Utkrisht Shah

Hershey Valerio
GENERAL DATA
This is a case of Mrs. L.S., 69 year old, female
Reliability 90%
Date of consultation: june 21, 2012
Time of interview: 8pm
Place of interview: Emergency room EAC-
Medical Center Cavite
CHIEF COMPLAINT:
According to the patient
I had fever for the past 5 days and I started
to vomit since today.
HISTORY OF PRESENT
ILLNESS
5 DAYS PTC, patient experienced general body
malaise followed by fever of 39 degrees celsius.
Self medicated of Paracetamol and fever
subsided.
2 DAYS PTC, persistence of symptoms, she
consulted a private physician where she was
allegedly diagnosed having Urinary Tract
Infection. She was given Medication Levofloxacin
500mg once daily for 7 days and was sent home.
10 hours PTC, pateint experienced dizziness
accompanied with an episode of non bilious,
non projectile vomiting , fever and epigastric
pain with a severity of 5/10, non radiating,
squeezing in character . No associated
vomiting and diarrhea hence consulted our
institution.
PAST MEDICAL HISTORY
Mrs. L.S. is a known hypertensive for the past
35 years.
Medication: Clonidine 75mg good compliant.
Known Diabetic took insulin as her
maintenance
In 2008, admitted at another institution for
having cardiomegaly.
FAMILY HISTORY
(+) hypertension : Father
(+) Diabetes: Mother
(+) Hypertensive : daughter and son
PERSONAL AND SOCIAL
HISTORY
Non smoker
Non alcoholic beverage drinker
REVIEW OF SYSTEMS
(+) easy fatigability
(+) weakness
(+) low grade fever
(+) chills
(+) dizziness
(+) sore throat
(+) cough
(-) weight loss
(-) loss of appetite
PHYSICAL EXAMINATION
GENERAL SURVEY:
Patient conscious, alert, ambulatory, oriented to
3spheres, not in cardiorespiratory disease.
VITAL SIGN:
BP: 140/80:
PR: 88
HR: 28
TEMPERATURE: 38.1 degrees celsius
SKIN: warm, good skin turgor, no rahes, no cyanosis
HEENT: anicteric sclerae, pink palpebral conjunctiva,
no nasoaural discharge , no lymphadenopathy.
CHEST AND LUNGS: symmetrical chest expansion,
no retractions, clear breath sounds
HEART: regular rate and rhythem , no murmur
ABDOMEN: flat, normoactive bowel sounds, tender
RECTUM AND GENITALIA: unremarkable
EXTREMITIES: no edema, full and equal pulses.
NEUROLOGIC
EXAMINATION
Motor response: 5/5
Sensory response: 100%
Cranial nerves: intact
LABORATORY RESULT
HEMATOLOGY
TEST RESULT REFERENCE TEST RESULT REFERENCE

HEMOGLOBIN 105 123-153 G/M LYMPHOCYTES 0.10 0.22-0.40

HEMATOCRIT 0.32 0.36-0.45 ESINOPHILS 0.02 0.22-0.40

WBC 16.5 10-15X10^9/L MONOCYTES 0.03 0.04-0.08

SEGMENTERS 0.83 0.36-0.68 STAB CELLS 0.02 0.02-0.06

URINALYSIS
COLOR- yellow
ALBUMIN- trace
CHARACTER- slightly cloudy
SUGAR- negative
SPECIFIC GRAVITY- 1.005
WBC- 170-180/hpf
PH- 5.0
BACTERIA +1
RBC- 2-4 hpf
EPITHELIAL CELLS- few
MUCUS THREADS +1
Management:
The patient was brought to ER at 8 pm and seen
by Dra Martinez . The following are the
chronological order of the ER management :
8 pm- CBG 221 mg/dl
8:40 pm-hooked to PNSS 1L X 200 cc FD- TE: 9
PM , Na , K done
8:45- Plasil 1 amp IV given
8:50- Ranitidine 1 amp IV given
8:55 Aeknil 300 mg IV given, ciprofloxacin skin
test done
9 pm- regulated IVF to q8 due @ 920pm ANST(-)
Laboratory done outside attached to chart,
UA/CBC done last 6-20-2012 . Blood chemistry
done last 6-1-2012.
CPG form inserted, chest x ray PA semi
settings done
9 pm- regulated IVF to q8
9:o5- human insulin 70/30 220 given sq
9:35- Ciprofloxacin 200 mg IV given as SQ
X ray plate @ bedside , ENDORSED
Course in Ward
The patient was admitted to ward. Vital signs
recorded and was put on PNSS IV q8 and set
on low salt low fat DM diet.
On the 1st hospital day the patient complained
of mild weakness with diarrhea so serum Na
and K was requested.
The patient was given Kcl along with her other
home medications and antibiotics. She was
scheduled for KUB ultrasound for the next day..
Day 2, KUB ultrasound was done which
showed no negative findings. The patient still
complained of weakness and epigastric pain
without diarrhea and vomiting.
Day 3, the patients condition improved and
was discharged under home medications.
Medications
Ciprofloxacin 200 mg IV Q12
Metoclopromide 1 amp IV
Ranitidine 50 mg IV Q8
Human insulin 70/30 22 U
Simvastatin 20 mg 1 tab
Cilostazol 509 mg 1 tab
Catapress 75 mcg/tab 1 tab
Combizar 100 mg
Levofloxacin 500 mg tab 1 tab PO
DISCUSSION
URINARY TRACT INFECTION
a bacterial infection that occurs when bacteria
invade the urinary tract system; the bacteria
multiply throughout the urinary track system.
they often cause severe symptoms such as pain
and/or burning upon urination.
Theurinary tract systemis the body's filtering
system for removal of liquid waste. The
urinary tract consists of
thekidneys,bladder,ureters, andurethra.
About half of all women will have at least one
UTI in her lifetime, while many women suffer
through several infections throughout their
lifetime.
Women are particularly susceptible to urinary
tract infections or UTI.
CAUSES:
The most common cause of UTIs is bacteria from
the bowel that live on the skin near the rectum or in
the vagina, which can spread and enter the urinary
tract through the urethra.
. Once these bacteria enter the urethra, they travel
upward; causing infection in the bladder and
sometimes other parts of the urinary tract.
Sexual intercourse is a common cause of urinary
tract infections because the female anatomy can
make women more prone to urinary tract infections.
During sexual activity, bacteria in the vaginal area
are sometimes massaged into the urethra.
Another cause of bladder infections or UTI is
waiting too long to urinate. The bladder is a
muscle that stretches to hold urine and
contracts when the urine is released.
Waiting too long past the time you first feel the
need to urinate can cause the bladder to
stretch beyond its capacity. Over time, this can
weaken the bladder muscle. When the bladder
is weakened, it may not empty completely and
some urine is left in the bladder.
This may increase the risk of urinary tract
infections or bladder infections. Other factors
that also may increase a woman's risk of
developing UTI includepregnancy, having urinary
tract infections as child, menopause or diabetes.
E. coli- most common cause of UTI 85-90%
Staphylococcus saprophyticus 5-10%
Other bacterial causes
include:Klebsiella,Proteus,Pseudomonas,
andEnterobacter.
These are uncommon and typically related to
abnormalities of the urinary system orurinary
catheterizationUrinary tract infections due
toStaphylococcus aureus typically occurs
secondary to blood born infections.
SIGNS AND SYMPTOMS:
frequent urge to urinate, accompanied by
pain or burning on urination.
The urine often appears cloudy and
occasionally dark, if blood is present. The
urine may develop an unpleasant odor.
Lower abdominal pain
Feel bloated and feeling of the bladder is full.
Fever
PATHOGENESIS:
The urinary tract should be viewed as a single
anatomic unit that is united by a continuous
column of urine extending from the urethra to
the kidney. In the vast majority of UTIs,
bacteria gain access to the bladder via the
urethra.
Ascent of bacteria from the bladder may
follow and is probably the pathway for most
renal parenchymal infections.
The vaginal introitus and distal urethra are
normally colonized by diphtheroids,
streptococcal species, lactobacilli, and
staphylococcal species but not by the enteric
gram-negative bacilli that commonly cause
UTIs.
In females prone to the development of
cystitis, however, enteric gram-negative
organisms residing in the bowel colonize the
introitus, the periurethral skin, and the distal
urethra before and during episodes of
bacteriuria.
The factors that predispose to periurethral
colonization with gram-negative bacilli remain
poorly understood, but alteration of the
normal vaginal flora by antibiotics, other
genital infections, or contraceptives
(especially spermicide) appears to play an
important role. Loss of the normally dominant
H2O2-producing lactobacilli from the vaginal
flora appears to facilitate colonization by E.
coli.
Small numbers of periurethral bacteria
probably gain entry to the bladder frequently,
and this process is facilitated in some cases
by urethral massage during intercourse.
Whether bladder infection ensues depends on
interacting effects of strain pathogenicity,
inoculum size, and local and systemic host
defense mechanisms. Recent data from both
animal models and human studies indicate
that E. coli sometimes invades the bladder
epithelium, forming intracellular colonies
(biofilms) that may persist and become a
source of recurrent infection.
Under normal circumstances, bacteria placed in the
bladder are rapidly cleared, partly through the flushing
and dilutional effects of voiding but also as a result of
the antibacterial properties of urine and the bladder
mucosa.
Owing mostly to a high urea concentration and high
osmolarity, the bladder urine of many healthy persons
inhibits or kills bacteria. Prostatic secretions possess
antibacterial properties as well. Bladder epithelial cells
secrete cytokines and chemokinesprimarily
interleukin (IL) 6 and IL-8upon interaction with
bacteria, causing polymorphonuclear leukocytes to
enter the bladder epithelium and the urine soon after
infection arises and play a role in clearing bacteriuria.
The role of locally produced antibody remains unclear.
CONDITION AFFECTING THE
PATHOGENESIS:
1. GENDER AND SEXUAL ACTIVITY
-The female urethra appears to be particularly prone to
colonization with colonic gram-negative bacilli because of
its proximity to the anus, its short length (~4 cm), and its
termination beneath the labia.
2. PREGNANCY
-This predisposition to upper tract infection during
pregnancy results from decreased ureteral tone,
decreased ureteral peristalsis, and temporary
incompetence of the vesicoureteral valves. Bladder
catheterization during or after delivery causes additional
infections. Increased incidences of low birth weight,
premature delivery, and neonatal death result from UTIs
(particularly upper tract infections) during pregnancy.
3. OBSTRUCTION
- Any impediment to the free flow of urine
tumor, stricture, stone, or prostatic
hypertrophyresults in hydronephrosis and a
greatly increased frequency of UTI.
- Infection superimposed on urinary tract
obstruction may lead to rapid destruction of
renal tissue.
4. NEUROGENIC BLADDER DYSFUNCTION
-Interference with bladder enervation, as in
spinal cord injury, tabes dorsalis, multiple
sclerosis, diabetes, and other diseases, may
be associated with UTI.
- The infection may be initiated by the use of
catheters for bladder drainage and is favored
by the prolonged stasis of urine in the bladder.
- An additional factor often operative in these
cases is bone demineralization due to
immobilization, which causes hypercalciuria,
calculus formation, and obstructive uropathy.
5. VESICOURETERAL REFLUX
- Defined as reflux of urine from the bladder
cavity up into the ureters and sometimes into
the renal pelvis, vesicoureteral reflux occurs
during voiding or with elevation of pressure in
the bladder.
- An anatomically impaired vesicoureteral
junction facilitates reflux of bacteria and thus
upper tract infection.