are also thought to play a role in triggering this comple" disorder. $&out 15 percent of SL% cases are thought to &e triggered &y drug e"posure, and more than <5 drugs that may &e involved have &een identified. !n people with SL%, cells that have undergone self+destruction (apoptosis &ecause they are damaged or no longer needed are not cleared away properly. 'he relationship of this loss of function to the cause or features of SL% is unclear. esearchers suggest that these dead cells may release su&stances that cause the immune system to react inappropriately and attack the &odys tissues, resulting in the signs and symptoms of SL% (*enetics )ome eference> QS /ational Li&rary for Medicine, une 2518
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6.
D!$*/ES'!C '%S' $ccording to the $merican College of heumatology (2517 the diagnostic test
that can &e done to the patients with SL% are> $&normal &lood testsH low &lood cell counts> anemia, low white &lood cells or low platelets,
positive antinuclear anti&ody>
referred to as $/$ and present in nearly all patients with lupus certain anti&odies that show an immune system pro&lem> anti+dou&le+strand D/$ (called anti+dsD/$, anti+ Smith (referred to as anti+Sm or antiphospholipid anti&odies, or a false+positive &lood test for syphilis (meaning you do not really have this infection .La& tests. !f your doctor suspects you have lupus from your symptoms, you will need a series of &lood tests to confirm that you do have the disease. 'he most important &lood screening test measures $/$, &ut you can have $/$ and not have lupus. 'herefore, if you have positive $/$, you may need more specific tests to prove the diagnosis. 'hese &lood tests include anti&odies to anti+dsD/$ and anti+Sm. 'he presence of antiphospholipid anti&odies can help doctors detect lupus. 'hese anti&odies signal a raised risk of certain complications such as miscarriage, difficulties with memory, or &lood clots that may lead to stroke or lung inFury. Doctors also may measure levels of certain complement proteins (a part of the immune system in the &lood, to help detect the disease and follow its progress. Diagnosis may reGuire urine and &lood tests as well as a kidney &iopsy.
•
Qrine test> Blood or protein in the urine is a sign of kidney damage. 17
Blood test> 'he kidneys remove waste materials like creatinine and urea from the
•
&lood. !f the &lood contains high levels of these su&stances, kidney function is declining. Jour doctor should estimate your glomerular filtration rate &ased on your creatinine score.
idney &iopsy> $ &iopsy is a procedure to o&tain a tissue sample for e"amination
•
with a microscope. 'o o&tain a sample of your kidney tissue, your doctor will insert a long needle through the skin. %"amining the tissue with a microscope can confirm the diagnosis of lupus nephritis and help to determine how far the disease has progressed.
6!.
M$/$*%M%/'4'%$'M%/' 'here is no cure for lupus, and treatment can &e a challenge. )owever, treatment
has improved a great deal. 'reatment depends on the type of symptoms you have and how serious they are. 0atients with muscle or Foint pain, fatigue, rashes and other pro&lems that are not dangerous can receive OconservativeP treatment. 'hese options include nonsteroidal anti+inflammatory drugs N referred to as /S$!Ds. Lupus is treated with drugs that &lock your &odys immune system. Some of these are prednisone, aathioprine, cyclophosphamide or cyclosporine. $ newer medication, &elimuma&, is a monloclonal
anti&ody
that
is
also
availa&le.
$ntimalarial
drugs,
such
as
hydro"ychloroGuine and chloroGuine, can also &e used to help control lupus. /onsteroidal anti+inflammatory drugs. /S$!Ds decrease swelling, pain and fever. 'hese drugs include i&uprofen (&rand names Motrin, $dvil and napro"en (/aprosyn, $leve. Some of these /S$!Ds can cause serious side effects like stomach &leeding or 18
kidney damage. $lways check with your doctor &efore taking any medications that are over the counter (without a prescription for your lupus. $ntimalarial drugs. 0atients with lupus also may receive an antimalarial medication such as hydro"ychloroGuine (0laGuenil. 'hough these drugs prevent and treat malaria, they also help relieve some lupus symptoms, such as fatigue, rashes, Foint pain or mouth sores. 'hey also may help prevent a&normal &lood clotting. Corticosteroids and immune suppressants are prescri&ed &y doctors. 0atients with serious or life+threatening pro&lems such as kidney inflammation, lung or heart involvement, and central nervous system symptoms need more OaggressiveP (stronger treatment. 'his may include high+dose corticosteroids such as prednisone (Deltasone and others and drugs that suppress the immune system. !mmune suppressants include aathioprine
(!muran,
cyclophosphamide
(Cyto"an
and
cyclosporine
(/eoral,
Sandimmune. ecently mycophenolate mofetil (CellCept has &een used to treat severe kidney disease in lupusNreferred to as lupus nephritis. 'his e"citing treatment advance occurred thanks to research studies in patientsNcalled clinical trials. !t provides hope tha t some of the other drugs that researchers are testing in patients will help lupus. !t also underscores the need for patients with lupus to take part in studies. Com&ination treatment> )ealth care providers may com&ine a few medications to control lupus and prevent tissue damage. %ach treatment has risks and &enefits. Most immune+suppressing medications, for instance, may cause maFor side effects. Side effects of these drugs may include a raised risk of infections as well as nausea, vomiting, hair loss, diarrhea, high &lood pressure and osteoporosis (weak &ones. heumatologists may lower the dose of a drug or stop a medicine &ecause of side effects or when the disease
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goes into remission. $s a result, it is important to receive careful and freGuent health e"ams and la& tests to track your symptoms and change your treatment as needed. ($merican College of heumatology, 2517. !f you develop kidney disease, you may need to eat less protein and sodium (salt. !f you have high &lood pressure, you should &e sure to take the drugs prescri&ed to control your pressure. !f you are overweight, losing weight may help to control your &lood pressure.
6!!.
0E*/ES!S
Systemic lupus erythematosus (SL% carries a highly varia&le prognosis for individual patients. 'he natural history of SL% ranges from relatively &enign disease to rapidly progressive and even fatal disease. SL% often wa"es and wanes in affected individuals throughout life, and features of the disease vary greatly &etween individuals. 'he disease course is milder and survival rate higher in persons with isolated skin and musculoskeletal involvement than in those with renal disease and C/S disease.$ consortium report of 2;< SL% patients followed for =.= years noted falls in SL% Disease $ctivity !nde" 2555 (SL%D$!+2 scores after the first year of clinical follow+up and gradual increases in cumulative mean Systemic Lupus !nternational Colla&orating Clinics (SL!CC damage inde" scores (Medscape &y Christie Bartels, Ae&. 2518.
$s longevity of people with SL% increases, the likelihood of complications also increases in four areas> cardiovascular disease, infections, osteoporosis, and cancer.
Standard preventive measures and screening for related diseases may &e necessary to deal with the increased risks, due to the side effects of medications. %"tra vigilance is 20
considered warranted especially for cancers affecting the immune system. SL% is considered incura&le, &ut highly treata&le.
6!!!.
%0!D%M!ELE*J
0revalence rates in lupus are estimated to &e as high as =1 per 155 555 people in the QS$. 'he incidence of lupus has nearly tripled in the last 85 years, mainly due to improved diagnosis of mild disease. %stimated incidence rates in /orth $merica, South $merica, and %urope range from 2 to < per 155 555 per year. @omen are affected nine times more freGuently than men and $frican $merican and Latin $merican mestios are affected much more freGuently than Caucasians, and have higher disease mor&idity. 'he disease appears to &e more common in ur&an than rural areas. Si"ty+five percent of patients with SL% have disease onset &etween the ages of 13 and == years, 25T present &efore age 13, and 1=T after the age of == (Boumpas et al., 2512.
'here are different prevalence rates for people of the same race in different areas of the world. 'he contrast &etween low reported rates of SL% in &lack women in $frica and high rates in &lack women in the Qnited ingdom suggests that there are environmental influences. !n general, &lack women have a higher rate of SL% than women of any other race, followed &y $sian women and then white women. !n the Qnited States, &lack women are 8 times more likely to have SL% than white women. $ review of SL% across $sia+0acific countries revealed considera&le variation in prevalence and survival rates. Aor e"ample, overall prevalence rates ranged from 8.7 to 8=.7 per 155,555, and the overall incidence ranged from 5.; to 7.1 per 155,555 per year. 21
Moreover, $sians with SL% had higher rates of renal involvement than whites did, and cardiovascular involvement was a leading cause of death in $sians. More than ;5T of cases of SL% occur in women, freGuently starting at child&earing age. 'he use of e"ogenous hormones has &een associated with lupus onset and flares, suggesting a role for hormonal factors in the pathogenesis of the disease. 'he risk of SL% development in men is similar to that in prepu&ertal or postmenopausal women. !nterestingly, in men, SL% is more common in those with linefelter syndrome (ie, genotype ::J, further supporting a hormonal hypothesis. !n fact, a study &y Dillon et al found that men with linefelter syndrome had a more severe course of SL% than women &ut a less severe course than other men.
'he female+to+male ratio peaks at 11>1 during the child&earing years.$ correlation &etween age and incidence of SL% mirrors peak years of female se" hormone production. Enset of SL% is usually after pu&erty, typically in the 25s and 75s, with 25T of all cases diagnosed during the first 2 decades of life.Men with lupus tend to have less photosensitivity, more serositis, an older age at diagnosis, and a higher 1 year mortality compared to women. SL% tends to &e milder in the elderly with lower incidence of malar rash, photosensitivity, purpura, alopecia, aynaud-s phenomenon, renal and central nervous system involvement, &ut greater prevalence of serositis, pulmonary involvement, sicca symptoms, and musculoskeletal manifestations (Bertsias and Cervera, 2512.
$ review of the worldwide literature (predominantly /orth $merica, %urope, and $sia found that the incidence of pediatric+onset SL% ranged from 5.73 to 2.= per 155,555 per year and the prevalence ranged from 1.<; to 2=.9 per 155,555. 'he
22
prevalence of SL% is highest in women aged 18 to 38 years. SL% does not have an age predilection in males, although it should &e noted that in older adults, the female+to+male ratio falls. 'his effect is likely due to loss of the estrogen effect in older females. (Medscape &y Christie Bartels, Ae&. 2518.
!:.
0!C'Q%S %L$'%D 'E CL!%/'-S !LL/%SS
Aig. 7. + Malar rash
Aig. =. $cute diffuse cutaneous lupus
Aig. 8 0eriungual erythema and nailfold
Aig.3.
vasculitis
23
Su´
cutaneous
lupus
erythematosus
Aig.9. Aacial discoid lupus rash with a malar distri&ution. /ote the erythema (indicating
disease
activity,
keratin
plugged follicles, and dermal atrophy.
24
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esult
Qnit
eference (/CCLS
@BC
15.87
15X;4L
=.5+15.5
BC
1.9=
15X124L
M 8.=+=.2 A 7.=+3.3
)%ME*LEB!/
8<
*4L
M17=+19= A 12=+1==
A!a#ys's a!d D's&uss'o!
Pat I utua! Med'&a# Ce!te
Ta,#e /7 He6ato#o$y Resu#t 'est
esult
Qnit
eference (/CCLS
@BC
15.87
15X;4L
=.5+15.5
BC
1.9=
15X124L
M 8.=+=.2 A 7.=+3.3
)%ME*LEB!/
8<
*4L
M17=+19= A 12=+1==
)%M$'EC!'
5.1=
MC6
<7.8
fL
<2+;2
MC)
29.8
0g
29+72
MC)C
72;
*4L
725 7<5
0L$'%L%'
22<
15X;4L
1=5+ 855
M 5.85+5.=2 A 5.73+5.8<
D!AA%%/' CEQ/' /%Q'E0)!LS
5.35
5.=5 +5.95
LJM0)ECJ'%S
5.13
5.25+ 5.85
ME/ECJ'%S %ES!/E0)!LS
5.53
5.52+5.53
5.1<
B$SE0)!LS
5.55
%S
1=5
5.52+5.5= 5.55=+5.51 MM4)
M 5+15 A 5+25
E#rythroyte Seimentation 'ate C ESRB Emean orpusular hemogloin onentration C"**B E mean orpusular olume C"*B
"ean
*
*orpusular emogloin onentration C"*B E Phite loo *ells CP*B E 'e loo *ell C'*B>
$ &rief description of each of the measured parameters> @BC @hite Blood Count> $ total count of the num&er of white cells per liter of &lood.
!ncreased in inflammation,
infection and in dyscrasias (such as leukemia. Decreased> !n various infections, &one marrow defects, drugs, etc. $n e"amination of the features descri&ed &elow will indicate which of the white cell types is causing the general lowering. BC ed Cell Count> $ total count of the num&er of red cells per liter of &lood. !ncreased in overproduction states of the marrow (polycythemia, chronic o"ygen deprivation. Decreased in anemia. $n e"amination of the red cell indices usually reveals the nature of the a&normality. )emoglo&in> 'he total amount of hemoglo&in in the &lood (irrespective of the num&er of cells containing the hemoglo&in. )ematocrit> 'he total volume of the red cells in the &lood. MC6 Mean Corpuscular 6olume is an indication of the sie of the red cells. MC) Mean Corpuscular )emoglo&in is a measure of the amount of hemoglo&in per red &lood cell. MC)C Mean Corpuscular )emoglo&in Concentration is the amount of hemoglo&in per liter of fluid in each cell. Lymphocytes 'he lymphocytes are the circulating immune response cells. Monocytes> 0hagocytic (engulfing white cells. Basophils> 0hagocytic white cells. 0latelets> 'he small cells which are intimately involved in coagulation and clot formation. Qpon the result of the )ematological test that was conducted last $pril 2517 the patient-s result of %S was noticea&ly five times high or a&ove the normal range. $n erythrocyte sedimentation rate test, measures the speed at which red &lood cells settle to the &ottom of an upright glass test tu&e. 'his measurement is important &ecause when a&normal proteins are present in the &lood, typically due to inflammation or infection,
they cause red &lood cells to clump together and sink more Guickly, which results in a high %S value. 'he %S is useful in detecting inflammation in the &ody that may &e caused &y infection, some cancers, and certain autoimmune diseases. 'hus, saying that the a&normally high %S rate is due to the said autoimmune disease (the SL%H Systemic Lupus %rythematosus. !n relation, with the high %S, the @BC was also slightly &eyond the normal range. @hite &lood cells are the mainstay of the immune system. Some white &lood cells, known as macrophages, play a function in innate immunity &y surrounding, ingesting, and destroying invading &acteria and other foreign organisms in a process called phagocytosis (literally, Ocell eatingP, which is part of the inflammatory reaction and in the patient-s case is virtually seen &y the presence of &ipedal edema thus makes us conclude that the macrophages phagocytic role malfunctions which results in not recogniing which cell should and should not &e eaten. Macrophages also play an important role in adaptive immunity in that they attach to invading antigens and deliver them to &e destroyed &y other components of the adaptive immune system. 'he eosinophil is also high, knowing that the eosinophil is attracted to sites of parasitic infections, antigen+anti&ody reactions and play a part in allergic reactions. 'hese may implicate that something is wrong inside the &ody causing this eosinophils to increase in num&er and this may correlated with the %S result (the a&normal increased of %S rate due to proteins. $nother a&normalities in the )ematologic test is that there is a drop of the BC, )emoglo&in, )ematocrit (description a&ove which indicates that the patient is anemic which reduces the o"ygen+carrying capa&ility of &lood and the patients history of pulmonary tu&erculosis may have any connection with the said results. Aor us to
understand the said results, red &lood cells are composed predominantly of a protein and iron compound, called hemoglo&in that captures o"ygen molecules as the &lood moves through the lungs, giving &lood its red color. $s &lood passes through &ody tissues, hemoglo&in then releases the o"ygen to cells throughout the &ody, in relation with the patients hematology results of low BC and hemoglo&in, due to the incapa&ility of the &lood to transport o"ygen, there is a deficiency of supply in o"ygen thus making the cell ina&ility or alter to function for the reason that o"ygen plays an important role in the cellular respiration and manufacturing $'0 (energy. ed &lood cells are so packed with hemoglo&in. )emoglo&in also takes up and releases nitric o"ide, which plays an important role in regulating &lood pressure. Due to lower count of the patient-s BC, she was advised and su&Fected to &lood transfusion. Ta,#e 7 Ceat'!'!e Lee#
Date Creatinine eference
$pril 75, 2517 21.15 5.3+2.5 mg4dl
May 3, 2517 22.1= 5.3+2.5 mg4dl
Serum creatinine levels and urinalysis are used in screening for renal involvement. %arly detection allows for prompt treatment so that renal damage can &e prevented (Smelter et al., 255<. enal involvement may lead to hypertension, which also reGuires careful monitoring and management. $s seen in the results that there is high level of creatinine which is related to the patient-s nephritis (kidney inflammation caused &y any infection.
'he patient-s spouse Mr. %llan Mantasa as noted from his interview said that his partner mentioned that she has a history of convulsion in her childhood years. 'heoretically speaking, her convulsion e"perience pro&a&ly contri&uted her autoimmune disease if she has taken any anti+convulsant medicine. @hen Mrs. Condrada 'iempo was asked, that the patient during that year received medication &ut was not sure and forgot the said drug &ecause that happens a long time ago. $s it was noted in the &ook of ohnson (Brunner Suddarths-s 'e"t&ook of Medical+Surgical /ursing, 11th edition, that certain medications like anticonvulsants, have &een implicated in chemical or drug that induced SL%. $ccording to Mr. %llan Mantasa, his partner (oann 'iempo has a history of lung pro&lem when she-s still working in Eamis City in her teenage years &ut doesn-t follow the proper medication due to financial pro&lemH he also once said that her wife had trou&le in her pregnancy leading to miscarriage of their child prior to her illness diagnosis. Lupus appears to increase the chance of miscarriage early in pregnancy. @hile studies vary, miscarriage rates with lupus have &een reported to &e up to 7=T during the first trimester. $ previous miscarriage, kidney disease, and the presence of specific anti&odies (antiphospholipid have &een associated with a higher chance of miscarriage in women with lupus. 'he final diagnoses of the patient were Chronic idney Disease due to Lupus /ephritis and Connective 'issue Disease Lupus S ystemic %rythematosus. 'he presence of /ephritis is the manifestation of the immune system complication. 'his may result to a further damage of the kidney that will lead for the advice for dialysis. 'he patient may not die &ecause of her illness &ut &ecause of the complications. 'he medication that was
prescri&ed &y the physicians may actually give cure to her said illness &ut may also give rise to another complication as &rought &y the side effects or contradictions of the drug. Pat II Ma!ue# 8 Sa!tos Hosp'ta#
'a&le 7> La&oratory esults 'est
esult Qnit
/ormal ange
emarks
$l&umin Coagulation>
2.< g4dL 21. 15 sec
(/CCLS 7.<+=.5 15+ 17.=5 Y18
Lower Slower
0rothrom&in time 0otassium )emoglo&in )ematocrit @BC Lymphocyte Band %osinophil Monocyte 0latelet count
9.< p nmol4L 39 L 5.25 L 22.== ) 5.58 L 5.55 L 5.55 5.57 L 122 L
7.=+=.7 119+185 5.78+5.88 =.5+1=.5 5.25+5.=5 5.52+5.5= 5.55+5.51 5.5<+5.18 1=5+7;5
)igher Lower Lower )igher Lower Lower Baseline Lower Lower
'he decrease in al&umin indicates kidney diseases or liver diseases. $l&umin helps move many small molecules through the &lood including &iliru&in (yellow &reakdown product of normal heme cata&olism. 0rothrom&in time (0' is a &lood test that measures how long it takes &lood to clot. $ prothrom&in time test can &e used to check for &leeding pro&lems. 0' is also used to check whether medicine prevent &lood clots is working. Blood clotting factors are needed for &lood to clot (coagulation. 0rothrom&in, or factor !!, is one of the clotting factors made &y the liver . Due to the result of 0' a&ove, we can say that another organ is also affected other than the kidney.
0rothrom&in time (0' is measured to>
•
Aind a cause for a&normal &leeding or &ruising.
•
Check to see if &lood+thinning medicine, such as warfarin (Coumadin, is working. !f the test is done for this purpose, a 0' may &e done every day at first. @hen the correct dose of medicine is found, you will not need so many tests.
•
Check for low levels of &lood clotting factors. 'he lack of some clotting factors can cause &leeding disorders such as hemophilia, which is passed in families (inherited.
•
Check for a low level of vitamin . 6itamin is needed to make prothrom&in and other clotting factors.
•
Check if it is safe to do a procedure or surgery that might cause &leeding.
•
Check how well the liver is working. 0rothrom&in levels are checked along with other liver tests, such as aspartate aminotransferase and alanine aminotransferase.
•
Check to see if the &ody is using up its clotting factors so Guickly that the &lood cant clot and &leeding does not stop. 'his may mean the person has disseminated intravascular coagulation (D!C.
0otassium is &oth an electrolyte and a mineral. !t helps keep the water (the amount of fluid inside and outside the &odys cells and electrolyte &alance of the &ody. 0otassium is also important in how nerves and muscles work. $&normal potassium levels may cause symptoms such as muscle cramps or weakness, nausea, diarrhea, freGuent, urination, dehydration, low &lood pressure, confusion, irrita&ility, paralysis, and changes in heart rhythm. $ &lood test to check potassium is done to>
•
Check levels in people &eing treated with medicines such as diuretics and for people having kidney dialysis.
•
Check to see whether treatment for too low or too high potassiumlevels is working.
•
Check people with high &lood pressure who may have a pro&lem with their kidneys or adrenal glands.
oann *alagar 'iempo was pre+operatively diagnosed of $cute enal Aailure with transition to Chronic enal Aailure and was ordered to &e su&Fected to dialysis. Dr. )ipol !!!, odrigo was the attending surgeon of the patient. Dr, )ipol !!! performed the operation using ultrasound to guide the !nternal ugular catheter placement. Dialysis is the artificial process of eliminating waste (diffusion and unwanted water (ultrafiltration from the &lood. Eur kidneys do this naturally. Some people, however, may have failed or damaged kidneys which cannot carry out the function properly + they may need dialysis. !n other words, dialysis is the artificial replacement for lost kidney function (renal replacement therapy. Dialysis may &e used for patients who have &ecome ill and have acute kidney failure (temporary loss of kidney function, or for fairly sta&le patients who have permanently lost kidney function (stage = chronic kidney disease. $ppro"imately 1,=55 liters of &lood are filtered &y a healthy persons kidneys each day. @e could not live if waste products were not removed from our kidneys. 0eople whose kidneys either do not work properly or not at all e"perience a &uildup of waste in their &lood. @ithout dialysis the amount of waste products in the &lood would increase and eventually reach levels that would cause coma and death. !nternal Fugular venous access (especially right+sided is associated with a low rate of catheter malposition, and is commonly used in situations that reGuire relia&le tip
positioning for immediate use, such as drug administration or transvenous pacing. Similarly, the direct route from the right internal Fugular vein to the superior vena cava facilitates hemodialysis access and pulmonary artery catheter placement. 'he Qltrasound shows that the !6 catheter was noted in place, tip of which is directed towards the superior vena cava region.
Aig.<. the location of !nternal ugular 6ein Catheteriation
Co!&#us'o!
'he SL% of oann 'iempo develops a new complication which leads to Lupus /ephritis that targets and damages the functional and &asic unit of the kidney and the filtering capa&ility of the kidney was altered. Based on the analysis, the patients SL%+ Lupus /ephritis can &e partially determine with the presence of edema. 'he patient-s
edema manifested the &ipedal inflammation (right leg> most affected part and facial inflammation (right eye> most affected part. 'he la&oratory result of 0rothrom&in time test resulted to reach at the a&normal rate thus saying that another complication of the liver was arising. $lmost all of the la&oratory results of the patient-s remarks goes down or lowered which directly implicates that the patient-s &ody in response to the illness was not proper or normal. 'he crucial stage of the patient-s dialysis though may add few days of her life &ut the procedure cannot give any assurance of healing &ut only maintenance. 'he patient actually died due to the said complications of the acute to chronic renal failure which was considered as %SD or the %nd+Stage+enal Disease. 'he monthly or yearly check up is very important for us to &e aware of the possi&le illness, diseases or a&normalities in our &ody. %arly detection of an y illness may e"tend one-s life together with proper medication or treatment and medical procedures. Life without money is lame &ut money without life is dead. Aor it was said that health is wealth.
Su66ay
'a&le 8. Systemic Lupus %rythematosus+ $utoimmune Disease Su mmary
%tiologic Aactors
Main 0ro&lem
Manifestations
Medical Management
2+genetic
Dysfunctional
S!/S+ &utterfly
S'%E!DS+
P+psychological
A+autoimmune
immune
rash
Suppress
support
9+viral factor
system
E!/'S+ $rthritis
inflammation
A+ administer
E+e"posure and produces
!D/%J+
and immune
medications
intake of
anti&odies
protenuria and
reaction
L+ lifetime
medications
against the
hematuria
0L$SM$
monitoring and
&ody cells
)%$'+
%:C)$/*%
lifestyle changes
'he anti&odies pericarditis
')%$0J-
M+ monitor for
attack multiple
B$!/+ psychosis,
remove the
seiure
organs>
seiures and
circulating
development
S!/,
depression
anti&odies
E!/'S, !D/%J, )%$', B$!/
APPE*DICES
!.
CL!%/'-S 0!C'Q% $/D DECQM%/'$'!E/ 0!C'Q%
/ursing !ntervention
Aig.;. @ay to the patient-s place or vicinity. 'he main road of San 6icente if travelled straightly will lead you to Dulag, Butuan City. $ motorcycle terminal is noticea&le &etween the way to 'ungao and Santa Cru. 'he way to Santa Cru will lead to Manila de Buga&us.
Aig. 15. %llan Mantasa residency. 0+1 Manila de Buga&us.
Aig. 11. 0hotos during interview and the patient-s images during her admission in M..Santos )ospital
!!.
CL!%/'-S $Q')E!Z$'!E/ L%''%
File Attached To Hard Copy
!!!.
CL!%/'-S D!SC)$*%S SQMM$J
File Attached To Hard Copy
!6.
CL!%/'-S L$BE$'EJ '%S' %SQL'S
File Attached To Hard Copy
Re%ee!&e
Book ohnson, .J, 255<,P )and&ook for Brunner-s and Suddarth-s Medical+ Surgical /ursing, 11th editionP p.97;+982 Smelter, S., Bare, B., )inkle, ., Cheever, ., 255<, OBrunner-s and Suddarth-s 'e"t&ook of Medical+ Surgical /ursing, 11thP v2.p.1;5;, 1;15. 0orth, C, M. and uhert, M.0. 0athophysiology> Concepts of $ltered )ealth States, 3th edition, 0hiladelphia> Lippincott, @illiams and @ilkins, 2557. 0ondang, , M. and 0ondang, .$, 0. /ursing ed Book, 2nd edition, 2512 0DA and @e&site $merican College of heumatology www.rheumatology.org Erganiation of 'eratology !nformation Specialists + www.E'!Spregnancy.org. Medscape $uthor> Christie M Bartels, MD, MSH Chief %ditor> )er&ert S Diamond, MD http>44www.lifela&s.com4Lifela&s[BC40atients4MedicalConditions4)ematology http>44emedicine.medscape.com4article4
Cu'&u#u6 9'tae
/ame> Mary Coleen L. Diango )ome $ddress> 0+11 Maha&a, Alorida, Butuan City Birth Date> Ae&ruary 13, 1;;8 Birth 0lace> 0+7 Alorida, Butuan City 0arents> Mr. Mateo Diango Mrs. Madeline Logroṅo Si&lings> $nthony Stephen L. Diango, Lorraine Diane L. Diango, 6erlyn ay L. Diango %ducational Background 0rimary %ducation>
Mariana L. 0ineda Memorial %lementary School, Butuan City )onor eceived> 9th )onor
Secondary %ducation> Alorida /ational )igh School, Butuan City )onor eceived> Salutatorian, ournalist of the Jear 'ertiary %ducation>
Caraga State Qniversity, Main Campus 0rogram> Bachelor of Science in Biology
