University of Perpetual Help

System
Dalta Medical Center

EMERGENCY ROOM CASE

Gacias, Albien Emmanuel E.

Pedia Clerk E.R
Case 1

GENERAL DATA
This is a case of CR, a 7 years old female, Filipino, Catholic, born on May 31, 2009, currently
residing in Las Pinas City and was admitted for the 1st time in our institution last Oct 4, 2016

CHIEF COMPLAINT: rashes

HISTORY OF PRESENT ILLNESS

1 day prior to consultation patient noticed rashes on her chest characterized as small macular
rashed associated with pruritus and fever with a Tmax of 38.1 degrees Celsius. Paracetamol 250mg/5ml
– 7.5ml was given when fever occur. No other associated signs and symptoms like cough, colds, vomiting
or loose bowel movement.
Few hours prior to consultation, patient and mother noticed that the rashes became a pimple like
characteristics and others were fluid filled which spread over the patients head and beginning on her
extremities accompanied by fever with a Tmax of 37.8 degrees Celsius. Due to progression of above
symptoms, mother decided to seek for consult.

PAST MEDICAL HISTORY

(-) Allergies (+) Asthma - Salbutamol (-) Heart diseases

(-) Hypertension (-)Diabetes (-) Cancer (-) TB

FAMILY HISTORY:
(-) Hypertension (-) heart disease (-) asthma (-) allergy
(-) blood disorder (-) diabetes (-) cancer (-) TB

PERSONAL AND SOCIAL HISTORY

Patient was living in a compound together with her relatives (Total of 13 people). They have 2
dogs and 1 cat. Primary care giver to the patient is the mother. Mother reported that one of their relative
has chicken pox.

MATERNAL HISTORY
Patient was born full term via Normal Spontaneous Vaginal Delivery from a G1P1 (1001) mother.
No complications at birth

IMMUNIZATION HISTORY
Immunized with 1 dose of BCG, 3 doses of Pentavalent vaccine( diphtheria, tetanus, pertussis,
hepatitis and haemophilus influenza) and 3 doses of IPV( inactivated polio vaccine). 3 doses of
pneumococcal conjugate. 1 dose of MMR and varicella. Patient stopped having immunization since she
was 1 year old.

NUTRITIONAL HISTORY
Patient eat solid foods. Patient is taking Celine as her vitamin.

REVIEW OF SYSTEMS

General: (-) Weakness (-) Fatigue (-) weight loss (-) irritability
Skin: (-) lumps (-) sores (-) dryness (-) color change (-) changes in hair or nails.
Head: (+) Headache (-) head injury (-) dizziness (-) lightheadedness
Eyes: (-) Vision changes (-) glasses or contact lenses (-) pain (-) redness (-) excessive tearing
(-) flashing lights
Ears: (-) decreased Hearing (-) tinnitus (-) vertigo (-) earaches (-) infection (-) discharge.
Nose and sinuses: (-) colds (-) nasal stuffiness (-) discharge (-) itching (-) nosebleeds
Throat: (-) bleeding gums (-) dry mouth (-) frequent sore throats,
Neck: (-) masses, (-) CLAD (-) stiffness in the neck.
Breasts: (-) Lumps (-) pain (-) discomfort (-) nipple discharge
Respiratory: (-) Cough (-) dyspnea
Cardiovascular: (-) chest pain or discomfort (-) palpitations (-) dyspnea (-) high blood pressure (-)
orthopnea
Gastrointestinal: (-) heartburn (-) decreased appetite (-) nausea (-) Vomiting (-) diarrhea (-) constipation,
(-) abdominal pain, (-) excessive belching or passing of gas
Urinary: (-) Frequency of urination, (-) nocturia (-) urgency (-) burning or pain on urination (-)
incontinence (-) hematuria
Musculoskeletal: (-) stiffness (-) backache
Hematologic: (-) easy bruising or bleeding
Endocrine: (-) heat or cold intolerance (-) excessive sweating (-) excessive thirst or hunger,
Neurologic: (-) Fainting (-) weakness (-) paralysis (-) numbness or loss of sensation
Immunologic: (-) allergies

PHYSICAL EXAMINATION

Vitals Signs
Vital Signs Findings Normal Value
Temperature 38.2 36.5-37.5 C Febrile
Heart Rate 116 60-95 Tachycardia
Respiratory Rate 24 14-22 Tachypnea

Blood Pressure Not taken 100-120/60-75

O2 saturation 99% 96-100% Normal

Weight: 20 kg

General Appearance: Awake, weak looking, not in respiratory distress

Skin: fair skin, vesicular rashes and some crusted lesions all over the patient body, no masses,
capillary refill <2 secs, warm to touch, acyanotic, no jaundice, not pale
Head: normocephalic, no lice, hair equally distributed, no lesions, no masses
Eyes: anicteric sclerae, pinkish conjunctiva, eyes equally round and reactive to light (direct and
consensual), with Red orange reflex
Ears: Symmetrical, no redness, no discharges, no lesions, no skin tags, intact tympanic membrane pearly
white in color
Nose: (-) Alar flaring, No discharges, non-foul smelling
Throat: Moist lips and buccal mucosa, no tonsillopharyngeal congestion
Neck: No nuchal rigidity, no palpable cervical lymphadenopathy
Chest and lungs: Symmetrical Chest expansion, (+) Tachypnea, (-) Bilateral Course Crackles, (-)
intercostal and subcostal retractions
Breast: no lesions, no discharges, nipples are symmetrical
Heart: adynamic precordium, (+) tachycardia, regular rhythm, no murmur, 4th ICS LMCL, equal
peripheral pulses
Abdomen: flabby no discoloration, no visible masses, no striae, normoactive bowel sounds, soft
Genital/rectum: No lesions, no discoloration, no masses, no discharges.
Extremities: no gross deformity, no edema, full and equal pulses
Neurologic: conscious
Cranial Nerves: No significant findings
Motor: no asymmetry, with good muscle tone and activity
Sensory: no obvious sensory deficit
GCS: 15/15
Salient features:
 7 years old
 female
 rashes
 fever
 (+) asthma
 exposed with person who has chicken pox
 incomplete dosage of immunization
 headache
 tachycardia
 tachypnea
 weak looking
 vesicular rashes and some crusted lesions all over the body

DIFFERNETIAL DIAGNOSIS

Differential Diagnosis Rule in Rule out

Varicella Zoster  Fever
 Incomplete dose of varicella
zoster vaccine
 Exposed to person with
chicken pox
 vesicular rashes and some
crusted lesions all over the
patient body
Herpes simplex virus  fever  Shallow ulcers
 vesicular rashes and some  Vesicular rashes with
crusted lesions all over the erythematous base
patient body  Submandibular
lymphadenopathy
 Pharyngitis tonsillitis
 Burning or tingling
sensations on affected areas

WORKING IMPRESSION
VARICELLA ZOSTER VIRUS

COURSE IN THE EMERGENCY ROOM

Patient was seen and examined at the Emergency room. History and Physical Examination were
done. Patient was given with Paracetamol 250mg/5ml – 4ml and advised the mother to do tepid sponge
bath. Patient was advised for discharge with home medications of Paracetamol 250mg/5ml syrup – 4ml
every 4 hours for Temp. of > 37.8 degrees Celsius, Acyclovir 200mg/5ml suspension – 2ml which will be
given every 4 hours for 7 days and Cetirizine 5mg/5ml syrup – 5ml given once a day for itchiness. Patient
was advised to eat citrus fruits which are high in Vitamin C like oranges to boost the patient’s immunity. No
physical activity restriction. Patient was also advised to be isolated in the house to prevent spread of
infection and to avoid scratching or removing crusted lesions. Mother was advised to complete the patient’s
immunization to prevent other disease which can be prevented by providing vaccination. Patient was
advised to rest for about 7 days and follow up with pediatrician of choice.

FINAL DIAGNOSIS
VARICELLA ZOSTER VIRUS INFECTION

Varicella Zoster Virus - causes primary, latent, and recurrent infections. The primary infection is
manifested as varicella (chickenpox) and results in establishment of a lifelong latent infection of sensory
ganglion neurons. Reactivation of the latent infection causes herpes zoster (shingles). Although often a
mild illness of childhood, varicella can cause substantial morbidity and mortality in otherwise healthy
children. Morbidity and mortality are higher in immunocompetent infants, adolescents, and adults as well
as in immunocompromised persons.
Primary clinical disease can be prevented by immunization with live-attenuated VZV vaccine
(varicella vaccine).
Base on our patient’s history and physical examination, patient was recently exposed to a person
who was diagnosed with chicken pox at the same time patient didn’t have a complete immunization for
varicella zoster. Other supportive basis on the diagnosis of varicella zoster in the patient is the
presentation of fever and the pattern or rashes which is centripetal in manner of spread as a macular
rash. Macular rashes then turned to fluid filled vesicles which is a clinical manifestation of varicella zoster.

DISCUSSION

Epidemiology

Most children were infected by 15 yr of age, with fewer than 5% of adults remaining susceptible.
This pattern of infection at younger ages remains characteristic in all countries in temperate climates. In
contrast, in tropical areas, children acquire varicella at older ages and a higher proportion of young adults
remain susceptible leading to a higher proportion of cases occurring among adults.
Within households, transmission of VZV to susceptible individuals occurs at a rate of 65-86%;
more casual contact, such as occurs in a school classroom, is associated with lower attack rates among
susceptible children. Persons with varicella are contagious 24-48 hr before the rash is evident and until
vesicles are crusted, usually 3-7 days after onset of rash. Susceptible persons may also acquire varicella
after close, direct contact with adults or children who have herpes zoster.

Etiology
VZV is a neurotropic human herpesvirus with similarities to herpes simplex virus. These
enveloped viruses contain double-stranded DNA genomes that encode more than 70 proteins, including
proteins that are targets of cellular and humoral immunity.

Pathophysiology
VZV is transmitted by contact with oropharyngeal secretions and the fluid of skin lesions of
infected individuals, either by airborne spread or through direct contact. Primary infection (varicella)
results from inoculation of the virus onto the mucosa of the upper respiratory tract and tonsillar lymphoid
tissue. During the early part of the 10-21 day incubation period, virus replicates in the local lymphoid
tissue, and then a brief subclinical viremia spreads the virus to the reticuloendothelial system.
Widespread cutaneous lesions occur during a 2nd viremic phase that lasts 3-7 days. Peripheral blood
mononuclear cells carry infectious virus, generating new crops of vesicles during this period of viremia.
VZV is also transported back to the mucosa of the upper respiratory tract and oropharynx during the late
incubation period, permitting spread to susceptible contacts 1-2 days before the appearance of rash.

Host immune responses limit viral replication and facilitate recovery from infection. In the
immunocompromised child, the failure of immune responses, especially cell-mediated immune
responses, results in continued viral replication that may lead to prolonged and/or disseminated infection
with resultant complications in the lungs, liver, brain, and other organs. Virus is transported in a
retrograde manner through sensory axons to the dorsal root ganglia throughout the spinal cord, where the
virus establishes latent infection in the neurons and satellite cells associated with these axons. Virus may
also reach the ganglia by the hematogenous route. Subsequent reactivation of latent virus causes
herpes zoster, a vesicular rash that usually is dermatomal in distribution.

Clinical Manifestation
Varicella is an acute febrile rash illness. It has variable severity but is usually self-limited.
 The illness usually begins 14-16 days after exposure, although the incubation period can range
from 10-21 days. Subclinical varicella is rare; almost all exposed, susceptible persons experience a rash,
albeit so mild in some cases that it may go unnoticed. Prodromal symptoms may be present, particularly
in older children and adults. Fever, malaise, anorexia, headache, and occasionally mild abdominal pain
may occur 24-48 hr before the rash appears. Temperature elevation is usually 37.8-38.9°C (100-102°F)
but may be as high as 41.1°C (106°F); fever and other systemic symptoms usually resolve within 2-4
days after the onset of the rash.
Varicella lesions often appear first on the scalp, face, or trunk. The initial exanthem consists of
intensely pruritic erythematous macules that evolve through the papular stage to form clear, fluid-filled
vesicles. Clouding and umbilication of the lesions begin in 24-48 hr. While the initial lesions are crusting,
new crops form on the trunk and then the extremities; the simultaneous presence of lesions in various
stages of evolution is characteristic of varicella. The distribution of the rash is predominantly central or
centripetal with the greatest concentration on the trunk and proximally on the extremities. Ulcerative
lesions involving the mucosa of the oropharynx and vagina are also common; many children have
vesicular lesions on the eyelids and conjunctivae, but corneal involvement and serious ocular disease are
rare.
The average number of varicella lesions is about 300, but healthy children may have fewer than
10 to more than 1,500 lesions. In cases resulting from secondary household spread and in older children,
more lesions usually occur, and new crops of lesions may continue to develop for more than 7 days. The
exanthem may be much more extensive in children with skin disorders, such as eczema or recent
sunburn. Hypopigmentation or hyperpigmentation of lesion sites persists for days to weeks in some
children, but severe scarring is unusual unless the lesions were secondarily infected.

Diagnosis
Varicella and herpes zoster have been diagnosed primarily by their clinical appearance.
Laboratory evaluation has not been considered necessary for diagnosis or management.
Complete Blood count may help in supporting the diagnosis of Varicelle Zoster, it usually shows
Leukopenia which is typical during the 1st 72 hr after onset of rash; it is followed by a relative and
absolute lymphocytosis. Results of liver function tests are also usually (75%) mildly elevated.

VZV can be identified quickly by direct fluorescence assay of cells from cutaneous lesions
(vesicular fluid) in 15-20 min, by PCR amplification testing (vesicular fluid, crusts) in hours to days,
depending on availability, and by rapid culture with specific immunofluorescence staining (shell vial
technique) in 48-72 hr. In the absence of vesicles or scabs, scrapings of maculopapular lesions can be
collected for PCR or direct fluorescence assay testing.

PCR is the most sensitive and allows for differentiation of wild-type and vaccine strains. Direct
fluorescence assay is specific and less sensitive than PCR but when available allows for rapid diagnosis.

TREATMENT
The only antiviral drug available in liquid formulation that is licensed for treatment of varicella for
pediatric use is acyclovir.

To be most effective, treatment should be initiated as early as possible, preferably within 24 hr of

the onset of the exanthem. There is less clinical benefit if treatment is initiated more than 72 hr after onset
of the exanthem.

Some experts recommend the use of famciclovir or valacyclovir in older children who can swallow
tablets. These drugs are highly active against VZV by the same mechanism as acyclovir and are better
absorbed by the oral route than acyclovir. Valacyclovir (20 mg/kg/dose; maximum: 1,000 mg/dose,
administered 3 times daily for 5 days) is licensed for treatment of varicella in children 2 to <18 yr of age,
and both valacyclovir and famciclovir are approved for treatment of herpes zoster in adults.
Intravenous therapy is indicated for severe disease and for varicella in immunocompromised
patients (even if begun more than 72 hr after onset of rash). Any patient who has signs of disseminated
VZV, including pneumonia, severe hepatitis, thrombocytopenia, or encephalitis, should receive immediate
treatment. IV acyclovir therapy (500 mg/m2 every 8 hr) initiated within 72 hr of development of initial
symptoms decreases the likelihood of progressive varicella and visceral dissemination in high-risk
patients. Treatment is continued for 7-10 days or until no new lesions have appeared for 48 hr.

Acyclovir-resistant VZV has been identified primarily in children infected with HIV. These children
may be treated with intravenous foscarnet (120 mg/kg/day divided every 8 hr for up to 3 wk). The dose
should be modified in the presence of renal insufficiency. Resistance to foscarnet has been reported with
prolonged use. Cidofovir is also useful in this situation. Because of the increased toxicity profile of
foscarnet and cidofovir, these 2 drugs should be initiated in collaboration with an infectious disease
specialist.

COMPLICATIONS
The most common complications among people who died from varicella were pneumonia, central
nervous system complications, secondary infections, and hemorrhagic conditions.
Varicella Zoster may be associated with severe complications, including staphylococcal and
streptococcal superinfection, pneumonia, encephalitis, bleeding disorders, congenital infection, and life-
threatening perinatal infection.

PROGNOSIS

Primary varicella has a mortality rate of 2-3 per 100,000 cases, with the lowest case fatality rates
among children 1-9 years of age (~1 death per 100,000 cases).

Herpes zoster among healthy children has an excellent prognosis and is usually self-limited. Severe
presentation with complications and sometimes fatalities can occur in immunocompromised children.

PREVENTION AND CONTROL

Person with varicella is contagious for 24-48 hour before the rash is apparent.

Infection control practices, including caring for patients with varicella in isolation rooms with
filtered air systems, are essential. All healthcare workers should have evidence of varicella immunity.
Unvaccinated healthcare workers without other evidence of immunity who have had a close exposure to
VZV should be furloughed for days 8-21 after exposure because they are potentially infectious during this
period.

Varicella vaccine contains live, attenuated VZV (Oka strain) and is indicated for subcutaneous
administration. Catch-up vaccination with the 2nd dose is recommended for children and adolescents
who received only 1 dose. Vaccination with 2 doses is recommended for all persons without evidence of
immunity. The minimum interval between the 2 doses is 3 mo for persons 12 yr of age or younger
and 4 week for older children, adolescents, and adults.
Administration of varicella vaccine within 4 wk of measles-mumps-rubella (MMR) vaccination is
associated with a higher risk for breakthrough disease; therefore, it is recommended that the varicella and
MMR vaccines either be administered simultaneously at different sites or be given at least 4 wk apart.
Varicella vaccine can be administered as a monovalent vaccine (for all healthy persons ≥12 mo of age) or
as the quadrivalent measles-mumps- rubella-varicella (MMRV) vaccine (for children age 12 mo
through 12 yr only).

HERPES SIMPLEX VIRUS

The 2 closely related herpes simplex viruses (HSVs), HSV type 1 (HSV-1) and HSV type 2 (HSV-2),
cause a variety of illnesses, depending on the anatomic site where the infection is initiated, the immune
state of the host, and whether the symptoms reflect primary or recurrent infection. Common infections
involve the skin, eye, oral cavity, and genital tract. Infections tend to be mild and self-limiting, except in
the immunocompromised patient and newborn infant, in whom they may be severe and life-threatening.

Etiology
 HSVs contain a double-stranded DNA genome of approximately 152 kb that encodes at least 84
proteins. The DNA is contained within an icosadeltahedral capsid, which is surrounded by an outer
envelope composed of a lipid bilayer containing at least 12 viral glycoproteins.

Clinical Manifestation
The hallmarks of common HSV infections are skin vesicles and shallow ulcers. Classic infections
manifest as small, 2-4 mm vesicles that may be surrounded by an erythematous base. These may persist
for a few days before evolving into shallow, minimally erythematous ulcers. The vesicular phase tends to
persist longer when keratinized epithelia is involved and is generally brief and sometimes just fleeting
when moist mucous membranes are the site of infection. Because HSV infections are common and their
natural history is influenced by many factors, including portal of entry, immune status of the host, and
whether it is an initial or recurrent infection, the typical manifestations are seldom classic. Most infections
are asymptomatic or unrecognized, and non classic presentations, such as small skin fissures and small
erythematous non vesicular lesions, are common.

Treatment
Three antiviral drugs are available in the United States for the management of HSV infections,
namely acyclovir, valacyclovir, and famciclovir. All 3 are available in oral form, but only acyclovir is
available in a suspension form.

Early initiation of therapy results in the maximal therapeutic benefit. All 3 drugs have exceptional
safety profiles and are safe to use in pediatric patients.
Doses should be modified in patients with renal impairment.

Prevention

Transmission of infection occurs through exposure to virus either as the result of skin-to-skin contact
or from contact with contaminated secretions. Good handwashing and, when appropriate, the use of
gloves provide healthcare workers with excellent protection against HSV infection in the workplace.
Healthcare workers with active oral facial herpes or herpes whitlow should take precautions, particularly
when caring for high-risk patients such as newborns, immunocompromised individuals, and patients with
chronic skin conditions. Patients and parents should be advised about good hygienic practices, including
handwashing and avoiding contact with lesions and secretions, during active herpes outbreaks. Schools
and daycare centers should clean shared toys and athletic equipment such as wrestling mats at least
daily after use. Athletes with active herpes infections who participate in contact sports such as wrestling
and rugby should be excluded from practice or games until the lesions are completely healed. Genital
herpes can be prevented by avoiding genital-genital and oral-genital contact. The risk for acquiring genital
herpes can be reduced but not eliminated through the correct and consistent use of condoms. Male
circumcision is associated with a reduced risk of acquiring genital HSV infection. The risk for transmitting
genital HSV-2 infection to a susceptible sexual partner can be reduced but not eliminated by the daily use
of oral valacyclovir by the infected partner.

References:

1. NELSONS TEXTBOOK OF PEDIATRICS

Case 2

GENERAL DATA

This is a case of VN, a 5 year male, Filipino, Catholic, born on June 24, 2011, currently residing in
Las Pinas City and was admitted for the 1st time in our institution last Oct 8, 2016

CHIEF COMPLAINT: loose bowel movement with abdominal pain

HISTORY OF PRESENT ILLNESS

1 day prior to consult, patient had 6 episodes of loose bowel movement, watery and some formed
stools. Brownish in color.it was assoiciated with abdominal pain during bowel movement and fever of 37.8
degrees Celsius. There is also 1 episode of vomiting with ingested food. Patient was given with Paracetamol
250mg/5ml – 5ml given whenever the patient’s temperature increases. Hydrite was also given as tolerated
by the patient. No others associated symptoms like cough, cold, difficulty of breathing, and dysuria. No
consultation was done.
Few hours prior to consult patient had 5 episodes of loose bowel movement watery and brownish
in characteristics. Parents estimated the amount of about 120ml. associated also with abdominal pain and
decrease in appetite.
Dew to increase progression of above symptoms, parents decided to sought for consult.

PAST MEDICAL HISTORY

(-) Allergies (+)Asthma – no maintenance (+) Pneumonia - treated

(-) Heart diseases (-) Hypertension
(-)Diabetes (-)Cancer (-) TB

FAMILY HISTORY:
(+) Hypertension - paternal (-) heart disease (+) asthma- paternal (-) allergy
(-) blood disorder (-) diabetes (-) cancer (-) TB

DEVELOPMENTAL MILESTONE

A 1 month old, patient was able to raise head from prone position and alerts to sound, at 2
months old, patient was able to hold head midline and lifts chest off the table, he smiles socially after
being stroked or talked to. At 3 months old, he supports on forearms in prone position. Hold head up
steadily, he is able to produce long vowel sounds in musical fashion (Coos). At 4 months old, patient rolls
over, supports on wrists and shifts weight, able to laugh and oriented to voice. At 6 months old, patient
was able to sit unsupported, puts feet in mouth in supine position, babbles, and laterally oriented to bell.
At 9 months, patient was able to pivot when sitting, crawls well, pulls to stand, cruises, able to say
“mama” “dada” indiscrimately, gestures, wave bye bye and understands “no”. at 12 months patient was
able to walk alone, uses 2 words other than mama and dada or proper nouns, jargoning started, and able
to do one step command with gesture. At 15 month, patient is able to creeps up the stairs, walk
backwards independently, uses 4-6 words, and follows 1 step comman without gesture. On 18th months
patient is able to run, throws object from standing without falling, mature jargoning, able to speak 7-10
words vocabulary and knows parts of the body. At 24th months old patient is able to walk up and down
and step without help. Patient is able to use pronouns (I, you, me) inappropriately, follows 2 step
commands, has 50 word vocabulary and uses two word sentences.
At 3 years old, patient can alternate feet when going up steps and can pedal tricycle. He was able
to use minimum of 250 words, 3 word sentences, uses plurals, knows all pronounce and repeats 2 digits.
On his 4th year, patient is able to hop, skip, alternates feet going down steps. He already knows colors,
says song or poem from memory and asks questions. On his 5th year, patient is able to skip alternating
feet, jumps over low obstacles. He is able to print first name and asks what a word means.

NUTRITION
Mostly patient eats solid foods. Take Celine as vitamins

REVIEW OF SYSTEM

General: (+) Weakness (-) Fatigue (-) weight loss (-) irritability
Skin: (-) lumps (-) sores (-) dryness (-) color change (-) changes in hair or nails.
Head: (-) Headache (-) head injury (-) dizziness (-) lightheadedness
Eyes: (-) Vision changes (-) glasses or contact lenses (-) pain (-) redness (-) excessive tearing
(-) flashing lights
Ears: (-) decreased Hearing (-) tinnitus (-) vertigo (-) earaches (-) infection (-) discharge.
Nose and sinuses: (-) colds (-) nasal stuffiness (-) discharge (-) itching (-) nosebleeds
Throat: (-) bleeding gums (-) dry mouth (-) frequent sore throats,
Neck: (-) masses, (-) CLAD (-) stiffness in the neck.
Breasts: (-) Lumps (-) pain (-) discomfort (-) nipple discharge
Respiratory: (-) Cough (-) dyspnea
Cardiovascular: (-) chest pain or discomfort (-) palpitations (-) dyspnea (-) high blood pressure (-)
orthopnea
Urinary: (-) Frequency of urination, (-) nocturia (-) urgency (-) burning or pain on urination (-)
incontinence (-) hematuria
Musculoskeletal: (-) stiffness (-) backache
Hematologic: (-) easy bruising or bleeding
Endocrine: (-) heat or cold intolerance (-) excessive sweating (-) excessive thirst or hunger,
Neurologic: (-) Fainting (-) weakness (-) paralysis (-) numbness or loss of sensation
Immunologic: (-) allergies

PHYSICAL EXAMINATION

Vitals Signs
Vital Signs Findings Normal Value
Temperature 36.7 36.5-37.5 C Afebrile
Heart Rate 110 65-110 Normal
Respiratory Rate 24 20-25 Normal

Blood Pressure Not taken 95-110/ 60-75

O2 saturation 99% 96-100% Normal

Weight: 17 kg

General Appearance: Awake, weak looking, not in respiratory distress

Skin: fair skin, moist skin, no masses, capillary refill <2 secs, warm to touch, acyanotic, no jaundice, not
pale
Head: normocephalic, no lice, hair equally distributed, no lesions, no masses
Eyes: anicteric sclerae, pinkish conjunctiva, eyes equally round and reactive to light (direct and
consensual), with Red orange reflex
Ears: Symmetrical, no redness, no discharges, no lesions, no skin tags, intact tympanic membrane pearly
white in color
Nose: (-) Alar flaring, No discharges, non-foul smelling
Throat: Dry lips, moist buccal mucosa, no tonsillopharyngeal congestion
Neck: No nuchal rigidity, no palpable cervical lymphadenopathy
Chest and lungs: Symmetrical Chest expansion, (-) Tachypnea with regular rhythm, (-) Bilateral Course
Crackles , (-) intercostal and subcostal retractions
Breast: no lesions, no discharges, nipples are symmetrical
Heart: adynamic precordium, (-) tachycardia, regular rhythm, no murmur, 4th ICS LMCL, equal peripheral
pulses
Abdomen: flabby no discoloration, no visible masses, no striae, hyperactive bowel sounds (43 per
min.), soft
Genital/rectum – No lesions, no discoloration, no masses, no discharges.
Extremities: no gross deformity, no edema, full and equal pulses
Neurologic: conscious
Cranial Nerves: No significant findings
Motor: no asymmetry, with good muscle tone and activity
Sensory: no obvious sensory deficit
GCS: 15/15

Salient Features:
 5 years old
 male
 loose watery bowel movement
 abdominal pain
 fever
 weakness
 hyperactive bowel sounds (43 per minute)

DIFFERENTIAL DIAGNOSIS

Differential Diagnosis Rule in Rule out

Intestinal Amoebiasis  Fever
 Abdominal pain
 Heme positive on stool
 Frequent bowel movement
Shigellosis  Fever  Gross bloody mucoid stool
 Abdominal pain  Abdominal tenderness
 Watery loose bowel
movement
 Hyperactive bowel sounds

Enteropathogenic  Fever
Escherichia Coli  Loose bowel movement

WORKING IMPRESSION
ACUTE GASTROENTERITIS WITH MILD DEHYDRATION

COURSE IN THE EMERGENCY ROOM

 Patient was seen and examined at the Emergency room. History and Physical Examination were
done. Laboratory that were done were: Complete blood count with actual platelet count and stool exam
was ordered. Therapeutics: Hydrite diluted to 200 ml of water. Laboratory results were interpreted
accordingly. Patient was advised for discharge with home medications: Metronidazole 125mg/5ml which
will be given 9ml 3 times a day for 7 days. ORS (Pedialyte) 1 sachet in 200ml of water as tolerated and
Paracetamol 250mg/5ml given 5ml every 4 hours for temp. of 37.8 degrees Celsius. Mother was advised
to put patient in soft diet such as porridge and soup with rice. Increase oral fluid intake was also advised
with bed rest until patient is able to increase his strength. Mother was advised to watch out for non for
persistence of fever which doesn’t relieve by medication, persistence of loose bowel movement after 7 days
of treatment, signs of dehydration like sunken eye balls, dry lips and increase pulses. Patient was advised
to follow up with pediatrician.

COMPLETE BLOOD COUNT:

Result Normal Values
Red Blood Cells 5.02 4.0 -5.0x 10^12 /L
Hematocrit 0.42 0.33-0.43L Normal
Hemoglobin 135 115.00-145.00 g/l Normal
White Blood Cells 14.1 4.0-12.0 x 10^9 /L Increased
Segmenters 0.75 0.54-0.62 Increased
Eosinophil 0.01 0.01-0.03 normal
Lymphocyte 0.16 0.25-.33 Decreased
Monocyte 0.08 0.03-0.07 Slightly increased
Platelet Count 426 150-400,000x 10^9/L Increased
MCV 83 76-90 fl Normal
MCH 26.8 25-31 pg Normal
MCHC 324 496-558 g/L Decreased

STOOL EXAM
RESULT
COLOR Brown
CONSISTENCY Mucoid
BLOOD (GROSS) Negative
BLOOD (CHEM)
PUS 15-20/ HPF
MUCUS Positive
BILE
OVA AND PARASITE E. Histolytica cyst seen
CELLS
REMARKS: RBC

FINAL DIAGNOSIS:
INTESTINAL AMOEBIASIS
In most infected individuals, Entamoeba histolytica or a related species parasitizes the lumen of
the gastrointestinal tract and causes few symptoms or sequelae. E. histolytica is the only invasive species
and can cause amebic colitis with parasitic invasion of the intestinal mucosa and amebic liver abscess
with dissemination of the parasite to the liver.
Base on the patient’s history, physical examination and laboratory tested, all the symptoms of
abdominal pain, loose bowel movement, fever and hyperactive bowel movement may give us an idea that
the condition is on gastrointestinal origin. Stool exam was done and showed that patient has heme
positive on stool with E. hystolytica seen. With these presentation patient is ought to have amoebiasis.

DISCUSSION

Epidemiology

It is estimated that infection with E. histolytica leads to 50 million cases of symptomatic disease
and 40,000-110,000 deaths annually. Amebiasis is the second leading parasitic cause of death
worldwide, after malaria. Prospective studies show that 4-10% of individuals infected with E. histolytica
develop amebic colitis and that <1% of infected individuals develop disseminated disease, including
amebic liver abscess.

Amebiasis is endemic to Africa, Latin America, India, and Southeast Asia. Residents of mental
health institutions and men who have sex with men are also at increased risk for invasive amebiasis.
Food or drink contaminated with Entamoeba cysts and oral-anogenital sex are the most common means
of infection. Untreated water and night soil (human feces used as fertilizer) are important sources of
infection. Food handlers shedding amebic cysts play a role in spreading infection. Direct contact with
infected feces can also result in person-to-person transmission.

Etiology

E. histolytica, the main pathogenic species, causes a spectrum of disease and can become
invasive in 4-10% of infected patients. Patients previously described as asymptomatic carriers of E.
histolytica based on microscopy findings were likely harboring E. dispar. Four other species of
nonpathogenic Entamoeba are known to colonize the human gastrointestinal tract: E. coli, E. hartmanni,
E. gingivalis, and E. polecki.

Infection is acquired through the ingestion of parasite cysts, which measure 10-18 μm in diameter
and contain 4 nuclei. Cysts are resistant to harsh environmental conditions, including chlorine
concentrations commonly used in water purification, but can be killed by heating to 55°C (131°F). After
ingestion, cysts are resistant to gastric acidity and digestive enzymes and germinate in the small intestine
to form trophozoites. These large, actively motile organisms colonize the lumen of the large intestine and
may invade the mucosal lining. Infection is not usually transmitted by trophozoites, as these rapidly
degenerate outside the body and are unable to survive the low pH of the stomach if swallowed.

Pathophysiology
 Trophozoites are responsible for tissue invasion and destruction. These attach to colonic epithelial
cells by a galactose and N-acetyl-dgalactosamine– specific lectin. This lectin is also thought to be
responsible for resistance to complement-mediated lysis. Once attached to the colonic mucosa, amebas
release proteases that allow for penetration through the epithelial layer. Host cells are destroyed by
cytolysis and apoptosis. Cytolysis is mediated by trophozoite release of amoebapores (pore-forming
proteins), phospholipases, and hemolysins. Amoebapores, which cause a massive influx of extracellular
calcium, may also be partially responsible for the induction of apoptosis that occurs with amebic liver
disease and colitis. Once host cells are partially digested by amebic proteases, the degraded material is
internalized through phagocytosis. Early invasive amebiasis produces significant inflammation, due in part
to parasite-mediated activation of nuclear factor-κB. Once E. histolytica trophozoites invade the intestinal
mucosa, the organisms multiply and spread laterally underneath the intestinal epithelium to produce the
characteristic flask-shaped ulcers. Amebas produce similar lytic lesions if they reach the liver. These
lesions are commonly called abscesses, although they contain no granulocytes. Well-established ulcers
and amebic liver abscesses demonstrate little local inflammatory response.

Immunity to infection is associated with a mucosal secretory IgA response against the galactose/N-
acetyl-d-galactosamine lectin. Neutrophils appear to be important in initial host defense, but E. histolytica–
induced epithelial cell damage releases neutrophil chemoattractants, and E. histolytica is able to kill
neutrophils, which then release mediators that further damage epithelial cells. The disparity between the
extent of tissue destruction by amebas and the absence of a local host inflammatory response in the
presence of systemic humoral (antibody) and cell-mediated responses may reflect both parasite-mediated
apoptosis and the ability of the trophozoite to kill not only epithelial cells but neutrophils, monocytes, and
macrophages.

Clinical Manifestation
Clinical presentations range from asymptomatic cyst passage to amebic colitis, amebic dysentery,
ameboma, and extraintestinal disease. Up to 10% of infected persons develop invasive disease within a
year. Thus, asymptomatic carriers should be treated. Severe disease is more common in young children,
pregnant women, malnourished individuals, and persons taking corticosteroids, and invasive disease is
more common in men. Extraintestinal disease usually involves the liver, but less common extraintestinal
manifestations include amebic brain abscess, pleuropulmonary disease, ulcerative skin, and genitourinary
lesions.

Amebic Colitis
Amebic colitis may occur within 2 wk of infection or may be delayed for months. The onset is usually
gradual, with colicky abdominal pains and frequent bowel movements (6-8/day). Diarrhea is frequently
associated with tenesmus. Almost all stool is heme-positive, but most patients do not present with grossly
bloody stools. Generalized constitutional symptoms and signs are characteristically absent, with fever
documented in only one third of patients. Amebic colitis affects all age groups but is strikingly common in
children 1-5 yr of age. Severe amebic colitis in infants and young children tends to be rapidly progressive
with more frequent extraintestinal involvement and high mortality rates, particularly in tropical countries.
Amebic dysentery can result in dehydration and electrolyte disturbances.

Diagnosis

A diagnosis of amebic colitis is made in the presence of compatible symptoms with detection of E.
histolytica antigens in stool. This approach has a >95% sensitivity and specificity and coupled with a positive
serology test is the most accurate means of diagnosis in developed countries.
The E. histolytica II stool antigen detection test (TechLab, Blacksburg, VA) is able to distinguish E.
histolytica from E. dispar infection. Microscopic examination of stool samples has a sensitivity of 60%.
Sensitivity can be increased to 85-95% by examining 3 stools, as excretion of cysts can be intermittent.
However, microscopy cannot differentiate between E. histolytica and E. dispar unless phagocytosed
erythrocytes (specific for E. histolytica) are seen.

TREATMENT
 Invasive amebiasis is treated with a nitroimidazole such as metronidazole or tinidazole and then
a luminal amebicide. simpler dosing and less-frequent adverse effects. These adverse effects include
nausea, abdominal discomfort, and a metallic taste that disappears after completion of therapy. Therapy
with a nitroimidazole should be followed by treatment with a luminal agent, such as paromomycin (which is
preferred) or iodoquinol. Paromomycin should not be given concurrently with metronidazole or tinidazole,
because diarrhea is a common side effect of paromomycin and may confuse the clinical picture.
Asymptomatic intestinal infection with E. histolytica should be treated preferably with paromomycin
or alternatively with either iodoquinol or diloxanide furoate. For fulminant cases of amebic colitis, some
experts suggest adding dehydroemetine (1 mg/kg/day subcutaneously or IM, never IV), available only
through the Centers for Disease Control and Prevention. Patients should be hospitalized for monitoring
if dehydroemetine is administered. Dehydroemetine should be discontinued if tachycardia, T-wave
depression, arrhythmia, or proteinuria develops.

COMPLICATIONS
Complications of amebic colitis include acute necrotizing colitis, amoebas, toxic megacolon,
extraintestinal extension, or local perforation and peritonitis. Less commonly, a chronic form of amebic
colitis develops, often recurring over several years. Amoebas are nodular foci of proliferative inflammation
that sometimes develop in the wall of the colon. Chronic amebiasis should be excluded before initiating
corticosteroid treatment for inflammatory bowel disease, as corticosteroid therapy given during active
amebic colitis is associated with high mortality rates.
An amebic liver abscess may rupture into the peritoneum, pleural cavity, skin, and pericardium.
Cases of amebic abscesses in extrahepatic sites, including the lung and brain, have been reported.

PROGNOSIS

Most infections evolve to either an asymptomatic carrier state or eradication. Extraintestinal

infection carries about a 5% mortality rate.

PREVENTION AND CONTROL

Control of amebiasis can be achieved by exercising proper sanitation and avoiding fecal-oral
transmission. Regular examination of food handlers and thorough investigation of diarrheal episodes may
help identify the source of infection. No prophylactic drug or vaccine is currently available for amebiasis.
Immunization with a combination of galactose/N-acetyl-d-galactosamine lectin and CpG
oligodeoxynucleotides is protective against amebic trophozoite challenge in animals, and an intranasal
galactose-lectin subunit vaccine is protective in baboons.

SHIGELLOSIS
 Shigella causes an acute invasive enteric infection clinically manifested by diarrhea that is often
bloody. The term dysentery is used to describe the syndrome of bloody diarrhea with fever, abdominal
cramps, rectal pain, and mucoid stools. Bacillary dysentery is a term often used to distinguish dysentery
caused by Shigella from amoebic dysentery caused by Entamoeba histolytica.

ETIOLOGY
Four species of Shigella are responsible for bacillary dysentery: Shigella dysenteriae (serogroup
A), Shigella flexneri (serogroup B), Shigella boydii (serogroup C), and Shigella sonnei (serogroup D). There
are 15 serotypes in group A, 19 serotypes in group B, 19 serotypes in group C, and one serotype in group
D. Species classification has important therapeutic implications because the species differ in both
geographic distribution and antimicrobial susceptibility.

CLINICAL MANIFESTATION
Severe abdominal pain, high fever, emesis, anorexia, generalized toxicity, urgency, and painful
defecation characteristically occur. The diarrhea may be watery and of large volume initially, evolving into
frequent, small-volume, bloody mucoid stools. Most children never progress to the stage of bloody diarrhea,
but some have bloody stools from the outset. Significant dehydration is related to the fluid and electrolyte
losses in feces and emesis. Untreated diarrhea can last 7-10 days; only approximately 10% of patients
have diarrhea persisting for longer than 10 days. Persistent diarrhea occurs in malnourished infants,
children with AIDS, and occasionally previously normal children. Even nondysenteric disease can be
complicated by persistent illness. Physical examination initially shows abdominal distention and
tenderness, hyperactive bowel sounds, and a tender rectum on digital examination. Rectal prolapse may
be present, particularly in malnourished children

TREATMENT
As with gastroenteritis from other causes, the first concern in a child with suspected shigellosis
should be for fluid and electrolyte correction and maintenance (see Chapter 340). Drugs that retard
intestinal motility (e.g., diphenoxylate hydrochloride with atropine [Lomotil] or loperamide [Imodium]) should
not be used because of the risk of prolonging the illness. Nutrition is a key concern in areas where
malnutrition is common. A high-protein and high-caloric diet during convalescence enhances growth in the
following 6 mo.

The next concern is a decision about the use of antibiotics. Although some authorities recommend
withholding antibacterial therapy because of the self-limited nature of the infection, the cost of drugs, and
the risk of emergence of resistant organisms, there is a persuasive logic in favor of empirical treatment of
all children in whom shigellosis is strongly suspected.

PREVENTION
Numerous measures have been recommended to decrease the risk of Shigella transmission to
children. Mothers should be encouraged to prolong breastfeeding of infants. Families and daycare
personnel should be educated in proper handwashing techniques and encouraged to wash hands after
using the toilet, changing diapers, or engaging in preparation of foods. They should be taught how to
manage potentially contaminated materials such as raw vegetables, soiled diapers, and diaper-changing
areas. Children with diarrhea should be excluded from childcare facilities. Children should be supervised
when handwashing after they use the toilet. Caretakers should be informed of the risk of transmission if
they prepare food when they are ill with diarrhea. Families should be educated regarding the risk of
swallowing contaminated water from ponds, lakes, or untreated pools. In developing countries, a safe water
supply and appropriate sanitation systems are important measures for reducing the risk for shigellosis.
There is not yet a vaccine that is effective for preventing infection by Shigella. Measles immunization can
substantially reduce the incidence and severity of diarrheal diseases, including shigellosis. Every infant
should be immunized against measles at the recommended age.

ENTEROPATHOGENIC ESCHERICHIA COLI

 EPEC are a major cause of acute, prolonged, and persistent diarrhea in children younger than 2 yr
of age in developing countries (20% of infant diarrhea). In developed countries, EPEC are responsible for
occasional outbreaks in daycare centers and pediatric wards. Profuse watery, nonbloody diarrhea with
mucus, vomiting, and low-grade fever are common symptoms. Prolonged diarrhea (>7 days) and persistent
diarrhea (>14 days) can lead to malnutrition, a potentially serious outcome of EPEC infection in infants in
the developing world. Studies show that breastfeeding is protective against diarrhea caused by EPEC.

References:

1. NELSONS TEXTBOOK OF PEDIATRICS