Boook

AGO MEDICAL AND EDUCATION CENTER
BICOL CRISTIAN COLLAGE OF MEDICINE

LEGAZPI CITY
In partial fulfillment of the

Requirements for the degree of
Doctor of Medicine
By
DeepakSingh Yadav
Junior Medical Intern
BCCM 2020
A Compilation of clinical histories in my one year clinical rotation in Bicol

Medical Center, Bicol Regional Teaching and Training Hospital, Don Susano Rodríguez
Medical Hospital, Legazpi Eye Center and Ago General Hospital.
OUTLINE
PEDIATRIC
1. Enteric Fever
2. Pneumonia
3. Dengue
INTERNAL MEDICINE
1. Pulmonary Tuberculosis
2. Dengue
3. Schizophrenia
SURGERY
1. Appendicitis
2. Cholecystitis
3. Burn
OBSTETRICS AND GYNAECOLOGIST

1. Ovarian dermoid cyst
2. Normal labor delivery
PEDIATRIC DEPARTMENT
ENTERIC FEVER
ABSTRACT
Children bear a substantial proportion of the enteric fever disease burden in endemic areas.
Controversy persists regarding which age groups are most affected, leading to uncertainty
about optimal intervention strategies. We performed a systematic review and meta-analysis of
studies in Asia and Africa to compare the relative proportion of children with enteric fever in
the age groups <5 years, 5–9 years, and 10–14 years. Overall, studies conducted in Africa
showed a relatively smaller occurrence of disease in the youngest age group, whereas in Asia
the picture was more mixed with a very large degree of heterogeneity in estimates. The
clinical features of enteric fever reviewed here differ between younger and older children and
adults, likely leading to further uncertainty over disease burden. It is evident from our review
that preschool children and infants also contribute a significant proportion of disease burden
but have not been adequately targeted via vaccination programs, which have been focusing
primarily on school-based vaccination campaigns.
Enteric fever, caused by Salmonella enterica subspecies enterica serovars Typhi, Paratyphi A,
Paratyphi B, and Paratyphi C, is a major cause of morbidity for human populations in
affected regions of the world. Currently, it is estimated that there are >26 million patients
with a blood culture positive for enteric fever annually with a 1% fatality rate. The majority
of existing epidemiological evidence comes from studies in adult populations. There are
conflicting opinions about the rate of disease in young children, especially infants, even
though a substantial burden of disease is suffered by young children in endemic regions.
PATIENT HISTORY
Informant: Mother
Reliability: 95%

GENERAL DATA:

This is a case of K.T. 1 year and 5 months-old male, Filipino, Roman Catholic, born
on May 21, 2018 from Zone 1, Pilar, Sorsogon , admitted for the first time at Bicol Medical
Center on December 19, 2019.

CHIEF COMPLAINT: fever

HISTORY OF PRESENT ILLNESS:

2 week prior to admission, patient had on and fever , This was accompanied by abdominal
pain and solid greenish mucoid stool, No consult was done. He was given Paracetamol 120
mg/ml syrup, 3 ml 3x a day which offered temporary relief of fever.
3 days prior to admission, above symptoms persisted. He was brought for consult at a local
health center and prescribed paracetamol and chloramphenicol with unrecalled doses , which
was given a temporary relief.
1 days prior to admission, still with fever, abdominal pain , now accompanied by cough and
colds.
Few hours prior to admission, signs and symptoms persisted. He was brought for consult at a
private pediatrician, then referred to this institution, hence admitted.

PERSONAL HISTORY:

Prenatal— At 6th months gestation, the mother had occasional cough and colds; no
medications taken. She had prenatal check-up at the Barangay Health Center once a month
from 1st month to 8th month AOG. TT4. Supplementation include ferrous sulfate taken for 8
months.

Birth/Postnatal— Born full term via SVD at home assisted by a midwife to a then 30 year-old
G4P4. No complications. Newborn had bowel movements and urine output within 24 hours
of life.

GROWTH & DEVELOPMENT:

Gross motor:
4 months old- held head
6 mo- rolled over
7 mo- sat without support
8 mo- stood without support
1 y/o- walked alone

Fine motor:
8 months old- pincer grasp
Expressive language:
7 months old- babbling
1 y/o- first word: ‘Mama’

Personal/Psychosocial:
3 mo- social smile
7 mo- stranger anxiety
8 mo- first tooth

IMMUNIZATION:
BCG at birth
Hepatitis B at birth, 1 mo, 6 mo
DPT at 6, 10, 14 weeks
OPV at 6, 10, 14 weeks
Hib at 2, 4, 6 months
Measles at 9 months

NUTRITIONAL HISTORY:

Patient was exclusively breastfed from birth up to 1 year and 1 month old. He
was bottle fed thereafter up to present with powdered milk drink (dilution of 3 scoops: 240
ml) 7-8x a day. He started solids at 6 months with baby food. Presently, he is able to take soft
foods such as rice and crackers.

PAST MEDICAL HISTORY:

No known medical conditions such as bronchial asthma, congenital disorders, seizure
disorder, cardiac disease, blood dyscrasia or other conditions.
No previous hospitalization, surgical operation and accidents.
No known allergy to food and drugs.

FAMILY HISTORY:
No relative with PTB, asthma, seizure disorder, HTN, DM, cardiac disease, stroke, renal
disease, gastrointestinal disease, malignancies and congenital defects.

SOCIAL HISTORY:

The patient is the youngest among 2 siblings. 23 year-old mother is a high school graduate
and housekeeper. 21 year-old father is a high school graduate working as a construction
worker. Sibling is a 4 year-old girl. The household has 4 members, composed of the
immediate family, together in a single-room owned house made of light materials, which has
a 15-meter distance from the neighboring house. Drinking source is a water pump,
with sterilization applied. They have no toilet facility at home; utilizes a common toilet.
Garbage disposal is through burning. They keep 3 dogs as pets.

REVIEW OF SYSTEMS:

General: No weight loss.
Skin: No pruritus and easy bruising.
HEENT: No headache, redness, ear discharge, nasal discharge, mouth sores,
Sore throat, neck lumps andstiffness.
Musculoskeletal: No muscle and joint pain/swelling, no limitation of movement.
Cardiovascular: No tachycardia, orthopnea, dyspnea, edema, and chest pain.
Gastrointestinal: No bowel changes. Abdominal pain.
Urinary: No urgency, frequency, gross hematuria, andenuresis.
Neurologic: No tics or seizures.

PHYSICAL EXAMINATION:

General Survey: Cuddled by mother, awake, conscious, not in respiratory distress, febrile

Vital Signs: Weigh 13 kg , Height 75 cm, CR 158 bpm, RR40/min, Temperature 38.1°C

Z-score:
Length-for-age: Below -3 StuntedWeight-for-age: Above -2 Normal
Skin: No pallor, jaundice or pigmentation, good turgor, no lesions.

HEENT: Normocephalic. Anicteric sclerae, pink palpebral conjunctivae, pupils 2-4
mm equally reactive and responsive to light and accommodation. Pinnae without deformity,
no ear discharge. Patent nasal septum. Pinkish oral mucosa.
No tonsillopharyngeal congestion. No cervical lymphadenopathy.

Chest & Lungs: Flat, no scars, symmetrical chest expansion, tachypneic, (-)
subcostal retractions. No palpable mass. (-) crackles and occasional wheezes on bibasal lung
fields.

Heart: Adynamic precordium, no heaves, no thrills. PMI at 4th left intercostal space
midclavicular line. Tachycardic, regular rhythm, no murmurs.

Abdomen: Globular. Normal active bowel sounds. Soft, non-tender, no palpable mass, liver
and spleen non-palpable.

Genitalia: Descended testes, good rugae, central urethral orifice; no phimosis, no hydrocoele.

Extremities: Equal length, no edema, no cyanosis, no joint swelling and tenderness. Full and
equal pulses. Full range of motion. CRT <2s
Neurologic Examination:
Mental status: Conscious, coherent, GCS 15

Cranial nerves:
CN I Not tested
II Pupils 2-3 mm equally reactive and responsive to light and
accommodation
III, IV, Extraocular movements intact
VI
V (+) corneal blink reflex
VII Symmetrical facial movements
VIII Responds to name-calling
IX, X (+) gag reflex
XI Can shrug shoulders
XII Midline tongue without fasciculations

Motor:Sensory:
Good muscle tone and bulk
Deep Tendon Reflexes:
Biceps Triceps Brachioradialis Patellar Achilles Babinski
R+2 +2 +2 +2 +2 Negative
L +2 +2 +2 +2 +2 Negative

IMPRESSION: Enteric Fever (Typhoid Fever)

COURSE IN THE WARD
DAY 0
Subjective –
➢ (+)Abdominal pain
➢ (+)fever
➢ (+)vomiting
➢ (+)Soft Stool
Objective –
➢ Tempt.: 38.1˚C
➢ CR: 122 Bpm
➢ RR : 40cpm
Assessment – Enteric Fever
Plan –
➢ Dat
➢ IVF - d5imb 320cc for 8 hr at 25-30 ugtts/min , 3 cycles
➢ Diagnostic
Cbc with pc
Typhidot
Blood g/s
U/A
Serum na,k,ca
➢ Therapeutic
Paracetamol IV(10mg/kg/dose)
Ceftriaxone IV(75mg/kg/day) q12
Monitor vital sign q2 with o2 monitoring
➢ Monitor I&O qshift
➢ Refer
DAY 1
Subjective –
➢ (+)Abdominal pain
➢ (+)fever
➢ (-)vomiting
➢ (-)lbm
Objective –
➢ Tempt.: 37.1˚C
➢ CR: 115 Bpm
➢ RR : 35cpm
Assessment – Enteric fever
Plan –
➢ Dat
➢ Ivf- D5 0.3NACL(maintenance +10%)
Therapeutic
➢ Refer
DAY 2
Subjective –
➢ (+)Abdominal pain(decrease)
➢ (-)fever
➢ (-)vomiting
➢ (-)lbm
Objective –
➢ Tempt.: 37.5˚C
➢ CR: 110 Bpm
➢ RR : 32cpm
Plan –
➢ Dat
➢ Ivf- D5nm maintenance
Therapeutic
➢ Refer
DAY 3
Subjective –
➢ (-)Abdominal pain
➢ (-)fever
➢ (-)vomiting
➢ (-)lbm
Objective –
➢ Tempt.: 37.5˚C
➢ CR: 95 Bpm
➢ RR : 26cpm
Plan –
➢ Dat
➢ Ivf- D5nm maintenance shift to heplock
Therapeutic
➢ Refer
DAY 4
Subjective –
➢ (-)Abdominal pain
➢ (-)fever
➢ (-)vomiting
➢ (-)lbm
Objective –
➢ Tempt.: 37.5˚C
➢ CR: 95 Bpm
➢ RR : 26cpm
Plan –
➢ May go home
➢ Home take meds
Cefixime 8mg/kg/day for 7 days
Multivitamins syrup 5ml once a day
Zinc sulfate 5ml once a day
➢ Follow up after 1 week
DIAGNOSTIC
Urinalysis-
Protein Negative
Glucose Negative
Pus cell 0-2/hpf
RBC 0-2/hpf
Urates Many
Serum electrolyte
Sodium 136 mmol/l
Potassium 3.4 mg/dl
Chloride 99mmol/l
Typhidot
IgG Negative
IgM Positive
CBC
White blood cell 8.32
Red blood cell 3.13
Hemoglobin 121
Hematocrit 0.34
Platelet count 308
Neutrophils 36
Lymphocytes 56
BLOOD C/S- no growth after 72 hr
DIFFERENTIAL DIAGNOSIS
Rule in Rule out

Dengue Fever Fever Ɵ Bleeding
Abdominal pain Ɵ Rashes
Vomiting
Rule in Rule out
AGE vomiting Can not be ruled out
Abdominal pain
Fever
Soft stool
Rule in Rule out
SVI Fever 3 weeks fever
Abdominal pain
Vomiting
FINAL DIAGNOSIS :- enteric fever

DISCUSSION ABOUT THE CASE:-
Enteric Fever (Typhoid Fever)

ETIOLOGY
Typhoid fever is caused by S. enterica serovar Typhi (S. Typhi), a Gramnegative bacterium.
A very similar but often less-severe disease is caused by Salmonella Paratyphi A and rarely
by S. Paratyphi B (Schotmulleri) and S. Paratyphi C (Hirschfeldii). The ratio of disease
caused by S. Typhi to that caused by S. Paratyphi is approximately 10 : 1, although the
proportion of S. Paratyphi A infections is increasing in some parts of the world for reasons
that are unclear. Although S. Typhi shares many genes with Escherichia coli and at least 95%
of genes with S. Typhimurium, several unique gene clusters known as pathogenicity islands
and other genes have been acquired during evolution. The inactivation of single genes, as
well as the acquisition or loss of single genes or large islands of DNA, may have contributed
to host adaptation and restriction of S. Typhi.
One of the most specific gene products is the polysaccharide capsule Vi (virulence), which is
present in approximately 90% of all freshly isolated S. Typhi and has a protective effect
against the bactericidal action of the serum of infected patients.
EPIDEMIOLOGY
It is estimated that more than 26.9 million typhoid fever cases occur annually, of which 1%
result in death. The vast majority of this disease burden is witnessed in Asia. Additionally, an
estimated 5.4 million cases caused by paratyphoid occur each year. In 2010, 13.5 million
cases of typhoid fever were recorded, and both typhoid and paratyphoid fevers together
accounted for more than 12 million disability-adjusted life years. The mortality caused by
typhoid fever in the same year was found to be 7.2 per 100,000 population for the sub-
Saharan region of Africa. Given the paucity of microbiologic facilities in developing
countries, these figures may be more representative of the clinical syndrome rather than of
culture-proven disease. In most developed countries, the incidence of typhoid fever is <15
cases per 100,000 population, with most cases occurring in travelers. In contrast, the
incidence may vary considerably in the developing world, with estimated rates ranging from
100-1,000 cases per 100,000 population. There are significant differences in the age
distribution and population at risk. Population-based studies from South Asia also indicate
that the age-specific incidence of typhoid fever may be highest in children younger than 5 yr
of age, in association with comparatively higher rates of complications and hospitalization.
Typhoid fever is notable for the emergence of drug resistance. Following sporadic outbreaks
of chloramphenicol-resistant S. Typhi infections, many strains of S. Typhi have developed
plasmid-mediated multidrug resistance to all 3 of the primary antimicrobials: ampicillin,
chloramphenicol, and trimethoprim-sulfamethoxazole. There is also a considerable increase
in nalidixic acid–resistant isolates of S. Typhi, as well as the emergence of fluoroquinolone-
resistant isolates. Nalidixic acid–resistant isolates first emerged in Southeast Asia and India,
and now account for the majority of travel-associated cases of typhoid fever in the United
States.
S. Typhi is highly adapted to infection of humans to the point that it has lost the ability to
cause transmissible disease in other animals. The discovery of the large number of
pseudogenes in S. Typhi suggests that the genome of this pathogen has undergone
degeneration to facilitate a specialized association with the human host. Thus, direct or
indirect contact with an infected person (sick or chronic carrier) is a prerequisite for infection.
Ingestion of foods or water contaminated with S. Typhi from human feces is the most
common mode of transmission, although waterborne outbreaks as a consequence of poor
sanitation or contamination have been described in developing countries. In other parts of the
world, oysters and other shellfish cultivated in water contaminated by sewage and the use of
night soil as fertilizer may also cause infection.
PATHOGENESIS
Enteric fever occurs through the ingestion of the organism, and a variety of sources of fecal
contamination have been reported, including street foods and contamination of water
reservoirs.
Human volunteer experiments established an infecting dose of about 10 5 -10 9 organisms,

with an incubation period ranging from 4-14 days, depending on the inoculating dose of
viable bacteria. After ingestion, S. Typhi organisms are thought to invade the body through
the gut mucosa in the terminal ileum, possibly through specialized antigen-sampling cells
known as M cells that overlie gut-associated lymphoid tissues, through enterocytes, or via a
paracellular route. S. Typhi crosses the intestinal mucosal barrier after attachment to the
microvilli by an intricate mechanism involving membrane ruffling, actin rearrangement, and
internalization in an intracellular vacuole. In contrast to NTS, S. Typhi expresses virulence
factors that allow it to downregulate the pathogen recognition receptor–mediated host
inflammatory response. Within the Peyer patches in the terminal ileum, S. Typhi can traverse
the intestinal barrier through several mechanisms, including the M cells in the follicle-
associated epithelium, epithelial cells, and dendritic cells. At the villi, Salmonella can enter
through the M cells or by passage through or between compromised epithelial cells.
On contact with the epithelial cell, S. typhi assembles type III secretion system encoded on
SPI-1 and translocates effectors into the cytoplasm. These effectors activate host Rho
guanosine triphosphatases, resulting in the rearrangement of the actin cytoskeleton into
membrane ruffles, induction of mitogen-activated protein kinase pathways, n are further
modulated by the actin-binding proteins SipA and SipC and lead to bacterial uptake.
Mitogen-activated protein kinase signaling activates the transcription factors activator
protein-1 and nuclear factor-κB, which turn on production of IL-8. The destabilization of
tight junctions allows the transmigration of polymorphonuclear leukocytes from the
basolateral surface to the apical surface, paracellular fluid leakage, and access of bacteria to
the basolateral surface. Shortly after internalization of S. Typhi by macropinocytosis,
salmonellae are enclosed in a spacious phagosome that is formed by membrane ruffles. Later,
the phagosome fuses with lysosomes, acidifies, and shrinks to become adherent around the
bacterium, forming the Salmonella-containing vacuole. type III secretion system encoded on
SPI-2 is induced within the Salmonella-containing vacuole and translocates effector proteins
SifA and PipB2, which contribute to Salmonella-induced filament formation along
microtubules. The S. Typhi toxin has been isolated and characterized composed of 2 A
subunits, PltA and CdtB, which are homologs of the A subunits of the pertussis and
cytolethal distending toxins, respectively. Its single B subunit, PltB, is a homolog of 1 of the
components of the heteropentameric B subunit of pertussis toxin. Although the cellular

targets of the adenosine diphosphate–ribosyl transferase activity of PltA have not yet been
identified, CdtB is a DNase that inflicts DNA damage and induces cell-cycle arrest. S. Typhi
produces typhoid toxin only within mammalian cells, and the toxin is then ferried to the
extracellular environment by a unique transport mechanism that involves vesi carrier
intermediates (Fig. 198-4). These findings open the door to future opportunities for
developing diagnostic and preventive strategies.
After passing through the intestinal mucosa, S. Typhi organisms enter the mesenteric
lymphoid system and then pass into the bloodstream via the lymphatics. This primary
bacteremia is usually asymptomatic, and blood culture results are frequently negative at this
stage of the disease. The bloodborne bacteria are disseminated throughout the body and are
thought to colonize the organs of the reticuloendothelial system, where they may replicate
within macrophages. After a period of bacterial replication, S. Typhi organisms are shed back
into the blood, causing a secondary bacteremia that coincides with the onset of clinical
symptoms and marks the end of the incubation period.In vitro studies with human cell lines
have shown qualitative and quantitative differences in the epithelial cell response to S. Typhi
and S. Typhimurium with regard to cytokine and chemokine secretion. Thus, by avoiding the
triggering of an early inflammatory response in the gut, S. Typhi could instead colonize
deeper tissues and organ systems. Infection with S. Typhi produces an inflammatory response
in the deeper mucosal layers and underlying lymphoid tissue, with hyperplasia of Peyer
patches and subsequent necrosis and sloughing of overlying epithelium. The resulting ulcers
can bleed but usually heal without scarring or stricture formation. The inflammatory lesion
may occasionally penetrate the muscularis and serosa of the intestine and produce
perforation. The mesenteric lymph nodes, liver, and spleen are hyperemic and generally have
areas of focal necrosis as well. A mononuclear response may be seen in the bone marrow in
association with areas of focal necrosis. The morphologic changes of S. Typhi infection are
less prominent in infants than in older children and adults.
It is thought that several virulence factors, including type III secretion system encoded on
SPI-2, may be necessary for the virulence properties and ability to cause systemic infection.
The surface Vi polysaccharide capsular antigen found in S. Typhi interferes with
phagocytosis by preventing the binding of C3 to the surface of the bacterium. The ability of
organisms to survive within macrophages after phagocytosis is an important virulence trait
encoded by the PhoP regulon and may be related to metabolic effects on host cells. The
occasional occurrence of diarrhea may be explained by the presence of a toxin related to
cholera toxin and E. coli heat-labile enterotoxin. The clinical syndrome of fever and systemic
symptoms is produced by a release of proinflammatory cytokines (IL-6, IL-1β, and TNF-α)
from the infected cells.
In addition to the virulence of the infecting organisms, host factors and immunity may also
play an important role in predisposition to infection. There is an association between
susceptibility to typhoid fever and human genes within the major histocompatibility complex
class II and class III loci. Patients who are infected with HIV are at significantly higher risk
for clinical infection with S. Typhi and S. Paratyphi. Similarly, patients with Helicobacter
pylori infection have an increased risk of acquiring typhoid fever.
CLINICAL FEATURES
The incubation period of typhoid fever is usually 7-14 days but depends on the infecting dose
and ranges between 3 and 30 days. The clinical presentation varies from a mild illness with
low-grade fever, malaise, and slight, dry cough to a severe clinical picture with abdominal
discomfort and multiple complications.
Many factors influence the severity and overall clinical outcome of the infection. They
include the duration of illness before the initiation of appropriate therapy, choice of
antimicrobial treatment, age, previous exposure or vaccination history, virulence of the
bacterial strain, quantity of inoculum ingested, and several host factors affecting immune
status.
The presentation of typhoid fever may also differ according to age. Although data from South
America and parts of Africa suggest that typhoid may manifest as a mild illness in young
children, presentation may vary in different parts of the world. There is emerging evidence
from south Asia that the presentation of typhoid may be more dramatic in children younger
than 5 yr of age, with comparatively higher rates of complications and hospitalization.
Diarrhea, toxicity, and complications such as disseminated intravascular coagulopathy are
also more common in infancy, resulting in higher case fatality rates. However, some of the
other features and complications of typhoid fever seen in adults, such as relative bradycardia,
neurologic manifestations, and gastrointestinal bleeding, are rare in children.
Typhoid fever usually manifests as high-grade fever with a wide variety of associated
features, such as generalized myalgia, abdominal pain, hepatosplenomegaly, abdominal pain,
and anorexia (Table 198-5).
In children, diarrhea may occur in the earlier stages of the illness and may be followed by
constipation. In the absence of localizing signs, the early stage of the disease may be difficult
to differentiate from other endemic diseases such as malaria and dengue fever. The fever may
rise gradually, but the classic stepladder rise of fever is relatively rare. In approximately 25%
of cases, a macular or maculopapular rash (rose spots) may be visible around the 7th-10th day
of the illness, and lesions may appear in crops of 10-15 on the lower chest and abdomen and
last 2-3 days (Fig. 198-5). These lesions may be difficult to see in dark-skinned children.
Patients managed as outpatients present with fever (99%) but have less emesis, diarrhea,
hepatomegaly, splenomegaly, and myalgias than patients who require admission to the
hospital.
The presentation of typhoid fever may be tempered by coexisting morbidities and early
diagnosis and administration of antibiotics. In malaria-endemic areas and in parts of the
world where schistosomiasis is common, the presentation of typhoid may also be atypical. It
is also recognized that multidrug-resistant S. Typhi infection is a more severe clinical illness
with higher rates of toxicity, complications, and case fatality rates, which may be related to
the greater virulence as well as higher numbers of circulating bacteria. The emergence of
typhoid infections resistant to nalidixic acid and fluoroquinolones is associated with higher
rates of morbidity and treatment failure. These findings may have implications for treatment
algorithms, especially in endemic areas with high rates of multidrug-resistant and nalidixic
acid– or fluoroquinolone-resistant typhoid.
If no complications occur, the symptoms and physical findings gradually resolve within 2-4
wk; however, the illness may be associated with malnutrition in a number of affected
children. Although enteric fever caused by S. Paratyphi organisms has been classically
regarded as a milder illness, there have been several outbreaks of infection with drug-resistant
S. Paratyphi A, suggesting that paratyphoid fever may also be severe, with significant
morbidity and complications.
COMPLICATIONS
Although altered liver function is found in many patients with enteric fever, clinically
significant hepatitis, jaundice, and cholecystitis are relatively rare and may be associated with
higher rates of adverse outcome. Intestinal hemorrhage (<1%) and perforation (0.5-1%) are
infrequent among children. Intestinal perforation may be preceded by a marked increase in
abdominal pain (usually in the right lower quadrant), tenderness, vomiting, and features of
peritonitis. Intestinal perforation and peritonitis may be accompanied by a sudden rise in
pulse rate, hypotension, marked abdominal tenderness and guarding, and subsequent
abdominal rigidity. A rising white blood cell count with a left shift and free air on abdominal
radiographs may be seen in such cases.
Rare complications include toxic myocarditis, which may manifest as arrhythmias, sinoatrial
block, or cardiogenic shock (Table 198-6). Neurologic complications are also relatively
uncommon among children; they include delirium, psychosis, increased intracranial pressure,
acute cerebellar ataxia, chorea, deafness, and Guillain-Barré syndrome. Although case fatality
rates may be higher with neurologic manifestations, recovery usually occurs with no
sequelae. Other reported complications include fatal bone marrow necrosis, disseminated
intravascular coagulopathy, hemolytic–uremic syndrome, pyelonephritis, nephrotic
syndrome, meningitis, endocarditis, parotitis, orchitis, and suppurative lymphadenitis.
The propensity to become a carrier follows the epidemiology of gallbladder disease,

increasing with patient age and the antibiotic resistance of the prevalent strains. Although
limited data are available, rates of chronic carriage are generally lower in children than
adults.
DIAGNOSIS
The mainstay of the diagnosis of typhoid fever is a positive result of culture from the blood or
another anatomic site. Results of blood cultures are positive in 40-60% of the patients seen
early in the course of the disease, and stool and urine culture results become positive after the
1st wk. The stool culture result is also occasionally positive during the incubation period.
However, the sensitivity of blood cultures in diagnosing typhoid fever in many parts of the
developing world is limited because widespread liberal antibiotic use may render
bacteriologic confirmation difficult. Although bone marrow cultures may increase the
likelihood of bacteriologic confirmation of typhoid, collection of the specimens is difficult
and relatively invasive.
Results of other laboratory investigations are nonspecific. Although blood leukocyte counts
are frequently low in relation to the fever and toxicity, there is a wide range in counts; in
younger children leukocytosis is common and may reach 20,000-25,000 cells/µL.
Thrombocytopenia may be a marker of severe illness and may accompany disseminated
intravascular coagulopathy. Liver function test results may be deranged, but significant
hepatic dysfunction is rare.
The classic Widal test measures antibodies against O and H antigens of S. Typhi but lacks
sensitivity and specificity in endemic areas. Because many false-positive and false-negative
results occur, diagnosis of typhoid fever by Widal test alone is prone to error. Other relatively
newer diagnostic tests using monoclonal antibodies have been developed that directly detect
S. Typhi–specific antigens in the serum or S. Typhi Vi antigen in the urine. However, few
have proved sufficiently robust in large-scale evaluations. A nested polymerase chain
reaction analysis using H1-d primers has been used to amplify specific genes of S. Typhi in
the blood of patients; it is a promising means of making a rapid diagnosis, especially given
the low level of bacteremia in enteric fever. Despite these innovations, the mainstay of
diagnosis of typhoid remains clinical in much of the developing world, and several diagnostic
algorithms have been evaluated in endemic areas.
TREATMENT
An early diagnosis of typhoid fever and institution of appropriate treatment are essential. The
vast majority of children with typhoid fever can be managed at home with oral antibiotics and
close medical follow-up for complications or failure of response to therapy. Patients with
persistent vomiting, severe diarrhea, and abdominal distention may require hospitalization
and parenteral antibiotic therapy.
There are general principles of typhoid fever management. Adequate rest, hydration, and
attention are important to correct fluid and electrolyte imbalance. Antipyretic therapy
(acetaminophen 10-15 mg/kg every 4-6 hr PO) should be provided as required. A soft, easily
digestible diet should be continued unless the patient has abdominal distention or ileus.
Antibiotic therapy is critical to minimize complications (Table 198-7). It has been suggested
that traditional therapy with either chloramphenicol or amoxicillin is associated with relapse
rates of 5-15% and 4-8%, respectively, whereas use of the quinolones and third-generation
cephalosporins is associated with higher cure rates. The antibiotic treatment of typhoid fever
in children is also influenced by the prevalence of antimicrobial resistance. Over the past 2
decades, emergence of multidrug-resistant strains of S. Typhi (i.e., isolates fully resistant to
amoxicillin, trimethoprim-sulfamethoxazole, and chloramphenicol) has necessitated
treatment with fluoroquinolones, which are the antimicrobial drug of choice for treatment of
salmonellosis in adults, with cephalosporins as an alternative. The emergence of resistance to
quinolones places tremendous pressure on public health systems because alternative
therapeutic options are limited.
Although some investigators suggest that children with typhoid fever should be treated with
fluoroquinolones like adults, others question this approach on the basis of the potential
development of further resistance to fluoroquinolones and the fact that quinolones are still not
approved for widespread use in children. A Cochrane systematic
review of the treatment of typhoid fever also indicates that there is little evidence to support
the carte blanche administration of fluoroquinolones in all cases of typhoid fever.
Azithromycin may be an alternative antibiotic for children with uncomplicated typhoid fever.
In addition to antibiotics, the importance of supportive treatment and maintenance of

appropriate fluid and electrolyte balance must be underscored. Although additional treatment
with dexamethasone (3 mg/kg for the initial dose, followed by 1 mg/kg every 6 hr for 48 hr)
is recommended for severely ill patients with shock, obtundation, stupor, or coma;
corticosteroids should be administered only under strict controlled conditions and
supervision, because their use may mask signs of abdominal complications.
REFERENCE:- Nelson book of Pediatric

PNEUMONIA
ABSTRACT
Pneumonia (from the Greek pneuma, “breath”) is a potentially fatal infection and
inflammation of the lower respiratory tract (i.e., bronchioles and alveoli) usually caused by
inhaled bacteria and viruses has both properties (Streptococcus pneumoniae, aka
pneumococcus). The illness is frequently characterized by high fever, shortness of breath,
rapid breathing, sharp chest pain, and a productive cough with thick phlegm. Pneumonia that
develops outside the hospital setting is commonly referred to as community-acquired
pneumonia. Pneumonia that develops 48 hours or later after admission to the hospital is
known as nosocomial or hospital acquired pneumonia. In this case report we review the
presentation and management of pneumonia involving the respiratory system. The aim of this
report is to alert the clinicians to the potential diagnosis of pneumonia treatment. This is the
case report of 3 months old boy with Pneumonia. He was diagnosed with pneumonia. His
treatment was starting and after 7 days, he became completely recovered. For his disease
diagnosis different tests are also performed.
PATIENT HISTORY
Informant: Mother
Reliability: 95%

GENERAL DATA:

This is a case of G.G., a 1 Months old female, Filipino, Roman Catholic, born on October
18, 2019 from Bato, San Fernando, Camarines Sur, admitted for the first time at Bicol
Medical Center on December 5, 2019.

CHIEF COMPLAINT: difficulty of breathing, poor suck


1 week prior to admission, patient had productive cough and colds with yellowish, mucoid,
non-blood streaked nasal discharge. Consultation was done in private clinic and ambroxal
given with unrecalled dose.
1 days prior to admission, patient had poor suck, cough, cold, tachypneic, now accompanied
by episodes of difficulty of breathing. No consult was done and no medications was given.
Few hours prior to admission, signs and symptoms persisted. He was brought for consult at a
private pediatrician, then referred to this institution, hence admitted.

PERSONAL HISTORY:

Prenatal— At 4th month gestation, the mother had UTI for 2 weeks. No consult done; took
unrecalled antibiotic capsule 3x a day for 1 week. She had prenatal check-up at the
Barangay Health Center once when she was at 5th month AOG. TT3. Supplementation
include ferrous sulfate taken for 1 month.

Birth/Postnatal— Born full term via SVD at a local health center to a then 23 year-old G1P1
(1001). No complications. Newborn had bowel movements and urine output within 24 hours
of life.

GROWTH & DEVELOPMENT:
Newborn:
Tonic nack reflex
Pelvic high when supine
Startle reflex
1 month:
Pelvic now flat when supine
Rises head slightly from prone position
Smiles, diminishes activity when talk to

IMMUNIZATION:

BCG at birth
Hepatitis B at birth, 1 mo.

NUTRITIONAL HISTORY:

Patient was exclusively breastfed from birth up to now.no formula milk was given to
this patient.


No known medical conditions such as bronchial asthma, congenital disorders,
seizure disorder, cardiac disease, blood dyscrasia or other conditions.
No previous hospitalization, surgical operation and accidents.
No known allergy to food and drugs.

FAMILY HISTORY:

No relative with PTB, asthma, seizure disorder, HTN, DM, cardiac disease, stroke,
renal disease, gastrointestinal disease, malignancies and congenital defects.

SOCIAL HISTORY:

The patient is the youngest among family members. 23 year-old mother is a high school
graduate and housekeeper. 21 year-old father is a high school graduate working in water
supply station. The household has 3 members, composed of the immediate family, together in
a single-room owned house made of light materials, which has a 15-meter distance
from the neighboring house. Drinking source is a water pump, with sterilization applied.
They have no toilet facility at home; utilizes a common toilet. Garbage disposal is through
burning.

REVIEW OF SYSTEMS:

General: No weight loss.
Skin: No pruritus and easy bruising.
HEENT: No headache, redness, ear discharge, nasal discharge, mouth sores, sore
throat, neck lumps andstiffness.
Musculoskeletal: No muscle and joint pain/swelling, no limitation of movement.
Cardiovascular: No tachycardia, orthopnea, dyspnea, edema, and chest pain.
Gastrointestinal: No bowel changes.
Urinary: No urgency, frequency, gross hematuria, andenuresis.
Neurologic: No tics or seizures.


General Survey: Cuddled by mother, awake, conscious, in respiratory distress, febrile

Vital Signs: Weight 3.5 kg, Height 54cm, CR 158 bpm, RR55/min, Temperature 38.1°C

Z-score:
Length-for-age: Below -3 StuntedWeight-for-age: Above -2 Normal
Skin: No pallor, jaundice or pigmentation, good turgor, no lesions.

HEENT: Normocephalic. Open Anterior and posterior frontanal, pink palpebral
conjunctivae, pupils 2-4 mm equally reactive and responsive to light and accommodation.
Pinnae without deformity, no ear discharge. Patent nasal septum. Pinkish oral mucosa.
No tonsillopharyngeal congestion. No cervical lymphadenopathy.

Chest & Lungs: Flat, no scars, symmetrical chest expansion, tachypneic, (+)
subcostal retractions. No palpable mass. (+) crackles and occasional wheezes on bibasal lung
fields.

Heart: Adynamic precordium, no heaves, no thrills. PMI at 4th left intercostal space
midclavicular line. Tachycardic, regular rhythm, no murmurs.

Abdomen: Globular. Normal active bowel sounds. Soft, non-tender, no palpable mass, liver
and spleen non-palpable.

Genitalia: Descended testes, good rugae, central urethral orifice; no phimosis, no hydrocoele.

Extremities: Equal length, no edema, no cyanosis, no joint swelling and tenderness. Full and
equal pulses. Full range of motion. CRT <2s

Neurologic Examination:

Mental status: Conscious, coherent, GCS 15

Cranial nerves:
CN I Not tested
II Pupils 2-3 mm equally reactive and responsive to light and
accommodation
III, IV, Extraocular movements intact
VI
V (+) corneal blink reflex
VII Symmetrical facial movements
VIII Not applicable for this age
IX, X Not applicable for this age
XI Not applicable for this age
XII Midline tongue without fasciculations

Motor:
Good muscle tone and bulk
Not applicable for this patient

IMPRESSION: Pneumonia Moderate Risk

COURSE IN WARD
DAY 0
Subjective –
➢ (+) poor suck
➢ (+) cough and cold
➢ (+) difficultly of breathing
Objective –
➢ (+)crackle
➢ (+) alar flaring
➢ (+) retractions
Assessment – pneumonia moderate risk
Plan –
➢ Npo
➢ Ivf- d5imb 180cc for 8 hr at 22-23 ugtts/min , 3 cycles
➢ Diagnostic
Cbc with pc
Cxr-apl
Cbg monitoring q8 while in npo
➢ Therapeutic
Ampicillin 45 mg iv q6
Gentamicin 23 mg iv q24
Paracetamol 45 mg iv q4 for fever
➢ Monitor vital sign q2 with o2 monitoring
➢ Refer
Day 1
Subjective –
➢ (+) poor suck
➢ (+) cough
➢ (-) difficultly of breathing
Objective –
➢ (+)crackle
➢ (+) alar flaring
➢ (+) retractions
Plan –
➢ May feed with sap
➢ Continue ivf
➢ Continue iv meds
➢ Refer
Day 2
Subjective –
➢ (+) poor suck
➢ (+) cough
Objective –
➢ (+)crackle
➢ (-) alar flaring
➢ (+) retractions
Plan –
➢ Continue feeding with sap
➢ Continue ivf
➢ Continue medications
➢ Refer
Day 3
Subjective –
➢ Good suck
➢ (+) cough
Objective –
➢ (+)crackle
➢ (-) retractions
Plan –
➢ Continue feeding with sap
➢ Continue ivf
➢ Continue medications
➢ Refer
Day 4
Subjective –
➢ Good suck
➢ (-) cough
Objective –
➢ (-) crackle
➢ (-) retractions
Plan –
➢ May go home
➢ Home take meds
Ampicillin 100mg/ml 0.8 ml , 3 times a day for 3 more days
➢ Follow up on opd after 3days
ANNEXURE
CBC
Red blood cell 3.21
Hemoglobin 97
Hematocrit 0.29
Platelet count 261
Neutrophils 15.4
Lymphocytes 60.3
Monocytes 17.8
Eosinophils 3.5
Basophils 3.0
Chest x-ray – Pneumonia in both lungs
CBG - 95
Rule in Rule out

Pneumonia (+) crackle
(+) tachypnea
(+) chest intracostal
retractions
(+) poor suck
Acute Bronchitis (+) crackle (-) cyanosis
(+) cough (-) dehydrated
(+) cold (-) wheezes
(+) poor sleep
FINAL DIAGNOSIS
Pneumonia moderate risk
DISCUSSION
PNEUMONIAE
EPIDEMIOLOGY
Pneumonia, defined as inflammation of the lung parenchyma, is the leading cause of death
globally among children younger than age 5 yr, accounting for an estimated 1.2 million (18%
total) deaths annually (Fig. 400-1). The incidence of pneumonia is more than 10-fold higher
(0.29 episodes vs 0.03 episodes), and the number of childhood-related deaths from
pneumonia ≈2,000 fold higher, in developing than in developed countries (Table 400-1).
Fifteen countries account for more than three-fourths of all pediatric deaths from pneumonia.
In the United States from 1939-1996, pneumonia mortality in children declined by 97%; in
1970, pneumonia accounted for 9% of all deaths of children younger than age 5 yr compared
to 2% in 2007. It is probable that this decline results from the introduction of antibiotics,
vaccines, and the expansion of medical insurance coverage for children. Haemophilus
influenzae type b was an important cause of bacterial pneumonia in young children but
became uncommon with the routine use of effective vaccines, while measles vaccine greatly
reduced the incidence of measles-related pneumonia deaths in developing countries.
Improved access to healthcare in rural areas of developing countries and the introduction of
pneumococcal conjugate vaccines were also important contributors to the further reductions
in pneumonia-related deaths achieved over the past decade.
ETIOLOGY
Although most cases of pneumonia are caused by microorganisms, noninfectious causes

include aspiration (of food or gastric acid, foreign bodies, hydrocarbons, and lipoid
substances), hypersensitivity reactions, and drug- or radiation-induced pneumonitis. The
cause of pneumonia in an individual patient is often difficult to determine because direct
culture of lung tissue is invasive and rarely performed. Cultures performed on specimens in
children obtained from the upper respiratory tract or sputum typically do not accurately
reflect the cause of lower respiratory tract infection. With the use of molecular diagnostic
testing, a bacterial or viral cause of pneumonia can be identified in 40-80% of children with
community-acquired pneumonia. Streptococcus pneumoniae (pneumococcus) is the most
common bacterial pathogen in children 3 wk to 4 yr of age, whereas Mycoplasma
pneumoniae and Chlamydophila pneumoniae are the most frequent bacterial pathogens in
children age 5 yr and older. I
viruses.
S. pneumoniae, H. influenzae, and S. aureus are the major causes of hospitalization and death
from bacterial pneumonia among children in developing countries, although in children with
HIV infection, Mycobacterium tuberculosis, atypical mycobacteria
Lower respiratory tract viral infections are much more common in the fall and winter in both
the northern and southern hemispheres in relation to the seasonal epidemics of respiratory
viral infection that occur each year. The typical pattern of these epidemics usually begins in
the fall, when parainfluenza infections appear and most often manifest as croup. Later in
winter, RSV, human metapneumovirus, and influenza viruses cause widespread infection,
including upper respiratory tract infections, bronchiolitis, and pneumonia. RSV is particularly
severe among infants and young children, whereas influenza virus causes disease and excess
hospitalization for acute respiratory illness in all age groups. Knowledge of the prevailing
viral epidemic may lead to a presumptive initial diagnosis.
Immunization status is relevant because children fully immunized against H. influenzae type
b and S. pneumoniae are less likely to be infected with these pathogens. Children who are
immunosuppressed or who have an underlying illness may be at risk for specific pathogens,
such as Pseudomonas spp. in patients with cystic fibrosis
PATHOGENESIS
The lower respiratory tract is normally kept sterile by physiologic defense mechanisms,
including mucociliary clearance, the properties of normal secretions such as secretory
immunoglobulin (Ig) A, and clearing of the airway by coughing. Immunologic defense
mechanisms of the lung that limit invasion by pathogenic organisms include macrophages
that are present in alveoli and bronchioles, secretory IgA, and other immunoglobulins.
Trauma, anesthesia, and aspiration increase the risk of pulmonary infection.
Viral pneumonia usually results from spread of infection along the airways, accompanied by
direct injury of the respiratory epithelium, which results in airway obstruction from swelling,
abnormal secretions, and cellular debris. The small caliber of airways in young infants makes
such patients particularly susceptible to severe infection. Atelectasis, interstitial edema, and
ventilation–perfusion mismatch causing significant hypoxemia often accompany airway
obstruction. Viral infection of the respiratory tract can also predispose to secondary bacterial
infection by disturbing normal host defense mechanisms, altering secretions, and modifying
the bacterial flora.
Bacterial pneumonia most often occurs when respiratory tract organisms colonize the trachea
and subsequently gain access to the lungs, but pneumonia may also result from direct seeding
of lung tissue after bacteremia. When bacterial infection is established in the lung
parenchyma, the pathologic process varies according to the invading organism. M.
pneumoniae attaches to the respiratory epithelium, inhibits ciliary action, and leads to cellular
destruction and an inflammatory response in the submucosa. As the infection progresses,
sloughed cellular debris, inflammatory cells, and mucus cause airway obstruction, with
spread of infection occurring along the bronchial tree, as it does in viral pneumonia.
S. pneumoniae produces local edema that aids in the proliferation of organisms and their
spread into adjacent portions of lung, often resulting in the characteristic focal lobar
involvement.
Group A streptococcus infection of the lower respiratory tract results in more diffuse
infection with interstitial pneumonia. The pathology includes necrosis of tracheobronchial
mucosa; formation of large amounts of exudate, edema, and local hemorrhage, with extension
into the interalveolar septa; and involvement of lymphatic vessels and the increased
likelihood of pleural involvement.
S. aureus pneumonia manifests in confluent bronchopneumonia, which is often unilateral and
characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas
of cavitation of the lung parenchyma, resulting in pneumatoceles, empyema, or, at times,
bronchopulmonary fistulas
Recurrent pneumonia is defined as 2 or more episodes in a single year or 3 or more episodes
ever, with radiographic clearing between occurrences. An underlying disorder should be
considered if a child experiences recurrent pneumonia.
CLINICAL MANIFESTATIONS
Pneumonia is frequently preceded by several days of symptoms of an upper respiratory tract

infection, typically rhinitis and cough. In viral pneumonia, fever is usually present but
temperatures are generally lower than in bacterial pneumonia. Tachypnea is the most
consistent clinical manifestation of pneumonia. Increased work of breathing accompanied by
intercostal, subcostal, and suprasternal retractions, nasal flaring, and use of accessory muscles
is common. Severe infection may be accompanied by cyanosis and lethargy, especially in
infants. Auscultation of the chest may reveal crackles and wheezing, but it is often difficult to
localize the source of these adventitious sounds in very young children with hyperresonant
chests. It is often not possible to distinguish viral pneumonia clinically from disease caused
by Mycoplasma and other bacterial pathogens.
Bacterial pneumonia in adults and older children typically begins suddenly with high fever,
cough, and chest pain. Other symptoms that may be seen include drowsiness with intermittent
periods of restlessness; rapid respirations; anxiety; and, occasionally, delirium. In many
children, splinting on the affected side to minimize pleuritic pain and improve ventilation is
noted; such children may lie on one side with the knees drawn up to the chest.
Physical findings depend on the stage of pneumonia. Early in the course of illness,
diminished breath sounds, scattered crackles, and rhonchi are commonly heard over the
affected lung field. With the development of increasing consolidation or complications of
pneumonia such as pleural effusion or empyema, dullness on percussion is noted and breath
sounds may be diminished. A lag in respiratory excursion often occurs on the affected side.
Abdominal distention may be prominent because of gastric dilation from swallowed air or
ileus. Abdominal pain is common in lower-lobe pneumonia. The liver may seem enlarged
because of downward displacement of the diaphragm secondary to hyperinflation of the lungs
or superimposed congestive heart failure.
Symptoms described in adults with pneumococcal pneumonia may be noted in older children
but are rarely observed in infants and young children, in whom the clinical pattern is
considerably more variable. In infants, there may be a prodrome of upper respiratory tract
infection and diminished appetite, leading to the abrupt onset of fever, restlessness,
apprehension, and respiratory distress. These infants appear ill, with respiratory distress
manifested as grunting; nasal flaring; retractions of the supraclavicular, intercostal, and
subcostal areas; tachypnea; tachycardia; air hunger; and often cyanosis. Results of physical
examination may be misleading, particularly in young infants, with meager findings
disproportionate to the degree of tachypnea. Some infants with bacterial pneumonia may
have associated gastrointestinal disturbances characterized by vomiting, anorexia, diarrhea,
and abdominal distention secondary to a paralytic ileus. Rapid progression of symptoms is
characteristic in the most severe cases of bacterial pneumonia.
DIAGNOSIS
An infiltrate on chest radiograph (posteroanterior and lateral views) supports the diagnosis of
pneumonia; the film may also indicate a complication such as a pleural effusion or empyema.
Viral pneumonia is usually characterized by hyperinflation with bilateral interstitial infiltrates
and peribronchial cuffing (Fig. 400-2). Confluent lobar consolidation is typically seen with
pneumococcal pneumonia (Fig. 400-3). The radiographic appearance alone is not diagnostic,
and other clinical features must be considered. Repeat chest radiographs are not required for
proof of cure for patients with uncomplicated pneumonia. Someexperts suggest that a chest
radiograph may not be necessary for older children with suspected pneumonia (cough, fever,
localized crackles, or decreased breath sounds) who are well enough to be managed as
outpatients.
Point-of-care use of portable or handheld ultrasonography is highly sensitive and specific in

diagnosing pneumonia in children by determining lung consolidations and air bronchograms
or effusions.
The peripheral white blood cell (WBC) count can be useful in differentiating viral from
bacterial pneumonia. In viral pneumonia, the WBC count can be normal or elevated but is
usually not higher than 20,000/mm 3 , with a lymphocyte predominance. Bacterial
pneumonia is often associated with an elevated WBC count, in the range of
15,00040,000/mm 3 , and a predominance of granulocytes. A large pleural effusion, lobar
consolidation, and a high fever at the onset of the illness are also suggestive of a bacterial
etiology. Atypical pneumonia caused by C. pneumoniae or M. pneumoniae is difficult to
distinguish from pneumococcal pneumonia on the basis of radiographic and laboratory
findings, and although pneumococcal pneumonia is associated with a higher WBC count,
erythrocyte sedimentation rate, procalcitonin, and C-reactive protein level, there is
considerable overlap, particularly with adenoviruses and enteroviruses.
The definitive diagnosis of a viral infection rests on the isolation of a virus or detection of the
viral genome or antigen in respiratory tract secretions. Reliable DNA or RNA tests for the
rapid detection of many respiratory pathogens, such as mycoplasma, pertussis, and viruses,
including RSV, parainfluenza, influenza, and adenoviruses, are available and accurate.
Serologic techniques can also be used to diagnose a recent respiratory viral infection but
generally require testing of acute and convalescent serum samples for a rise in antibodies to a
specific viral agent. This diagnostic technique is laborious, slow, and not generally clinically
useful because the infection usually resolves by the time it is confirmed serologically.
Serologic testing may be valuable as an epidemiologic tool to define the incidence and
prevalence of the various respiratory viral pathogens. Patient peripheral cell gene expression
patterns determined by microarray reverse transcription polymerase chain reaction is an
emerging technology that may help differentiate viral from bacterial causes of pneumonia.
The definitive diagnosis of a bacterial infection requires isolation of an organism from the
blood, pleural fluid, or lung. Culture of sputum is of little value in the diagnosis of
pneumonia in young children, while percutaneous lung aspiration is invasive and not
routinely performed. Blood culture results are positive in only 10% of children with
pneumococcal pneumonia and are not recommended for nontoxic appearing children treated
as an outpatient. Blood cultures are recommended for those who fail to improve or have
clinical deterioration, in thosewith complicated pneumonia (Table 400-5) and those requiring
hospitalization. Cold agglutinins at titers >1 : 64 are found in the blood in ≈50% of patients
with M. pneumoniae infections. Cold agglutinin findings are nonspecific because other
pathogens such as influenza viruses may also cause increases. Acute infection caused by M.
pneumoniae can be diagnosed on the basis of a positive polymerase chain reaction test result
or seroconversion in an IgG assay. Serologic evidence, such as the antistreptolysin O titer,
may be useful in the diagnosis of group A streptococcal pneumonia.
TREATMENT
Treatment of suspected bacterial pneumonia is based on the presumptive cause and the age
and clinical appearance of the child. For mildly ill children who do not require
hospitalization, amoxicillin is recommended. With the emergence of penicillin-resistant
pneumococci, high doses of amoxicillin (80-90 mg/kg/24 hr) should be prescribed unless
local data indicate a low prevalence of resistance. Therapeutic alternatives include
cefuroxime axetil and amoxicillin/clavulanate. For school-age children and in children in
whom infection with M. pneumoniae or C. pneumoniae is suggested, a macrolide antibiotic
such as azithromycin is an appropriate choice. In adolescents, a respiratory fluoroquinolone
(levofloxacin, moxifloxacin) may be considered as an alternative. Despite substantial gains
over the past decade, in developing countries only ≈60% of children with symptoms of
pneumonia (≈50% in sub-Saharan Africa) are taken to an appropriate caregiver, and less than
one-third receive antibiotics. The World Health Organization and other international groups
have developed systems to train mothers and local healthcare providers in the recognition and
treatment of pneumonia.
The empiric treatment of suspected bacterial pneumonia in a hospitalized child requires an

approach based on the clinical manifestations at the time of presentation. In areas without
substantial high-level penicillin resistance among S. pneumoniae, children who are fully
immunized against H. influenzae type b and S. pneumoniae and are not severely ill should
receive ampicillin or penicillin G. For children who do not meet these criteria, ceftriaxone or
cefotaxime should be used. If clinical features suggest staphylococcal pneumonia
(pneumatoceles, empyema), initial antimicrobial therapy should also include vancomycin or
clindamycin.
If viral pneumonia is suspected, it is reasonable to withhold antibiotic therapy, especially for

those patients who are mildly ill, have clinical evidence suggesting viral infection, and are in
no respiratory distress. However, up to 30% of patients with known viral infection,
particularly influenza viruses, may have coexisting bacterial pathogens. Therefore, if the
decision is made to withhold antibiotic therapy on the basis of presumptive diagnosis of a
viral infection, deterioration in clinical status should signal the possibility of superimposed
bacterial infection, and antibiotic therapy should be initiated.
Table 400-5 notes the indications for admission to a hospital. The optimal duration of
antibiotic treatment for pneumonia has not been well-established in controlled studies.
However, antibiotics should generally be continued until the patient has been afebrile for 72
hr, and the total duration should not be less than 10 days (or 5 days if azithromycin is used).
Shorter courses (5-7 days) may also be effective, particularly for children managed on an
outpatient basis, but further study is needed. Available data do not support prolonged courses
of treatment for uncomplicated pneumonia. In developing countries, oral zinc (10 mg/day for
<12 mo, 20 mg/day for ≥12 mo) reduces mortality among children with clinically defined
severe pneumonia.
PROGNOSIS
Typically, patients with uncomplicated community-acquired bacterial pneumonia show

response to therapy, with improvement in clinical symptoms (fever, cough, tachypnea, chest
pain), within 48-96 hr of initiation of antibiotics. Radiographic evidence of improvement lags
substantially behind clinical improvement. A number of possibilities must be considered
when a patient does not improve with appropriate antibiotic therapy: (1) complications, such
as empyema (see Table 4005); (2) bacterial resistance; (3) nonbacterial etiologies such as
viruses or fungi and aspiration of foreign bodies or food; (4) bronchial obstruction from
endobronchial lesions, foreign body, or mucous plugs; (5) preexisting diseases such as
immunodeficiencies, ciliary dyskinesia, cystic fibrosis, pulmonary sequestration, or
congenital pulmonary airway malformation, formerly called cystic adenomatoid
malformation; and (6) other noninfectious causes (including bronchiolitis obliterans,
hypersensitivity pneumonitis, eosinophilic pneumonia, aspiration, and granulomatosis with
polyangiitis, formerly called Wegener granulomatosis). A repeat chest radiograph is the first
step in determining the reason for delay in response to treatment. Bronchoalveolar lavage
may be indicated in children with respiratory failure; high-resolution CT scans may better
identify complications or an anatomic reason for a poor response to therapy.
Mortality from community-acquired pneumonia in developed nations is rare, and most

children with pneumonia do not experience long-term pulmonary sequelae. Some data
suggest that up to 45% of children have symptoms of asthma 5 yr after hospitalization for
pneumonia; this finding may reflect either undiagnosed asthma at the time of presentation or
a propensity for development of asthma after pneumonia.
COMPLICATIONS
Complications of pneumonia (see Table 400-5) are usually the result of direct spread of
bacterial infection within the thoracic cavity (pleural effusion, empyema, and pericarditis) or
bacteremia and hematologic spread (Fig. 400-4). Meningitis, suppurative arthritis, and
osteomyelitis are rare complications of hematologic spread of pneumococcal or
H. influenzae type b infection.
S. aureus, S. pneumoniae, and S. pyogenes are the most common causes of parapneumonic
effusions and empyema (Table 400-6). Nonetheless many effusions that complicate bacterial
pneumonia are sterile. Universal 16S ribosomal RNA gene polymerase chain reaction
identifies the bacterial genome and can determine the bacterial etiology of the effusion if the
culture is negative. The treatment of empyema is based on the stage (exudative,
fibrinopurulent, organizing). Imaging studies including ultrasonography and CT are helpful in
determining the stage of empyema. The mainstays of therapy include antibiotic therapy and
drainage with tube thoracostomy. Additional effective approaches include the use of
intrapleural fibrinolytic therapy (urokinase, streptokinase, tissue plasminogen activator) and
selected video-assisted thoracoscopy to debride or lyse adhesions and drain loculated areas of
pus. Early diagnosis and intervention, particularly with fibrinolysis or less often video-
assisted thoracoscopy, may obviate the need for thoracotomy and open debridement.
Fibrinolysis is more cost-effective than video-assisted thoracoscopy.
REFERENCE — NELSONE BOOK OF PEDIATRIC

DENGUE FEVER
ABSTRACT:-
As the outbreaks of Dengue fever increasing in Philippines, one part after other
getting affected, it is very essential to know more about this disease and prevalence, any
change in the viral strain, severity of the disease pattern, early detection of the virus and early
management of the disease resulting in good recovery . Population growth, rapid
urbanization, increase in international travel from endemic areas and global warming are
playing a major role in disease spread. Measures should be taken to control the
aforementioned causes to prevent disease spread and reduce epidemic flare up.
PATIENT’S HISTORY
Informant: Auntie & Uncle

Reliability: 85%

GENERAL DATA:

This is a case of patient S.F, a 16 yr old child, Filipino, Roman Catholic, born on MARCH
10, 2003 and currently residing at P1 BALABA, POLANGUI, Albay, admitted on JUNE 19,
2019 for the 1ST time in our institution.

CHIEF COMPLAINT: fever for 7 day


7 DAYS PRIOR TO ADMISSION PATIENT HAD UNDOCUMENTED INTERMITTENT
FEVER ASSOCIATED WITH EPIGASTRIC PAIN WITH 1 EPISODE OF VOMITING.
4 DAYS PRIOR TO ADMISSION SYMPTOMS PERSIS AND PATIENT WAS
ADMITTED AT JBMMOH AND WAS DIAGNOSED AS A CASE OF DF WITH
WARNING SIGNS.
1 DAY PRIOIR TO ADmISSION PATIENT HAD AN EPISODE NOSE BLEED
ASSOCIATED WITH THE PERSISTING SYMPTOMS.
PATIENT WAS REFERRED TO OUR INSTITUTION FOR FUTHER MANAGEMENT
AND EVALUATION.

Maternal and Obstetric History
Patient was born to a 32- yr old then G1P1 mother. She had regular prenatal check-ups since
2ND month of pregnancy until before giving birth. She took ferrous sulfate and multivitamins
during the course of her pregnancy. Mother denies any vices and any exposure to radiation
and teratogenic drugs or any infection. No complications were noted such as gestational
hypertension and diabetes.
Birthing History
The patient was born FULL term, NVD attended by a MIDWIFE. The mother claimed that
the baby had good cry and motor activity upon birth. Baby was not born in cardiorespiratory
distress. Baby’s birth weight was 3 kg.
Neonatal History
(-) spontaneous respiration (-) cyanosis (-) pallor (-) cry (-) jaundice (-) convulsions (-)
hemorrhage (-) respiratory difficulties (-) feeding difficulties (-) birth injury (-) congenital
abnormality
Nutritional History
The patient was breastfed until 6 months. Since then, the mother started to feed her child with
formula milk. His mother introduced semisolid food at 6 mos. At present, the patient has (-)
good appetite.
FAMILY HISTORY:

Paternal grandparents are deceased; age and cause of death are unrecalled.
Maternal grandparents are deceased; age and cause of death are unrecalled.
No heredofamilial disorders such as HTN, stroke, cardiac disease, kidney
disease, gastrointestinal disease, asthma, PTB, seizures, and malignancies noted among blood
relatives.

PERSONAL AND SOCIAL HISTORY:

Home: Patient lives with his parents .
Environment: The patient lives in a NON congested area, GOOD-ventilated, WOODEN
house.
Education: Patient is in ELEMENTARY.
Source of drinking water: TAP.
Garbage disposal: DAILY.
REVIEW OF SYSTEMS:

Constitutional: No weight gain/loss, fatigue.
Skin: No itching, lumps, dryness, color changes, changes in nails.
HEENT: No dizziness, lightheadedness, syncope, trauma, eye pain, redness, double vision,
blurred vision, hear loss, earache, ear discharge, mouth sores, bleeding gums, sore throat,
hoarseness, dysphagia.
Neck: No pain or stiffness.
Respiratory: No cough, hemoptysis, dyspnea.
Cardiovascular: No chest pain, edema, orthopnea, palpitations, cyanosis, paroxysmal
nocturnal dyspnea, easy fatigability.
Gastrointestinal: No nausea, vomiting, loss of appetite, dysphagia, hematochezia, diarrhea,
hemorrhoids, constipation.
Renal: No dysuria, gross hematuria, incontinence, urinary retention, urinary urgency,
hesitancy, dribbling.
Genitalia: No discharge and ulcers.
Peripheral Vascular: No leg cramps and varicose veins.
Musculoskeletal: No backache, joint swelling.
Neurologic: No numbness, tremors, seizures, memory loss.
Hematologic: No easy bruising, bleeding, pallor.
Endocrine: No heat/ cold intolerance, excessive sweating.
Psychiatric: No nervousness, depression, anxiety, hallucinations.


General Survey: Ambulatory, conscious, coherent, not in cardiorespiratory distress, afebrile.

Vital Signs: BP 90/60 mmHg, CR 110 bpm, RR 21/min, Temp 37.4 °C

Skin: Fair complexion, (+) erythematous maculopapular rash all over the face and body; no
jaundice, pallor or pigmentation; good turgor, warm

HEENT: Anicteric sclerae, pink palpebral conjunctivae, pupils 2-3 mm equally reactive and
responsive to light and accommodation. No ear discharge. No nasal discharge. Dry pinkish
lips, no mouth ulcers. No tonsillopharyngealcongestion.
Neck: Supple, midline trachea, thyroid lobes not felt, no jugular vein distention, no cervical
lymphadenopathy.

Chest: No scars, symmetrical chest expansion, no retractions. No palpable mass, symmetric
tactile and vocal fremitus. Resonant on percussion. Clear breath sounds on bilateral lung
fields; no wheeze, no crackles.
Heart: Adynamic precordium; no heaves, no thrills, PMI at 5th L ICS
MCL. Tachycardic, regular rhythm, no murmurs.
Abdomen: Flabby, no scars or visible veins. Normal active bowel sounds. Soft, (+) epigastric
tenderness on deep palpation, no palpable mass. Liver and spleen non-enlarged.

Digital Rectal Examination: No perirectal lesions or fissures. External sphincter tone intact.
Rectal vault without masses. Brown stool on examining finger, no blood.

Extremities: Equal length, no edema, no cyanosis, no limitation of movement, no joint
swelling; full and equal radial, popliteal, posterior tibial and dorsalis pedis pulses;CRT <2s.

Neurologic:
Mental Status: Conscious, coherent, GCS 15, oriented to time, place and person
Motor: Good muscle tone and bulk,Sensory:
stable gait
Cranial Nerves:
I – Able to smell the scent of orange peel
II - Pupils 2-3 mm equally reactive and responsive to light and accommodation
III, IV, VI - (+) extraocular movements
V - (+) corneal blink reflex
VII - Symmetrical facial movements
VIII - Able to hear
IX, X - (+) gag reflex
XI - Can shrug both shoulders
XII - Midline tongue without fasciculations

R L
Biceps +2 +2
Triceps +2 +2
Brachioradia +2 +2
lis
Patellar +2 +2
Achilles +2 +2
Babinski Negati Negati

ve ve

IMPRESSION: Dengue with Warning Signs

COURSE IN THE WARD:-
Day on admission
• Secure consent for admission and management,
• Low salt diet, more liquid and high fiber and iron
• IVF : PNSS 500ml infused with 44 ugtt/min
• Labs : CBC w/ pc , urinalysis and chext x ray serum • Meds : paracetamol 250
mg/5ml , 4 ml q 4° RTC
APPEBON 1 tsp BID
Citrizine 10 mg/tab OD Cont.. to monitor pt for complication.
Day 2 (sept 05,2017)
• V/S ; B P ; 90/60 mmHg, pulse: 98, RR ; 22,temp : 37.8 c
• Maintenance fluid : replace PNSS to D5 1/4NS with KCL 20meq/l with 16 ugtt/min.
• Labs: repeat CBC
• Meds : paracetamol 250 mg/5ml , 4 ml q 4° RTC
APPEBON 1 tsp BID
Citrizine 10 mg/tab OD Amoxicillin 375 mg TID
Day 3 ( sept 06,2017)
• V/S : B P 100/70mmHg, pulse; 96 , RR; 20 , temp; 37.2 • Cont.. replacement fluid
• Labs : repeat CBC w/pc
• Meds : paracetamol 250mg/5ml, 4 ml q 4° RTC
D/C; appebon and citrizine
Amoxicillin 375 mg TID
Azithromycin 165 mg , 55mg every 8 hrs.
Discharge meds ( oral medicine)
• Paracetamol 125mg/ml, 4ml TID
• Amoxicillin 125mg/5ml, 4 ml TID
• Azithromycin 200mg/5ml, 4 ml TID
ANNEXURE:-
CBC
Parameter Day 1 Day2 Day3
WBC 12 12.5 9.5
HCT 36 34.9 38
HBG 12 12.3 16
SEGMENT 0.80 0.80 0.80
LYMPHOCYTES 0.30 0.04 0.40
Platelet 58 102 250
URINALYSIS
DIFFERENTIAL DIAGNOSIS :-
FINAL DIAGNOSIS:- Dengue with Warning Sign
DENGUE
INTUBATION PERIOD: Uncertain. Probably 6 days to 10 days

PERIOD OF COMMUNICABILITY: Unknown. Presumed to be on the 1 St week of illness
when virus is still present in the blood
CLINICAL MANIFESTATIONS:
First 4 days:
>febrile or invasive stage --- starts abruptly as high fever, abdominal pain and headache; later
flushing which may be accompanied by vomiting, conjunctival infection and epistaxis
4th to 7th day:
>toxic or hemorrhagic stage --- lowering of temperature, severe abdominal pain, vomiting
and frequent bleeding from GIT in the form of melena; unstable BP ,narrow pulse pressure
and shock; death may occur; vasomotor collapse
7thto 10th day:
>convalescent or recovery stage --- generalized flushing with intervening areas of blanching
appetite regained and blood pressure already stable
MODE OF TRANSMISSION: Dengue viruses are transmitted to humans through the

infective bites of female Aedes mosquito. Mosquitoes generally acquire virus while feeding
on the blood of an infected person. After virus incubation of 8-10 days, an infected mosquito
is capable, during probing and blood feeding of transmitting the virus to
susceptible.individualsfortherestofitslife.Infectedfemalemosquitoes may also transmit the
virus to
their offspring by transovarial (via the eggs) transmission.
Humans are the main amplifying host of the virus. The virus circulates in the blood of
infected humans for two to seven days, at approximately the same time as they have fever.
Aedes mosquito may have acquired the virus when they fed on an individual during this
period. Dengue
cannot be transmitted through person to person mode.
CLASSIFICATION
1.Severe, frank type
>flushing, sudden high fever, severe hemorrhage, followed by sudden drop of temperature,
shock and terminating in recovery or death
2. Moderate
>with high fever but less hemorrhage, no shock present
3. Mild
>with slight fever, with or without petichial hemorrhage but epidemiologically related to
typical cases usually discovered in the course of invest or typical cases.
GRADING THE SEVERITY OF DENGUE FEVER:
Grade 1:
>fever >non-specific constitutional symptoms such as anorexia, vomiting and
>absence of spontaneous bleeding
>positive tourniquet test
Grade 2:
>signs and symptoms of Grade 1: plus>presence of spontaneous bleeding: mucocutaneous,
gastrointestinal
Grade 3:
>signs and symptoms of Grade 2 with more severe bleeding: plus>evidence of circulatory
failure: cold, clammy skin, irritability, weak tocompressible pulses, narrowing of pulse
pressure to 20 mmhg or less, coldextremities, mental confusion
Grade 4:
>signs and symptoms of Grade 3, declared shock, massive bleeding, pulse lessand arterial
blood Pressure = 1 mmhg (Dengue Syndrome/DS) .
SUSCEPTABILITY, RESISTANCE, AND OCCURRENCE:
>all persons are susceptible

>both sexes are equally affected
>age groups predominantly affected are the pre-school age and school age
>adults and infants are not exempted
>peak age affected: 5-9 years old
DF is sporadic throughout the year. Epidemic usually occurs during rainy seasons (June –
November). Peak months are September – October. It occurs wherever vector mosquito
exists.
DIAGNOSTIC TEST:
Tourniquet test
>Inflate the blood pressure cuff on the upper arm to a point midway between the systolic and
diastolic pressure for 5 minutes.
>Release cuff and make an imaginary 2.5 cm square or 1 inch square just below the cuff, at
the anticubital fossa
.>Count the number of petechiae inside the box. A test is positive when 20 or more petechiae
per suare are observed.
Dengue haemorrhagic fever (DHF), a potentially lethal complication, was firstrecognized in

the 1950s during the dengue epidemics in the Philippines and Thailand, but today DHF
affects most Asian countries and has become a leading cause of hospitalization and death
among children in several of them .Last June 16, 2008, I encountered a patient with such kind
of infection. This patient has caught my attention and has given the opportunity to study his
case. The objective of this study is to help me understand the disease process of Dengue
Fever and to orient myself for appropriate nursing interventions that I could offer to the
patient. This approach enables me to exercise my duties as student nurse which is to render
care. I was given the chance to improve the quality of care I can offer and to pursue my
chosen profession as future nurse. humble myself to present my studied case and submit
myself for further corrections to widen the scope of my knowledge and understanding.
DENGUE PREVENTION: There is no vaccine to prevent dengue. Prevention centers on

avoiding mosquito bites when traveling to areas where dengue occurs and when in U.S. areas,
especially along the Texas-Mexico border, where dengue might occur. Eliminating mosquito
breeding sites in these areas is another key prevention measure. Avoid mosquito bites
when traveling in tropical areas:
Use mosquito repellents on skin and clothing.

When outdoors during times that mosquitoes are biting, wear long-sleeved shirts and long
pants tucked into socks.
Avoid heavily populated residential areas.
When indoors, stay in air-conditioned or screened areas. Use bed nets if sleeping areas are
not screened or air-conditioned.
If you have symptoms of dengue, report your travel history to your doctor. Eliminate
mosquito breeding sites in areas where dengue might occur:
Eliminate mosquito breeding sites around homes. Discard items that can collect rain or run-
off water, especially old tires.
Regularly change the water in outdoor bird baths and pet and animal water containers.
References
1. Siler JF, Hall MW, Hitchens AP (2010) Dengue: its history, epidemiology, mechanism of
transmission, etiology, clinical manifestations, immunity, and prevention. Philipp J Sci 29: 1–
302.
2. Simmons JS, St John JH, Reynolds FHK (2009) Experimental studies of dengue. Philipp J
Sci 44: 1–247.
INTERNAL MEDICINE
PULMONARY TUBERCULOSIS
ABSTRACT :-
Background: Pulmonary tuberculosis (PTB) and paragonimiasis remain as health problems in
certain areas in the Philippines. Both share similar clinical manifestations, which include
chronic productive cough, hemoptysis, dyspnea, fever, weight loss, and night sweats. This
study aimed to determine the prevalence of PTB, paragonimiasis, and co-infections in
Zamboanga del Norte, Philippines. Methods: This study was conducted in selected villages in
two municipalities in Zamboanga del Norte. Patients with chronic cough were interviewed,
examined, and requested to submit two sputum samples which were processed using Ziehl-
Neelsen method to detect acid-fast bacilli (AFB), and NaOH concentration technique for the
detection of Paragonimus ova. Results: A total of 836 patients submitted sputum samples for
examination. Prevalence was 6·7% (2·5-12·7%) for paragonimiasis and 1·9% (0·9-6·3%) for
PTB. Co-infection rate was 0·3%, with two identified cases. Positivity rates for males and
females were 9·6 and 5·8% for paragonimiasis and 3·4 and 1·2% for PTB. Conclusion:
Pulmonary tuberculosis and paragonimiasis are co-endemic in Zamboanga del Norte,
suggesting the need to integrate surveillance and control efforts. Strengthening local health
systems through collaboration between different sectors is recommended for effective disease
control. Development of more sensitive diagnostic tests is important for more accurate
disease surveillance.
PATIENT HISTORY
Informant: Self-referred
Reliability: fair

GENERAL DATA:

This is a case of BD, a 42 year-old male, married, Filipino, farmer, Roman Catholic, born on
September 4,1978, from Zone 3, Ombao Polpog, Bula, Camarines Sur, admitted for the first
time at Bicol Medical Center on February 8 may 2020.

CHIEF COMPLAINT: coughing out of blood


2 week prior to admission, patient had productive cough with yellowish, mucoid, non-
bloodstreaked sputum. No associated fever or dyspnea. No consult done; no medications
taken.
2 days prior to admission, cough persisted. Sputum was now noted to be bloodstreaked. No
construction done; no medication was taken.
Few hours prior to admission, he had an episode of coughing out of blood amounting to 2
cups. This was accompanied by difficulty of breathing. He was brought for consult at a local
health center, was referred to BMC, hence admitted.
No other known medical conditions such as stroke, hypertension ,renal

disease, PTB, asthma, GI disease, thyroid disease, blood dyscrasia, or malignancies.
No known allergies to food and drugs.
No previous hospitalization, surgical operation or accident.

FAMILY HISTORY:

Paternal grandparents are deceased; age at and cause of death were attributed to old age.
Maternal grandparents are deceased; age at and cause of death are unrecalled.
Father died at 77 years old due to Acute Myocardial Infarction.
75 year-old mother is hypertensive.
4 siblings are otherwise well.
No other heredofamilial disorders such as DM, stroke, renal disease, gastrointestinal
disease, asthma, PTB, seizures, and malignancies noted among blood relatives.


Patient is a non-smoker, non-alcoholic and non-user of illicit drugs.
He is a working as a farmer. He had been married for 18 years to a now 37-year old
housekeeper. They have 3 children.The patient lives with his family. The household is
composed of 6 members, together in an owned house made of mixed concrete and light
materials with a water-sealed toilet and 2 bedrooms, which is 5 meters away from the
neighboring house. Garbage disposal is via the municipal garbage collection system; waste
segregation is practiced.
He has a regular diet of rice, fish, meat, vegetables and fruits; prefers meat. Drinking water
source is from the local water system, unsterilized.

REVIEW OF SYSTEMS:

Constitutional: weight loss was noted ,No fever, chills, fatigue.
Skin: No rash, itching, lumps, dryness, color changes, changes in nails.
HEENT: No headache, dizziness, lightheadedness, syncope, trauma, eye
pain, redness, double vision, blurred vision, hear loss, earache, ear discharge, mouth
sores, bleeding gums, sore throat, hoarseness, dysphagia
Cardiovascular: (+) chest pain, no edema, no palpitations; no
orthopnea, cyanosis, paroxysmal nocturnal dyspnea, easy fatigability.
Gastrointestinal: No loss of appetite, nausea, vomiting, hematemesis, abdominal
pain, dysphagia, hematochezia, diarrhea, hemorrhoids, constipation.
Renal: No dysuria, gross hematuria, incontinence, urinary retention, urinary
urgency, hesitancy, dribbling.
Genitalia: No pain, swelling, discharge and ulcers.
Musculoskeletal: No muscle pain, backache, joint swelling, joint pain.
Endocrine: No polyuria, polyphagia, heat/ cold intolerance, excessive sweating.



Vital Signs: BP 1010/80 mmHg, CR 95 bpm, RR 30/min, Temp 37.5°C, O2 sat 94%

Skin: Pale, no pigmentation, no rashes. Good turgor, cold, clammy.

HEENT: Anicteric sclerae, pale palpebral conjunctivae, pupils 2-3 mm equally reactive and
responsive to light and accommodation. No ear discharge. No nasal discharge. Pale dry lips,
no mouth ulcers. No tonsillopharyngealcongestion.

Neck: Supple, midline trachea, thyroid lobes not felt, no cervical lymphadenopathy.

Chest: No scars, symmetrical chest expansion, no retractions. No palpable mass,
decreased vocal and tactile fremitus on the right. Dull lungs. Decreased breath sounds on
right lung field; no wheeze, no crackles.
Abdomen: Flat, no scars or visible veins. Normal active bowel sound. Soft, non-tender, no
palpable mass. Liver and spleen non-enlarged.

swelling, full and equal radial, dorsalis pedis and posterior tibial pulses,, CRT <2s.

Neurologic:
Motor: Good muscle tone and bulkSensory
Cranial Nerves:

I - Not tested
VIII - Able to hear

R L
Biceps +2 +2
Triceps +2 +2
Brachioradial +2 +2
is
Patellar +2 +2
Achilles +2 +2
Babinski Negativ Negativ
e e

IMPRESSION: Pulmonary Tuberculosis
Course in the ward:

Patient was admitted to the medical ward, upon admission patient was
hook to the O2 support . Patient is for DAT, and iv fluid was given. Upon admission
laboratory was requested and clinically corrected. Patient is under antibiotic therapy,
regularly medications given . Also upon admission sputum examination, chest xray was
requested for further case studies. Result shows that patient diagnosed with pulmonary
tuberculosis. We referred this patient to the TB-dot Center. Upon advice patient was
discharged and followed up to tb dot Center.
DIAGNOSTIC :-
CBC
Parameter
Wbc 13.5
Hct 41
Hbg 14
Segmenter 0.68
Lymphocyte 0.47
Platelet 550
URINALYSIS- NORMAL
CHEST XRAY- TB in both lungs.
SPUTUM EXAMINATION- POSITIVE
Differential diagnosis:
Community-acquired Signs of lobar or atypical Sputum examination with

pneumonia pneumonia including presence of bacteria other
crackles and dyspnea. than normal flora.
Generally, shorter duration
of symptoms compared
with TB. If there is doubt,
one should consider
treating for bacterial
pneumonia first (without
using fluoroquinolones or
other antibiotics with
significant antituberculous
activity) and assess for
response.
Nontuberculous Mycobacterium avium If sputum AFB culture is

mycobacteria (NTM) complex and M kansasii positive, DNA probe may
may both present as be used for species
cavitary lesions. Patient identification. Similarly a
risk factors for TB may nucleic acid amplification
point to most likely test (NAAT) that is
diagnosis. negative for TB on a
smear-positive sputum
(95% sensitivity) makes M
tuberculosis less likely.
NTM is more common in
patients with underlying
lung disease.
FINAL DIAGNOSIS:- Pulmonary tuberculosis

DISCUSSION ABOUT CASE:-
TUBERCULOSIS
INTRODUCTION
· One of the oldest diseases known to affect humans and a major cause of death
worldwide
· Emerged -70 000 years ago in Africa · If properly treated, TB caused by drug –
susceptible strains is curable in the vast majority of cases
· If untreated, it can be fatal within 5 years in 50 – 65% of cases
ETIOLOGIC AGENT
· Mycobacterium tuberculosis
· The most common and important agent of human disease
· Rod-shaped, non-spore-forming aerobic, neutral on gram’s staining acid fast bacilli
EPIDEMEOLOGY
· The WHO estimated that 9 million new cases of TB occurred worldwide in 2013
· 95% of cases were reported from developing countries
· Of the estimated 9 million new cases of TB in 2013, 13% (1.1 million) were
associated with HIV infection
· Estimated 480 000 cases of MDR-TB cases worldwide may actually be XDR-TB
FROM EXPOSURE TO INFECTION

· TB is most commonly transmitted from a person with infectious PTB by droplet
nuclei
· Aerosolized by coughing, sneezing or speaking
· May remain suspended in the air for several hours
· Crowding in poorly ventilated rooms is one of the most important factors in the
transmission of tubercle bacilli
· The most infectious patients have cavitary pulmonary disease or, much less
commonly laryngeal TB
· Sputum smear negative are the less infectious
· Culture – negative PTB and extrapulmonary are essentially non infectious
· Persons with both HIV infection and TB may be less infectious than persons without
HIV co-infection because they are less likely to have cavitations
· The risk of developing disease after being infected depends largely on endogenous
factors
· Individuals innate immunologic and nonimmunologic defences
· Clinical illness directly following infection is classified as primary TB and is
common among children
· Not associated with high level of transmissibility
· 10% of infected persons may eventually develop active TB in their lifetime
· Among infected persons, the incidence of TB is highest during late adolescence and
early adulthood; the reasons are unclear
· This incidence among women peaks at 25 – 34 years of age
· The risk increases with the elderly, possibly because of waning immunity and
comorbidity
· The most potent risk factor for TB among infected individuals is clearly HIV co-
infection
NATURAL HISTORY OF DISEASE

· Before the advent of chemotherapy
· Untreated TB is fatal One third of patient died within one year after diagnosis
· More than 50% died within 5 years
PATHOGENESIS and IMMUNITY

· The interaction of M. Tuberculosis with human host begins when droplet nuclei
containing viable microorganisms propelled into the air by infectious patients are
inhaled by a close bystander.
· Majority of the inhaled bacilli are trapped in the upper airways and expelled by
ciliated mucosal cells
· A fraction (usually <10%) reach the alveoli
· Alveolar macrophages phagocytose the bacilli
· After a phagosome forms,the survival of M. Tuberculosis within it seems to depend in
part on reduced acidification due to lack of assembly of complete vesicular proton-
adenosine triphosphatase
· A complex of series of events is generated by the bacterial cell-wall lipoglycan
lipoarinomannan (ManLAM)
· ManLAM inhibits the intracellular increase of calcium. Thus, the calcium/calmodulin
pathway (leading to pphagosome-lysosome fusion) is impaired
· The bacilli survive within the phagosome
· If the bacilli is successful in arresting the phagosome maturation, then replication
begins and the macrophage eventually ruptures and releases its bacillary contents
· Other uninfected phagocytic cells are then recruited to continue the infection cycle by
ingesting dying macrophages and their bacillary content, thus expanding the infection.
THE HOST RESPONSE, GRANULOMA FORMATION and LATENCY

· M. Tuberculosis disseminates widely through the lymph vessels, spreading to other
sites in the lungs and other organs and undergoes a period of extensive growth within
naïve unactivated macrophages
· Additional naïve unactivated macrophages are recruited to the early granuloma
· 2 – 4 weeks after infection. Two host responses to M. Tuberculosis develop. A
macrophage activating response and a tissue damaging response
· The macrophage-activating response is a T-cell mediated phenomenon resulting in
the activation of macrophages that are capable of killing and digesting bacilli
· The tissue – damaging response is a result of delayed-type hypersensitivity reaction to
various bacillary antigens; it destroys unactivated macrophages that contain
multiplying bacilli but also causes caseation necrosis
· The growth of M. Tuberculosis is inhibited within necrotic environment by low
oxygen tension and low pH.
· Some lesions may heal by fibrosis, with subsequent calcification. Whereas,
inflammation and necrosis occur with other lesions
· Latency may not be an accurate term because bacilli may remain active during this
“latent” stage, forming biofilms in necrotic areas within which they temporarily hide
· The term persister is probably more accurate to indicate the behaviour of the bacilli
· It is important to recognize that latent infection and disease represent not a binary
state but rather a continuum along which infection will eventually move to a direction
of full containment or disease
CLINICAL MANIFESTATIONS
· TB can be classified as pulmonary, extrapulmonary or both
· Extrapulmonary TB may occur in 10 – 40% of patients
· Up to two – thirds of HIV – infected patients with TB may have both or
extrapulmonary TB alone
PULMONARY TUBERCULOSIS
· Categorized as primary or postprimary (adult-type, secondary)
PRIMARY DISEASE
· Occurs soon after the initial infection with tubercle bacilli
· May be asymptomatic or present with fever and occasionally pleuritic chest pain
· Seen often in children
· Involves in middle and lower lung zones
· GHON FOCUS
· The lesion formed after initial infection
· Usually peripheral and accompanied by transient hilar or paratracheal
lymphadenopathy
· GHON COMPLEX
· Ghon focus with or without overlying pleural reaction, thickening and regional
lymphadenopathy
POSTPRIMARY DISEASE
· Usually localized in the apical and posterior segments of the upper lobes
· Substantially higher mean oxygen tension (compared with that in the lower zones)
· The superior segments of the lower lobes are also more frequently involved
· Early in the course of the disease, symptoms and signs are often non-specific and
insidious.
· Diurnal fever, night sweats due to deferescence, weight loss, anorexia, general
malaise and weakness
· Cough develops up to 90% of cases
· Initially non-productive and limited to the morning and subsequently
accompanied by production of purulent sputum, sometimes with blood streaking
· Hemoptysis develops in 20 – 30% of cases · Massive hemoptysis may ensue as a
consequence of erosion of blood vessels in the wall of the cavity
· Many patients have no abnormalities detectable by chest examination whereas
others have rales especially after coughing
· Systemic features include fever (low grade and intermittent) in up to 80% of
cases and wasting
· The absence of fever does not exclude TB
· The most common hematologic finding is anemia, leukocytosis, thrombocytosis
with a slightly elevated ESR/or C reactive protein level
· None of these findings is consistent or sufficiently accurate for the diagnostic
purposes.
EXTRAPULMONARY TB
· Most commonly affected, in order of frequency: o Lymph nodes o Pleura o
Genitourinary tract o Bones and joints o Meninges o Peritoneum o Pericardium
LYMPH NODE TB
· Most common presentation of extrapulmonary T in both HIV-seronegative and
HIV-infected patients
· Presents as painless swelling of the lymph nodes
· Posterior cervical and supraclavicular sites (scrofula) · The diagnosis is
established by FNAB (with a yield of 80%) or surgical excision biopsy
PLEURAL TB
· Isolated pleural effusion usually reflects recent primary infection · The effusion
may be small, remain unnoticed and resolve spontaneously
· May be sufficiently large to cause symptoms such as fever, pleuritic chest pain
and dyspnea
· Thoracentesis is required to ascertain the nature of the effusion and to differentiate
it from manifestationsof other etiologies
· The fluid is straw colored or sometimes hemorrhagic
· It is an exudates with a protein concentration of >50% of that in the serum
(usually 4-6 g/dl)
· Norma to low glucose concentration
· pH of 7.3 (occasionally <7.2)
· WBC (usually 600 – 6000uL) neutrophils predominate early but lymphocyte
predominance is typical finding later
· Mesothilial cells are rare or absent
· Needle biopsy of the pleura is often required for diagnosis and is recommended
over pleural fluid
· It reveals granuloma and/or yields a positive culture in up to 80% of cases
· Pleura biopsy can yield a positive result in 75% of cases when real-time
automated nucleic acid amplification is used
· Tuberculous empyema is less common complication of pulmonary TB
· Usually the result of the rupture of a cavitywith spillage of a large number of
organisms into the pleural space
· This process may create a bronchopleural fistula with evident air in the pleural
space
TB OF THE UPPER AIRWAYS

· Nearly always a complication of advanced cavitary pulmonary TB
· May involve the larynx, pharynx and epiglottis
· Symptoms include hoarseness, dysphonia and dysphagia and chronic productive
cough
· Carcinoma of the larynx may have similar features but is usually painless
GENITOURINARY TB
· 10 – 15% of all extrapulmonary TB cases
· May involve any part of the genitourinary tract
· 75% of patients have chest radiographic abnormalities suggesting previous or
concomitant pulmonary disease
· Urinary frequency dysuria, nocturia, hematuria and flank or abdominal pain are
common symptoms
· Urinalysis reveals pyuria and hematuria
· Culture negative pyuria should raise suspicion of TB
SKELETAL TB
· 10% of extrapulmonary cases
· Pathogenesis is related to reactivation of hematogenous foci or to spread from
adjacent paravertebral lymph nodes
· Spinal TB (Pott’s disease or tuberculous spondylitis)
· Often involves two or more adjacent vertebra bodies
· The lower thoracic and upper lumbar vertebrae are usually affected in adults
· In advanced disease, collapse of the vertebral bodies results in kyphosis (gibbus)
· May present as psoas abscess
· CT scan or MRI reveals the characteristic lesion and suggests its etiology
· Aspiration of the abscess or bone biopsy confirms the tuberculous etiology
· A catastrophic complication is paraplegia
TUBERCULOUS MENINGITIS
· 5% of extrapulmonary TB
· Results from hematogenous spread of primary or postprimary pulmonary TB or
from a rupture of subependymal tubercle into the subarachnoid space
· Presents as headache, slight mental changes after a prodrome of weeks of low-
grade fever, malaise, anorexia and irritability
· If not recognized, may evolvd acutely with severe headache, confusion, lethargy,
altered sensorium and neck rigidity
· Evolves over 1 – 2 weeks a course longer than bacterial meningitis
· Lumbar puncture is the cornerstone of the diagnosis
· CSF exam reveals: high leukocyte count (uo to 1000/uL) with lymphocytic
predominance, protein content of 1 – 8g/L (100 – 800 g/L); and a low glucose
concentration
· Cuture of CSF diagnosis in up to 80% of cases and remains the gold standard
· Dexamethasone significantly enhance the chances of survival among >14years of
age but did not reduce the frequency of neurologic sequela GI TB
· Uncommon
· Swallowing of sputum with direct seeding, hematogenous spread
· Terminal ileum and the cecum are the sites most frequently involved
· Abdominal pain and swelling, obstruction, hematochezia and a palpable mass are
common findings
· Surgery is required in most cases, the diagnosis can be established by histologic
exam and culture of specimens obtained intraoperatively
PERICARDIAL TB
· Due to direct extension from mediastina or hilar lymph nodes or to hematogenous
spread
· Disease of the elderly in countries with low TB prevalence
· Acute presentation with dyspnea, fever, dull retrosternal pain and pericardial
friction rub
· Effusion may develop and signs and symptoms of tamponade may appar
· Definitive diagnosis is made by pericardiocentesis
· Fatal without treatment; case fatality of 40%
MILIARY TB
· Due to hematogenous spread
· Physical findings include hepatomegaly, splenomegaly, and lymphadenopathy.
Eye exam may reveal choroidal tubercles which are pathognomonic of military
TB
· Chest radiography reveals a military reticulonodular pattern (more easily seen in
underpenetrated film)
· Sputum smear microscopy is negative in most cases
· Hematologic abnormalities: anemia, leukopenia, lymphopenia, neutrophilic
leukocytosis, leukemoid reactions and polycythemia.
DIAGNOSIS
· The key to diagnosis of TB remain a high index of suspicion
· A presumptive diagnosis is commonly based on the finding of AFB on
microscopic examination of a diagnostic specimen
· Such as a smear of expectorated sputum
· It has been recommended that 2 or 3 sputum specimens preferably collected early
in the morning, should be submitted to the laboratory for AFB smear
· Two specimens collected on the same visit may be as effective as three
· Nucleic acid amplification technology ü Known as the Xpert MTB/RIF
· Can simultaneously detect TB and rifampicin resistance in less than 2 hours
· Sensitivity of 98% among AFB-positive cases and 70% among AFB negative
specimens
· The WHO recommends its use worldwide as the initial diagnostic test in adults
and children presumed to have MDR-TB or HIV-associated TB
· Mycobacterial culture
· Definitive diagnosis depends on the isolation and identification of M. tuberculosis
from a clinica specimen or identification of specific DNA sequences in a nuclear
acid amplification test
· Inoculation onto an egg or agar – based medium (eg., Lowenstein – Jensen or
Middlebrook 7H10) and incubated 37C (under 5% CO2 for middlebrook medium)
· Grows slowly 4 – 8 weeks may be required before growth is detected
· Radiographic procedures
· Upper lobe disease with infiltrates and cavities
· Virtually any radiographic pattern from a normal film to a solitary pulmonary
nodule to diffuse alveolar infiltrates
TREATMENT
· The two aims of TB treatment are: o To prevent morbidity and death by curing TB
while preventing the emergency of drug resistance o To interrupt transmission by

rendering patient non-infectious
RECOMMENDED DOSAGE
TREATMENT REGIMEN
· Standard regimen are divided into initial or bactericidal phase and a continuation
or sterilizing phase
· Initial phase o The majority of the tubercle bacilli are klled o Symptoms resolve o
Patient becomes non infectious
· Continuation phase o Eliminate persisting mycobactera and prevent relapse
· The treatment regimen of choice for virtually all forms of drug susceptible TB in
adults consist of 2 month initial (or intensive phase) of HRZE followed by 4 –
month continuation phase of HR
· The regimen can cure TB in more than 90% of patients o In children, most
forms of TB in the absence of HIV infection can be safely treated without
ethambutol
MONITORING TREATMENT RESPONSE
· Patients with pulmonary disease should have their sputum examined monthly
until cultures become negative By the end of the third month, the sputum of
virtually all patients should be culture negative o If mycobacteria culture is
not practical, then monitoring AFB smear exam should be undertaken at 2, 5
and 6 months Monitoring of response by during chemotherapy by nucleic acid
amplification technology is has not been shown to be suitable Serial chest
radiographs are not recommended o Because radiographic changes may lag
behind bacteriologic response and are not highly sensitive The most common
adverse reaction of significance is hepatitis Baseline assessment of liver

function (e.g. measurement of serum levels of aminotransferases) o Treatment
should be stopped if serum aminotransferases are five to sixfold elevated
· TREATMENT OF PULMONARY AND EXTRA PULMONARY
TUBERCULOSIS IN ADULT
DENGUE FEVER
ABSTRACT:-
As the outbreaks of Dengue fever increasing in Philippines, one part after other
getting affected, it is very essential to know more about this disease and prevalence, any
change in the viral strain, severity of the disease pattern, early detection of the virus and early
management of the disease resulting in good recovery . Population growth, rapid
urbanization, increase in international travel from endemic areas and global warming are
playing a major role in disease spread. Measures should be taken to control the
aforementioned causes to prevent disease spread and reduce epidemic flare up.
PATIENT’S HISTORY
Reliability: 90%

GENERAL DATA:

This is a case of MD, a 37 year-old female, married, Filipino, born on May 30, 1981,
college graduate, currently residing in Concepcion Pequeña, Naga
City, Camarines Sur, admitted for the first time at Bicol Medical Center on February 20,
2020.

CHIEF COMPLAINT: fever for 6 day


6 days prior to admission, patient had undocumented fever, intermittent. This was
accompanied by joint pain and appearance of reddish non-pruritic rashes all over the body.
She self-medicated with Paracetamol 500 mg/tab 3x a day which offered temporary relief of
fever.
4 days prior to admission, still with intermittent fever, joint pain and rashes, now associated
with dry cough. No accompanying abdominal pain, vomiting, epistaxis, passage of bloody or
black stools, or dysuria.
1 day prior to admission, signs and symptoms persisted. She consulted at a private hospital in
Naga City and was admitted as a case of dengue fever. She was given IVF of D5NSS and
D5LR and Paracetamol 500 mg/tab every 4 hours PRN.
Few hours prior to admission, she had epigastric pain, hence referred for further evaluation
and management, then subsequently admitted.

Patient was born via Spontaneous Vaginal Delivery at home assisted by a traditional birth
attendant. She had measles and chickenpox during her primary school years, but with no
history of rheumatic fever, mumps and polioduring childhood.
No known medical conditions such as HTN, stroke, renal disease, asthma, PTB, DM, cardiac
disease, GI disease, thyroid disease, blood dyscrasias, malignancies.

FAMILY HISTORY:

Paternal grandparents are deceased; age and cause of death are unrecalled.
Maternal grandparents are deceased; age and cause of death are unrecalled.
55 year-old father, 50 year-old mother, and siblings aged 28, 25 and 21 are otherwise
well.
No heredofamilial disorders such as HTN, stroke, cardiac disease, kidney
disease, gastrointestinal disease, asthma, PTB, seizures, and malignancies noted among blood
relatives.


Patient is a non-smoker, non-alcoholic beverage drinker, and non-user of illicit drugs.
She is married for 5 years to a now 32 year-old government employee. She is a graduate of
BS Business Administration who is a full-time mother to a 5 year-old girl and a 2 year-old
boy. The family lives in an owned housemade of concrete materials with a water-sealed
toilet, which is 10 meters away from the neighboring house. Garbage disposal is via the
city garbage collection system; waste segregation is practiced.
She has a regular diet of rice, fish, meat, vegetables and fruits; prefers meat. Drinking water
source is from a water refilling station.

REVIEW OF SYSTEMS:

Constitutional: No weight gain/loss, fatigue.
Skin: No itching, lumps, dryness, color changes, changes in nails.
Gastrointestinal: No nausea, vomiting, loss of appetite, dysphagia, hematochezia, diarrhea,
hemorrhoids, constipation.
Musculoskeletal: No backache, joint swelling.
Endocrine: No heat/ cold intolerance, excessive sweating.



Vital Signs: BP 90/60 mmHg, CR 110 bpm, RR 21/min, Temp 37.4 °C

Skin: Fair complexion, (+) erythematous maculopapular rash all over the face and body; no
jaundice, pallor or pigmentation; good turgor, warm

responsive to light and accommodation. No ear discharge. No nasal discharge. Dry pinkish
lips, no mouth ulcers. No tonsillopharyngealcongestion.
Neck: Supple, midline trachea, thyroid lobes not felt, no jugular vein distention, no cervical
lymphadenopathy.

tactile and vocal fremitus. Resonant on percussion. Clear breath sounds on bilateral lung
fields; no wheeze, no crackles.
Abdomen: Flabby, no scars or visible veins. Normal active bowel sounds. Soft, (+) epigastric
tenderness on deep palpation, no palpable mass. Liver and spleen non-enlarged.

Digital Rectal Examination: No perirectal lesions or fissures. External sphincter tone intact.
Rectal vault without masses. Brown stool on examining finger, no blood.

swelling; full and equal radial, popliteal, posterior tibial and dorsalis pedis pulses;CRT <2s.

Neurologic:
Motor: Good muscle tone and bulk,Sensory:
stable gait
Cranial Nerves:
VIII - Able to hear

R L
Biceps +2 +2
Triceps +2 +2
Brachioradia +2 +2
lis
Patellar +2 +2
Achilles +2 +2
Babinski Negati Negati

ve ve

IMPRESSION: Dengue with Warning Signs

Day on admission
• Secure consent for admission and management,
• Low salt diet, more liquid and high fiber and iron
• IVF : PNSS 500ml infused with 44 ugtt/min
• Labs : CBC w/ pc , urinalysis and chext x ray serum • Meds : paracetamol 250
mg/5ml , 4 ml q 4° RTC
APPEBON 1 tsp BID
Citrizine 10 mg/tab OD Cont.. to monitor pt for complication.
Day 2 (sept 05,2017)
• V/S ; B P ; 90/60 mmHg, pulse: 98, RR ; 22,temp : 37.8 c
• Maintenance fluid : replace PNSS to D5 1/4NS with KCL 20meq/l with 16 ugtt/min.
• Labs: repeat CBC
• Meds : paracetamol 250 mg/5ml , 4 ml q 4° RTC
APPEBON 1 tsp BID
Citrizine 10 mg/tab OD Amoxicillin 375 mg TID
Day 3 ( sept 06,2017)
• V/S : B P 100/70mmHg, pulse; 96 , RR; 20 , temp; 37.2 • Cont.. replacement fluid
• Labs : repeat CBC w/pc
• Meds : paracetamol 250mg/5ml, 4 ml q 4° RTC
D/C; appebon and citrizine
Amoxicillin 375 mg TID
Azithromycin 165 mg , 55mg every 8 hrs.
Discharge meds ( oral medicine)
• Paracetamol 125mg/ml, 4ml TID
• Amoxicillin 125mg/5ml, 4 ml TID
• Azithromycin 200mg/5ml, 4 ml TID
ANNEXURE:-
CBC
Parameter Day 1 Day2 Day3
WBC 12 12.5 9.5
HCT 36 34.9 38
HBG 12 12.3 16
SEGMENT 0.80 0.80 0.80
LYMPHOCYTES 0.30 0.04 0.40
Platelet 58 102 250
URINALYSIS
DIFFERENTIAL DIAGNOSIS :-
FINAL DIAGNOSIS:- Dengue with Warning Signs

DENGUE
INTUBATION PERIOD: Uncertain. Probably 6 days to 10 days

PERIOD OF COMMUNICABILITY: Unknown. Presumed to be on the 1 St week of illness
when virus is still present in the blood
CLINICAL MANIFESTATIONS:
First 4 days:
>febrile or invasive stage --- starts abruptly as high fever, abdominal pain and headache; later
flushing which may be accompanied by vomiting, conjunctival infection and epistaxis
4th to 7th day:
>toxic or hemorrhagic stage --- lowering of temperature, severe abdominal pain, vomiting
and frequent bleeding from GIT in the form of melena; unstable BP ,narrow pulse pressure
and shock; death may occur; vasomotor collapse
7thto 10th day:
>convalescent or recovery stage --- generalized flushing with intervening areas of blanching
appetite regained and blood pressure already stable
MODE OF TRANSMISSION: Dengue viruses are transmitted to humans through the

infective bites of female Aedes mosquito. Mosquitoes generally acquire virus while feeding
on the blood of an infected person. After virus incubation of 8-10 days, an infected mosquito
is capable, during probing and blood feeding of transmitting the virus to
susceptible.individualsfortherestofitslife.Infectedfemalemosquitoes may also transmit the
virus to
their offspring by transovarial (via the eggs) transmission.
Humans are the main amplifying host of the virus. The virus circulates in the blood of
infected humans for two to seven days, at approximately the same time as they have fever.
Aedes mosquito may have acquired the virus when they fed on an individual during this
period. Dengue
cannot be transmitted through person to person mode.
CLASSIFICATION
1.Severe, frank type

>flushing, sudden high fever, severe hemorrhage, followed by sudden drop of temperature,
shock and terminating in recovery or death
2. Moderate
>with high fever but less hemorrhage, no shock present
3. Mild
>with slight fever, with or without petichial hemorrhage but epidemiologically related to
typical cases usually discovered in the course of invest or typical cases.
GRADING THE SEVERITY OF DENGUE FEVER:
Grade 1:
>fever >non-specific constitutional symptoms such as anorexia, vomiting and
>absence of spontaneous bleeding
>positive tourniquet test
Grade 2:
>signs and symptoms of Grade 1: plus>presence of spontaneous bleeding: mucocutaneous,
gastrointestinal
Grade 3:
>signs and symptoms of Grade 2 with more severe bleeding: plus>evidence of circulatory
failure: cold, clammy skin, irritability, weak tocompressible pulses, narrowing of pulse
pressure to 20 mmhg or less, coldextremities, mental confusion
Grade 4:
>signs and symptoms of Grade 3, declared shock, massive bleeding, pulse lessand arterial
blood Pressure = 1 mmhg (Dengue Syndrome/DS) .
SUSCEPTABILITY, RESISTANCE, AND OCCURRENCE:
>all persons are susceptible

>both sexes are equally affected
>age groups predominantly affected are the pre-school age and school age
>adults and infants are not exempted
>peak age affected: 5-9 years old
DF is sporadic throughout the year. Epidemic usually occurs during rainy seasons (June –
November). Peak months are September – October. It occurs wherever vector mosquito
exists.
DIAGNOSTIC TEST:
Tourniquet test
>Inflate the blood pressure cuff on the upper arm to a point midway between the systolic and
diastolic pressure for 5 minutes.
>Release cuff and make an imaginary 2.5 cm square or 1 inch square just below the cuff, at
the anticubital fossa
.>Count the number of petechiae inside the box. A test is positive when 20 or more petechiae
per suare are observed.
Dengue haemorrhagic fever (DHF), a potentially lethal complication, was firstrecognized in

the 1950s during the dengue epidemics in the Philippines and Thailand, but today DHF
affects most Asian countries and has become a leading cause of hospitalization and death
among children in several of them .Last June 16, 2008, I encountered a patient with such kind
of infection. This patient has caught my attention and has given the opportunity to study his
case. The objective of this study is to help me understand the disease process of Dengue
Fever and to orient myself for appropriate nursing interventions that I could offer to the
patient. This approach enables me to exercise my duties as student nurse which is to render
care. I was given the chance to improve the quality of care I can offer and to pursue my
chosen profession as future nurse. humble myself to present my studied case and submit
myself for further corrections to widen the scope of my knowledge and understanding.
DENGUE PREVENTION: There is no vaccine to prevent dengue. Prevention centers on

avoiding mosquito bites when traveling to areas where dengue occurs and when in U.S. areas,
especially along the Texas-Mexico border, where dengue might occur. Eliminating mosquito
breeding sites in these areas is another key prevention measure. Avoid mosquito bites
When traveling in tropical areas:

Use mosquito repellents on skin and clothing.
When outdoors during times that mosquitoes are biting, wear long-sleeved shirts and long
pants tucked into socks.
Avoid heavily populated residential areas.
When indoors, stay in air-conditioned or screened areas. Use bed nets if sleeping areas are
not screened or air-conditioned.
If you have symptoms of dengue, report your travel history to your doctor. Eliminate
mosquito breeding sites in areas where dengue might occur:
Eliminate mosquito breeding sites around homes. Discard items that can collect rain or run-
off water, especially old tires.
Regularly change the water in outdoor bird baths and pet and animal water containers.
References
1. Siler JF, Hall MW, Hitchens AP (2010) Dengue: its history, epidemiology, mechanism of
transmission, etiology, clinical manifestations, immunity, and prevention. Philipp J Sci 29: 1–
302.
2. Simmons JS, St John JH, Reynolds FHK (2009) Experimental studies of dengue. Philipp J
Sci 44: 1–247.
SCHIZOPHRENIA
ABSTRACT
Schizophrenia is a chronic and severe disorder that affects how a person thinks, feels, and
acts. Although schizophrenia is not as common as other mental disorders, it can be very
disabling. Approximately 7 or 8 individuals out of 1,000 will have schizophrenia in their
lifetime.
People with the disorder may hear voices or see things that aren’t there. They may believe
other people are reading their minds, controlling their thoughts, or plotting to harm them.
This can be scary and upsetting to people with the illness and make them withdrawn or
extremely agitated. It can also be scary and upsetting to the people around them.
People with schizophrenia may sometimes talk about strange or unusual ideas, which can
make it difficult to carry on a conversation. They may sit for hours without moving or
talking. Sometimes people with schizophrenia seem perfectly fine until they talk about what
they are really thinking.
Families and society are impacted by schizophrenia too. Many people with schizophrenia
have difficulty holding a job or caring for themselves, so they may rely on others for help.
Stigmatizing attitudes and beliefs about schizophrenia are common and sometimes interfere
with people’s willingness to talk about and get treatment for the disorder.
People with schizophrenia may cope with symptoms throughout their lives, but treatment
helps many to recover and pursue their life goals. Researchers are developing more effective
treatments and using new research tools to understand the causes of schizophrenia. In the
years to come, this work may help prevent and better treat the illness.
PATIENT HISTORY
General Data
This is a case of 30 years old, Male, married with two children, born on November 19,
1990 at Labo Camarines Norte and currently residing at Baklad, Labo Camarines Norte.
Admitted at Bicol Medical Center- Cadlan for the first time.
Chief Complaint
Violent episodes at public place
History of Present Illness
Patient is apparently well until 4 months prior to admission, he had episodes of

depression due to his father’s medical condition (kidney failure) who is currently admitted at
BMC. Patient was unable to sleep.
1 week prior to admission, patient had episode of violence at home when provoked.
The wife reported that he smiles and talk alone and sometimes wonder outside the house. He
was caught mumbling many times which makes his wife worried because he left the care of
her young child to his husband. She medicated with tegretol 200mg/tab once a day,
haloperidol 5mg once a day, flucarizine 5mg once a day for 1 week as advised by family
friend.
1 day prior to admission, above symptoms was observed, wife reportedthat patient
had auditory hallucination as verbalized by patient described as unfamilliar and commanding.
He also go out nude in public places at times.
MSE:adult, male clad in t-shirt with jacket, pants with slippers on. Patient is conscious and
uncooperative. Oriented to person with good eye contact. He is conversant with
normoproductive and normal rate and tone of voice. Poor impulse control, judgement and
insight.
Past Medical History
· Non hypertensive, non diabetic, no blood dyscrasia and cardiac disease illicited
Prenatal history
· Born to a 30 year old G2P2 (2002) mother via spontaneous vaginal delivery by
traditional birth attendant with complete prenatal check up with multivitamins and
ferrous sulfate
· No history of other childhood illnes
· No surgery, no blood transfusion – history of blood donation
· No known allergy
Family History
· Father is presently admitted due to kidney failure
· Mother has hypertension
· Sibling is essentially well
Personal and Social History

· Provider to his family and parents
· Work as garbage collector in municipality of Labo, Camarines Norte
· Graduated highschool
· Non smoker, non alcoholic and denies illicit of illegal drugs.
Review of System
◦ General data: undocumented fever
◦ Skin: (-)rashes, (-)itchiness, (-)dryness
◦ HEENT: (-) headache, (-) dizziness, (-) lightheadedness, unable to sleep
◦ C/L: (-) DOB, (-)wheezing, (-)crackles
◦ CARDIO: (-)orthopnea, (-)cyanosis, (-) palpitations, (-)PNd
◦ GI: (+) loss of appetite, (-)constipation, (-) diarrhea
◦ GUT: (-)pain, (-)swelling, (-)itching
◦ MUSCULO: (-) muscle pain, (-)stiffness, (-)joint swelling
◦ ENDO: (-)polydipsia, (-)polyuria, (-)
◦ NEURO: (-) tremor, (-)paralysis
Physical Examination
◦ General data: afebrile, tachycardia

◦ Skin: no lesion
◦ HEENT: normocephalic, atraumatic, pupils equally reactive to light and accommodation,
yellowish sclera, pale conjunctiva, symmetrical ala nasi, no lymphadenopathy
◦ C/L: symmetrical chest expansion, normal rate and rhythm, clear breath sound
◦ CARDIO: AP, no heaves, lifts or thrills, no neck vein engorgement, carotid upstrokes are
brisk
without bruits, PMI at 5th ICS mid clavicular, s2 louder than s1
◦ GI: flabby with no visible masses, no visible pulsation, soft, no tenderness, normative
bowel,
(+) murphy’s sign
◦ GUT: grossly normal,
◦ MUSCULO: no observe swelling of joints or gross deformity, no signs of muscle wasting
or
atrophy, no tenderness or crepitus over the joints, full range of motion in all joints
◦ eXTREMITIES: warm without edema, poor skin turgor, no varicosities, 2+
◦ NEURO: alert, relaxed, uncooperative, not oriented to person, place and time, obeys simple
Command
IMPRESSION:- schizophrenia
DIAGNOSTIC
CBC
Parameter
Wbc 10.1
HCT 45
HBG 14
Segment 0.71
Lymphocytes 0.31
Platelet 345
URINALYSIS
FINAL DIAGNOSIS :- schizophrenia
DISCUSSION
SCHIZOPHRENIA
symptoms of schizophrenia:-
The symptoms of schizophrenia fall into three broad categories: positive, negative,
and cognitive symptoms.
POSITIVE SYMPTOMS
Positive symptoms are psychotic
behaviors not generally seen in
healthy people. People with positive
symptoms may “lose touch” with
some aspects of reality. For some
people, these symptoms come and go. For others, they stay stable over time.
Sometimes they are severe, and at other times hardly noticeable. The severity of
positive symptoms may depend on whether the individual is receiving treatment.
Positive symptoms include the following:
Hallucinations
are sensory experiences that occur in the absence of a stimulus. These can occur in
any of the five senses (vision, hearing, smell, taste, or touch). “Voices” (auditory
hallucinations) are the most common type of hallucination in schizophrenia. Many
people with the disorder hear voices. The voices can either be internal, seeming to
come from within one’s own mind, or they can be external, in which case they can
seem to be as real as another person speaking. The voices may talk to the person
about his or her behavior, command the person to do things, or warn the person of
danger. Sometimes the voices talk to each other, and sometimes people with
schizophrenia talk to the voices that they hear. People with schizophrenia may hear
voices for a long time before family and friends notice the problem.
Other types of hallucinations include seeing people or objects that are not there,
smelling odors that no one else detects, and feeling things like invisible fingers
touching their bodies when no one is near.
Delusions
are strongly held false beliefs that are not consistent with the person’s culture.
Delusions persist even when there is evidence that the beliefs are not true or logical.
People with schizophrenia can have delusions that seem bizarre, such as believing that
neighbors can control their behavior with magnetic waves. They may also believe that
people on television are directing special messages to them, or that radio stations are
broadcasting their thoughts aloud to others. These are called “delusions of reference.”
Sometimes they believe they are someone else, such as a famous historical figure.
They may have paranoid delusions and believe that others are trying to harm them,
such as by cheating, harassing, poisoning, spying on, or plotting against them or the
people they care about. These beliefs are called “persecutory delusions.”
Thought disorders
are unusual or dysfunctional ways of thinking. One form is called “disorganized
thinking.” This is when a person has trouble organizing his or her thoughts or
connecting them logically. He or she may talk in a garbled way that is hard to
understand. This is often called “word salad.” Another form is called “thought
blocking.” This is when a person stops speaking abruptly in the middle of a thought.
When asked why he or she stopped talking, the person may say that it felt as if the
thought had been taken out of his or her head. Finally, a person with a thought
disorder might make up meaningless words, or “neologisms.”
Movement disorders
may appear as agitated body movements. A person with a movement disorder may
repeat certain motions over and over. In the other extreme, a person may become
catatonic. Catatonia is a state in which a person does not move and does not respond
to others. Catatonia is rare today, but it was more common when treatment for
schizophrenia was not available.
NEGATIVE SYMPTOMS
Negative symptoms are associated with disruptions to normal emotions and
behaviors. These symptoms are harder to recognize as part of the disorder and can be
mistaken for depression or other conditions. These symptoms include the following:
• “Flat affect” (reduced expression of emotions via facial expression or voice tone)
• Reduced feelings of pleasure in everyday life
• Difficulty beginning and sustaining activities
• Reduced speaking
People with negative symptoms may need help with everyday tasks. They may
neglect basic personal hygiene.
This may make them seem lazy or unwilling to help themselves, but the problems are
symptoms caused by schizophrenia.
COGNITIVE SYMPTOMS
For some people, the cognitive symptoms of schizophrenia are subtle, but for others,
they are more severe and patients may notice changes in their memory or other
aspects of thinking. Similar to negative symptoms, cognitive symptoms may be
difficult to recognize as part of the disorder. Often, they are detected only when
specific tests are performed. Cognitive symptoms include the following:
• Poor “executive functioning” (the ability to understand information and use it to
make decisions)
• Trouble focusing or paying attention
• Problems with “working memory” (the ability to use information
immediately after learning it)
Poor cognition is related to worse employment and social outcomes and can be
distressing to individuals with schizophrenia.
When does schizophrenia start, and who gets it?

Schizophrenia affects slightlymore males than females. It occurs in all ethnic groups
around the world. Symptoms such as hallucinations anddelusions usually start
between ages 16 and 30. Males tend to experience symptoms a little earlier than
females. Most commonly, schizophrenia occurs in late adolescence and early
adulthood. It is uncommon to be diagnosed with schizophrenia after age 45.
Schizophrenia rarely occurs in children, but awareness of childhood-onset
schizophrenia is increasing.
It can be difficult to diagnose schizophrenia in teens. This is because the first signs
can include a change of friends, a drop in grades, sleep problems, and irritability—
behaviors that are common among teens. A combination of factors can predict
schizophrenia in up to 80 percent of youth who are at high risk of developing the
illness. These factors include isolating oneself and withdrawing from others, an
increase in unusual thoughts and suspicions, and a family history of psychosis. This
pre-psychotic stage of the disorder is called the “prodromal” period.
Are people with schizophrenia violent?

Most people with schizophrenia are not violent. In fact, most violent crimes are not
committed by people with schizophrenia. People with schizophrenia are much more
likely to harm themselves than others. Substance abuse may increase the chance a
person will become violent. The risk of violence is greatest when psychosis is
untreated and decreases substantially when treatment is in place.
Schizophrenia and suicide

Suicidal thoughts and behaviors are very common among people with schizophrenia.
People with schizophrenia die earlier than people without a mental illness, partly
because of the increased suicide risk.
It is hard to predict which people with schizophrenia are more likely to die by suicide,
but actively treating any co-existing depressive symptoms and substance abuse may
reduce suicide risk. People who take their antipsychotic medications as prescribed are
less likely to attempt suicide than those who do not. If someone you know is talking
about or has attempted suicide, help him or her find professional help right away or
call 911.
Schizophrenia and substance use disorders

Substance use disorders occur when frequent use of alcohol and/or drugs interferes
with a person’s health, family, work, school, and social life. Substance use is the most
common co-occurring disorder in people with schizophrenia, and the complex
relationships between substance use disorders and schizophrenia have been
extensively studied. Substance use disorders can make treatment for schizophrenia
less effective, and individuals are also less likely to engage in treatment for their
mental illness if they are abusing substances. It is commonly believed that people with
schizophrenia who also abuse substances are trying to “self-medicate” their
symptoms, but there is little evidence that people begin to abuse substances in
response to symptoms or that abusing substances reduces symptoms.
Nicotine is the most common drug abused by people with schizophrenia. People with
schizophrenia are much more likely to smoke than people without a mental illness,
and researchers are exploring whether there is a biological basis for this. There is
some evidence that nicotine may temporarily alleviate a subset of the cognitive
deficits commonly observed in schizophrenia, but these benefits are outweighed by
the detrimental effects of smoking on other aspects of cognition and general health.
Bupropion has been found to be effective for smoking cessation in people with
schizophrenia. Most studies find that reducing or stopping smoking does not make
schizophrenia symptoms worse.
Cannabis (marijuana) is also frequently abused by people with schizophrenia, which
can worsen health outcomes. Heavy cannabis use is associated with more severe and
earlier onset of schizophrenia symptoms, but research has not yet definitively
determined whether cannabis directly causes schizophrenia.
Drug abuse can increase rates of other medical illnesses (such as hepatitis, heart
disease, and infectious disease) as well as suicide, trauma, and homelessness in people
with schizophrenia.
It is generally understood that schizophrenia and substance use disorders have strong
genetic risk factors. While substance use disorder and a family history of psychosis
have individually been identified as risk factors for schizophrenia, it is less well
understood if and how these factors are related.
When people have both schizophrenia and a substance abuse disorder, their best
chance for recovery is a treatment program that integrates the schizophrenia and
substance abuse treatment.
What causes schizophrenia?
Research has identified several factors that contribute to the risk of developing
schizophrenia.
GENES AND ENVIRONMENT

Scientists have long known that schizophrenia sometimes runs in families. The illness
occurs in less than 1 percent of the general population, but it occurs in 10 percent of
people who have a first-degree relative with the disorder, such as a parent, brother, or
sister. People who have second- degree relatives (aunts, uncles, grandparents, or
cousins) with the disease also develop schizophrenia more often than the general
population. The risk is highest for an identical twin of a person with schizophrenia.
He or she has a 40 to 65 percent chance of developing the disorder. Although these
genetic relationships are strong, there are many people who have schizophrenia who
don’t have a family member with the disorder and, conversely, many people with one
or more family members with the disorder who do not develop it themselves.
Scientists believe that many different genes contribute to an increased risk of
schizophrenia, but that no single gene causes the disorder by itself. In fact, recent
research has found that people with schizophrenia tend to have higher rates of rare
genetic mutations. These genetic differences involve hundreds of different genes and
probably disrupt brain development in diverse and subtle ways.
Research into various genes that are related to schizophrenia is ongoing, so it is not
yet possible to use genetic information to predict who will develop the disease.
Despite this, tests that scan a person’s genes can be bought without a prescription or a
health professional’s advice. Ads for the tests suggest that with a saliva sample, a
company can determine if a client is at risk for developing specific diseases, including
schizophrenia. However, scientists don’t yet know all of the gene variations that
contribute to schizophrenia and those that are known raise the risk only by very small
amounts. Therefore, these “genome scans” are unlikely to provide a complete picture
of a person’s risk for developing a mental disorder like schizophrenia.
In addition, it certainly takes more than genes to cause the disorder. Scientists think
that interactions between genes and aspects of the individual’s environment are
necessary for schizophrenia to develop. Many environmental factors may be involved,
such as exposure to viruses or malnutrition before birth, problems during birth, and
other, not yet known, psychosocial factors.
DIFFERENT BRAIN CHEMISTRY AND STRUCTURE

Scientists think that an imbalance in the complex, interrelated chemical reactions of
the brain involving the neurotransmitters dopamine and glutamate, and possibly
others, plays a role in schizophrenia. Neurotransmitters are substances that brain cells
use to communicate with each other. Scientists are learning more about how brain
chemistry is related to schizophrenia.
Also, the brain structures of some people with schizophrenia are slightly different
than those of healthy people. For example, fluid-filled cavities at the center of the
brain, called ventricles, are larger in some people with schizophrenia. The brains of
people with the illness also tend to have less gray matter, and some areas of the brain
may have less or more activity. These differences are observed when brain scans from
a group of people with schizophrenia are compared with those from a group of people
without schizophrenia. However, the differences are not large enough to identify
individuals with the disorder and are not currently used to diagnose schizophrenia.
Studies of brain tissue after death also have revealed differences in the brains of
people with schizophrenia. Scientists have found small changes in the location or
structure of brain cells that are formed before birth. Some experts think problems
during brain development before birth may lead to faulty connections. The problem
may not show up in a person until puberty. The brain undergoes major changes during
puberty, and these changes could trigger psychotic symptoms in people who are
vulnerable due to genetics or brain differences. Scientists have learned a lot about
schizophrenia, but more research is needed to help explain how it develops.
How is schizophrenia treated?

Because the causes of schizophrenia are still unknown, treatments focus on
eliminating the symptoms of the disease. Treatments include antipsychotic
medications and various psychosocial treatments. Research on “coordinated specialty
care,” where a case manager, the patient, and a medication and psychosocial treatment
team work together, has shown promising results for recovery.
ANTIPSYCHOTIC MEDICATIONS
Antipsychotic medications have been available since the mid-1950s. The older types
are called conventional or typical antipsychotics.
In the 1990s, new antipsychotic medications were developed. These new medications
are called second-generation or atypical antipsychotics.
WHAT ARE THE SIDE EFFECTS?

Some people have side effects when they start taking medications. Most side effects
go away after a few days. Others are persistent but can often be managed successfully.
People who are taking antipsychotic medications should not drive until they adjust to
their new medication. Side effects of many antipsychotics include:
• Drowsiness
• Dizziness when changing positions • Blurred vision
• Rapid heartbeat
• Sensitivity to the sun
• Skin rashes
• Menstrual problems for women
Atypical antipsychotic medications can cause major weight gain and changes in a
person’s metabolism. This may increase a person’s risk of getting diabetes and high
cholesterol. A doctor should monitor a person’s weight, glucose levels, and lipid
levels regularly while the individual is taking an atypical antipsychotic medication.
Typical antipsychotic medications can cause side effects related to physical
movement, such as:
• Rigidity
• Persistent muscle spasms • Tremors
• Restlessness
Doctors and individuals should work together to choose the right medication,
medication dose, and treatment plan, which should be based on a person’s individual
needs and medical situation. Information about medications is frequently updated.
Check the U.S. Food and Drug Administration (FDA) website (http://www.fda.gov)
for the latest information on warnings, patient medication guides, or newly approved
medications.
Long-term use of typical antipsychotic medications may lead to a condition called
tardive dyskinesia (TD). TD causes muscle movements a person can’t control. The
movements commonly happen around the mouth. TD can range from mild to severe,
and in some people the problem cannot be cured. Sometimes people with TD recover
partially or fully after they stop taking the medication.
TD happens to fewer people who take the atypical antipsychotics, but some people
may still get TD. People who think that they might have TD should check with their
doctor before stopping their medication.
How are antipsychotic medications taken, and how do people respond to them?
Antipsychotic medications are usually taken daily in pill or liquid form. Some
antipsychotics are injections that are given once or twice a month.
Symptoms of schizophrenia, such as feeling agitated and having hallucinations,
usually improve within days after starting
antipsychotic treatment. Symptoms like delusions usually improve within a few
weeks. After about 6 weeks, many people will experience improvement in their
symptoms. Some people will continue to have some symptoms, but usually
medication helps to keep the symptoms from getting very intense.
However, people respond in different ways to antipsychotic medications, and no one
can tell beforehand how a person will respond. Sometimes a person needs to try
several medications before finding the right one. Doctors and patients can work
together to find the best medication or medication combination, as well as the right
dose.
Most people will have one or more periods of relapse—their symptoms come back or
get worse. Usually, relapses happen when people stop taking their medication or when
they take it less often than prescribed.
Some people stop taking the medication because they feel better or they may feel they
don’t need it anymore. But no one should stop taking an antipsychotic medication
without first talking to his or her doctor. Medication should be gradually tapered off,
never stopped suddenly.
HOW DO ANTIPSYCHOTIC MEDICATIONS INTERACT WITH OTHER

MEDICATIONS?
Antipsychotic medications can produce unpleasant or dangerous side effects when
taken with certain other medications. For this reason, all doctors treating a patient
need to be aware of all the medications that person is taking. Doctors need to know
about prescription and over-the- counter medicine, vitamins, minerals, and herbal
supplements. People also need to discuss any alcohol or street drug use with their
doctor.
PSYCHOSOCIAL TREATMENTS
Psychosocial treatments can help people with schizophrenia who are already
stabilized. Psychosocial treatments help individuals deal with the everyday challenges
of their illness, such as difficulty with communication, work, and forming and
keeping relationships. Learning and using coping skills to address these problems
helps people with schizophrenia to pursue their life goals, such as attending school or
work. Individuals who participate in regular psychosocial treatment are less likely to
have relapses or be hospitalized. For more information on psychosocial treatments,
see the psychotherapies section on the National Institute of Mental Health (NIMH)
website at http:// www.nimh.nih.gov/health/topics/psychotherapies/index.shtml.
ILLNESS MANAGEMENT SKILLS

People with schizophrenia can take an active role in managing their own illness. Once
they learn basic facts about schizophrenia and its treatment, they can make informed
decisions about their care. If they know how to watch for the early warning signs of
relapse and make a plan to respond, patients can learn to prevent relapses. Patients can
also use coping skills to deal with persistent symptoms.
REHABILITATION
Rehabilitation emphasizes social and vocational training to help people with
schizophrenia participate fully in their communities. Because schizophrenia usually
develops during the critical career-development years (ages 18 to 35), the career and
life trajectories for individuals with schizophrenia are usually interrupted and they
need to learn new skills to get their work life back on track. Rehabilitation programs
can include employment services, money management counseling, and skills training
to maintain positive relationships.
FAMILY EDUCATION AND SUPPORT

Family education and support teaches relatives or interested individuals about
schizophrenia and its treatment and strengthens their capacity to aid in their loved
one’s recovery.
COGNITIVE BEHAVIORAL THERAPY

Cognitive behavioral therapy (CBT) is a type of psychotherapy that focuses on
changing unhelpful patterns of thinking and behavior. The CBT therapist teaches
people with schizophrenia how to test the reality of their thoughts and perceptions,
how to “not listen” to their voices, and how to manage their symptoms overall. CBT
can help reduce the severity of symptoms and reduce the risk of relapse. CBT can be
delivered individually or in groups.
SELF-HELP GROUPS
In self-help groups for people with schizophrenia, group members support and
comfort each other and share information on helpful coping strategies and services.
Professional therapists usually are not involved. People in self-help groups know that
others are facing the same problems, which can help everyone feel less isolated and
more connected.
How can you help a person with schizophrenia?
Family and friends can help their loved one with schizophrenia by supporting their
engagement in treatment and pursuit of their recovery goals. Positive communication
approaches will be most helpful. It can be difficult to know how to respond to
someone with schizophrenia who makes strange or clearly false statements.
Remember that these beliefs or hallucinations seem very real to the person. It is not
helpful to say they are wrong or imaginary. But going along with the delusions is not
helpful, either. Instead, calmly say that you see things differently. Tell them that you
acknowledge that everyone has the right to see things his or her own way. In addition,
it is important to understand that schizophrenia is a biological illness. Being
respectful, supportive, and kind without tolerating dangerous or inappropriate
behavior is the best way to approach people with this disorder.
What is the outlook for the future?

The outlook for people with schizophrenia continues to improve. Treatments that
work well are available, and new ones are being developed. Many people with
schizophrenia experience recovery and lead independent, satisfying lives.
Continued research and understanding in genetics, neuroscience, and behavioral
science will help scientists and health professionals understand the causes of the
disorder and how it may be predicted and prevented. This work will help experts
develop better treatments to help people with schizophrenia achieve their full
potential. In 2009, NIMH launched the Recovery After an Initial Schizophrenia
Episode (RAISE) research project (http://www.nimh.nih.gov/raise). RAISE seeks to
fundamentally change the trajectory and prognosis of schizophrenia through
coordinated treatment in the earliest stages of the disorder. RAISE is designed to
reduce the likelihood of long-term disability that people with schizophrenia often
experience and help people with this disorder lead productive, independent lives.
REFERENCE :- NATIONAL INSTITUTE OF MENTAL HEALTH

SURGERY
APPENDICITIS
ABSTRACT
Acute appendicitis is still one of the most common abdominal emergencies necessitating
operative treatment. For the past century, the conventional management of appendicitis has
been open appendectomy. Since the introduction of laparoscopic appendectomy, it has been
performed with increased frequency. Clinical trials evaluating outcomes comparing open
appendectomy with laparoscopic appendectomy indicate that laparoscopic appendectomy is
associated with lower complication rate and lower mortality and is to be considered the
procedure of choice for patients with suspected acute appendicitis.
PATIENT’S HISTORY
Reliability: 95%
GENERAL DATA:
This is a case of Mj, a 27 year-old male, married, farmer , Filipino, Roman Catholic, born on
May 20, 1990 at Legazpi City, from Pinaric, Legazpi City, Albay, admitted for the second
time at Bicol Regional Training and Teaching Hospital on October 10, 2017.
CHIEF COMPLAINT: abdominal pain
Patient was apparently well until 8 hours prior to admission, he had pain at the right lower
quadrant of the abdomen, stabbing in character, non-radiating, 8/10, continuous. No
associated fever, vomiting, or dysuria. No medications taken.
Due to persistence of RLQ pain, he immediately consulted at BRTTH and was admitted.
Patient had hypertension 1 year ago detected during a consult at the local health office at
Legazpi City, with highest BP of 150/90. He took Losartan 50 mg tablet once a day for 2
months, then allegedly became normotensive, so he stopped the medication. No other known
medical conditions such as stroke, renal disease, PTB, asthma, DM, cardiac disease, GI
disease, thyroid disease, blood dyscrasia, or malignancies.
He was admitted at BRTTH on May 2016 for 7 days where he underwent cholecystectomy.
He was discharged as well, and was asymptomatic thereafter.
FAMILY HISTORY:
Paternal grandparents are deceased; age at and cause of death are unrecalled.
Father died at 67 years old due to stroke.
Mother is 71 years old and is hypertensive, on medications.
6 siblings are otherwise well.
No other heredofamilial disorders such as renal disease, gastrointestinal disease, asthma,
PTB, seizures, and malignancies noted among blood relatives.
Patient is a non-smoker, non-alcoholic and denies illicit drug use.

He is a high school graduate working as a tricycle driver. He is married for 23 years to a now
46 year-old housekeeper. They have 3 children 24, 22 and 19. The patient lives with his
family. The household is composed of 5 members, together in a house made of mixed
concrete and light materials with a water-sealed toilet and 2 bedrooms, which is 2 meters
away from the neighboring house. Garbage disposal is via the city waste collection system;
waste segregation is practiced.
He has a regular diet of rice, fish, meat, vegetables and fruits; prefers meat. Drinking water
source is from the local water system, unsterilized. He does not do exercise. He gets 7 hours
of sleep per day from 9 pm to 4 am, with no interruptions.
REVIEW OF SYSTEMS:
Constitutional: No fever, weight gain/loss, chills, fatigue.

HEENT: No headache, dizziness, lightheadedness, syncope, trauma, eye pain, redness,
double vision, blurred vision, hear loss, earache, ear discharge, mouth sores, bleeding gums,
sore throat, hoarseness, dysphagia. No neck or neck stiffness.
Cardiovascular: (+) history of hypertension. No chest pain, edema, orthopnea, palpitations,
cyanosis, paroxysmal nocturnal dyspnea, easy fatigability.
Gastrointestinal: No hematemesis, dysphagia, hematochezia, diarrhea, hemorrhoids,
constipation.
Renal: No polyuria, nocturia, gross hematuria, incontinence, urinary retention, urinary
urgency, hesitancy, dribbling.
Genitalia: No discharge, ulcers, or pain associated with coitus.
Peripheral Vascular: No leg cramps, varicose veins, pain, numbness.
Neurologic: No numbness, tremors, seizures, memory loss, insomnia, somnolence,
irritability.
Endocrine: No polydypsia, polyphagia, heat/ cold intolerance, excessive sweating.

Vital Signs: BP 130/90 mmHg, CR 88 bpm, RR 20/min, Temp 36.1°C
Skin: Dark complexion, no lesions.
HEENT: Anicteric sclerae, pink palpebral conjunctivae, pupils 2-3 mm, equally reactive and
responsive to light and accommodation. No ear discharge. No nasal discharge. Pinkish lips,
no mouth ulcers. No tonsillopharyngeal congestion. Supple neck, midline trachea, thyroid
lobes not felt, no cervical lymphadenopathy.
Chest: Flat, no scars, symmetrical chest expansion, no retractions. No palpable mass,

symmetric vocal and tactile fremitus. Resonant on percussion. Clear breath sounds on
bilateral lung fields; no wheeze, no crackles
Heart: Adynamic precordium; no heaves, no thrills, PMI at 5th L ICS MCL. Normal rate
beats, regular rhythm, no murmurs.
Abdomen: Flabby, (+) incision scar on RUQ, no visible veins. Normal active bowel sounds.
Soft, (+) tenderness at RLQ on direct palpation, no palpable mass. Liver span 4 cm in
midsternal line and 6 cm in right midclavicular line; spleen non-enlarged. (+) rebound
tenderness, negative Rovsing sign.
Extremities: No scars or pigmentations, equal length; no edema; no joint swelling; no
limitation of movement. Full and equal pulses. CRT <2s
Neurologic:
Motor: Good muscle tone and bulk
Cranial Nerves:
VIII - Able to hear

IMPRESSION: Acute Suppurative Appendicitis
· Upon admission
· secure consent for admission and management
o Diet : NPO
o IVF line : D5LR @ 30 gtt/min
o Labs : CBC,urinalysis
o Meds : paracetamol 600 mg iv q 8 hrs
o Omeprazol 40mg iv q 12 hr
o Taramadol HCL 50mg IVTT PRN for pain • Refer to OR
· Pre –operative
o Anesthesia notes
o NPO
o Secure consent for procedure
o Meds : omeprazole 40mg TIVt
o To OR on call
o Surgery started at 7 pm am procedure appendectomy
· Post –operative
o Limited movement related to pain as manifested by:
o Subjective:“Anay, hinay hinay la ke maol-ol tak samad” asverbalized by the
patient. Objective:
o V/S : B P ; 100/70, PR : 82 , RR ; 24
o positionfrom lying in bed, andknow the proper way inseating from a
supineposition. Refer to ward
· DAY 2
o Impaired skin integrity related to surgical incision
o SUBJECTIVE:“katapus ko la ka operahe”as verbalize by the patient
o OBJECTIVE:- open wound- visible surgical incision- post-operative patient
Temp - 36.6 c CPR - 80 bpm
o RR - 22 cpm
o BP - 110/70mmhg
o IVF : PNSS 1L @ 18 gtt/min
o Meds : metronidazole 500mg iv drip q 8 hrs Mefanemic acid 500mg/tab BID
o Erythromycin 500 mg/tab TID
o Paracetamol 500mg/tab TID
o After 12 hours of nursing interventions the patient’s wound appears to be dry
and freed from drainage or purulent substances there fore goal was met.
· Day 3 :
o Risk for infection related tosurgical incision at right lower quadrant of the
body. Objective
o incised skin @ rightlower quadrant
o RR – 20 cpm
o PR – 79 bpm
o Temp – 36.6 C
o B P – 110/70
o Incision pain
o Meds : start oral meds
o Metronidazole 500mg/tab BID
o Mefanemic acid 500mg/tab BID
o Dressing to wound mupirocin ointment
Discharge meds:-
o Metronidazole 500mg/tab BID
o Mefanemic acid 500mg/tab BID
o Dressing to wound mupirocin ointment
DIAGNOSTIC:-
CBC
Parameter
Wbc 18.3
Hct 46
Hbg 15
Segmenter 0.60
Lymphocyte 0.10
Platelet 445
URINALYSIS
DIFFERENTIAL DIAGNOSIS:-
Rule in Rule out

Cholecystitis Abdominal Pain Tenderness in RUQ
Nausea and vomiting No radiation to right
Loss of appeti shoulder
Fever
Acute mesenteric adenitis bdominal Pain Diffuse pain with
17 year old tenderness not localized
to the RLQ
Generalized
lymphadenopathy
Diverticulitis Abdominal Pain Tenderness in LLQ
17 year old Fever and chills
Nausea and vomiting Diarrhea or constipation
Loss of appetite Bloated feeling
FINAL DIAGNOSIS:- Acute Suppurative Appendicitis
DISCUSSION:-
APPENDICITIS
the most common cause of acute inflammation in the right lower quadrant of the
abdomen, is the most common reason for emergency abdominal surgery especially
when ruptured occurs. According to Brunner & Suddarth, “about 7% of the
population will have appendicitis at some time in their lives; males are affected more
than females and teenagers more than adults. Although it can occur at any age, it
occurs most frequently between the ages of 10 and 30 years old”. It is thought that
appendicitis begins when the opening from the appendix into the cecum becomes
blocked. The blockage may be due to a build-up of thick mucus within the appendix
orto stool that enters the appendix from the cecum. The mucus or stool hardens,
becomes rock-like, and blocks the opening Appendicitis usually happens after an
infection in the digestive tract, or when the tube connecting the large intestine and
appendix is blocked by trapped feces or food. Both situations cause inflammation,
which can lead to infection or rupture of the appendix. Untreated, mortality is high,
mainly because of the risk of rupture leading to peritonitis and shock .Also, if the
abdomen on palpation is also involuntary guarded (rigid) there should be a strong
suspicion of peritonitis.
Signs and Symptoms:

Pain starting around the navel, then moving down and to the right side of the
abdomen. The pain gets worse when moving, taking deep breaths, coughing
sneezing or being touched (Mc Burney’s point).
Loss of appetite
Nausea, and Vomiting
Change in bowel movements, including diarrhea or constipation or unable to pass gas.
Fever
Rovsing’s sign
: continuous deep palpation starting from the left iliac fossa upwards
(counterclockwise along the colon) may cause pain in the right iliac fossa, by pushing
bowel contents towards the ileocaecal valve and thus increasing pressure around the
appendix.
Psoas sign
: is the right lower-quadrant pain that is produced with either the passive extension of
the patients right hip (pt. lying on the left side, with knee in
flexion) or the patient’s active flexion of the right hip while supine. Straightening
out the legs causes pain because it stretches these muscles, while flexing the hip
activated the ilio psoas and therefore causes pain
Obturator sign:
if an inflamed appendix is in contact with the obturator internus, spasm of the muscle
can be demonstrated by flexing and internal rotation of the hip. This maneuver will
cause pain in the hypogastrium.
Dunphy’s sign:
increased pain in the right lower quadrant with coughing.
Kocher’s Sign:
the appearance of pain in the epigastric region or around the stomach at the beginning
of disease with a subsequent shift to the right iliac region.
Stikovskiy (resenstein’s) sign:
increased pain on palpation at the right iliac region as patient lies on his/her left side.
Blumberg sign:
also referred as rebound tenderness. Deep palpation of the viscera over the suspected
inflamed appendix followed by sudden release of the pessue causes the severe pain on
the site indicating positing Blumberg’s sign and peritonitis.
Risk Factors
Risk factors for Appendicitis are factors that do not seem to be a direct cause of the
disease, but seem to be associated in some way. Having a risk factor for Acute
Appendicitis makes the chances of getting the condition higher but does not always
lead to Acute Appendicitis.
Age:
Appendicitis can occur in all age groups but it is more common between the ages of
11 and 20.
Gender:
A male preponderance exists, with a male to female ratio (1.4: 1) and theoverall
lifetime risk is 8.6% for males and 6.7% for females. A male child suffering from
cysticfibrosis is at a higher risk for developing appendicitis.
Diet:
People whose diet is low in fiber and rich in refined carbohydrates have an increased
risk getting appendicitis.
Hereditary:
A particular position of the appendix which predisposes it to infection, runs in certain
families. Having a family history of appendicitis may increase a child's risk for the
illness.
Seasonal variation:
Most cases of appendicitis occur in the winter months - between the months of
October and May.
Infections:
Gastrointestinal infections such as Amebiasis, Bacterial Gastroenteritis, Mumps,
Coxsackie virus B and Adenovirus can predispose an individual to Appendicitis
Causes
On the basis of experimental evidence, acute appendicitis seems to be the end result
of a primary obstruction of the appendix lumen(the inside space of a tubular
structure). Once this obstruction occurs the appendix subsequently becomes filled
with mucus and swells, increasing pressures within the lumen and the walls of the
appendix, resulting in thrombosis and occlusion of the small vessels, and stasis of
lymphatic flow. Rarely, spontaneous recovery can occur at this point. As the former
progresses, the appendix becomes ischemic and then necrotic .As bacteria begin to
leak out through the dying walls, pus forms within and around the
appendix(suppuration). The end result of this cascade is appendiceal rupture (a 'burst
appendix') causing peritonitis, which may lead to septicemia and eventually death.
The causative agents include foreign bodies ,trauma, intestinal worms, lymphadenitis,
and most commonly calcified fecal deposits known as appendicoliths or fecalith. The
occurrence of an obstructing fecalith has attracted attention since their presence in
patients with appendicitisis significantly higher in developed than in developing
countries, and an appendiceal fecalith is commonly associated with complicated
appendicitis. Also, fecal stasis and arrest may play a role, as demonstrated by a
significantly lower number of bowel movements per week in patients with acute
appendicitis compared with healthy controls. The occurrence of a fecalith in the
appendix seems to be attributed to a right side fecal retention reservoir in the colon
and a prolonged transit time. From epidemiological data it has been stated that
diverticular disease and adenomatous
polyps were unknown and colon cancer exceedingly rare in communities exempt for
appendicitis. Also, acute appendicitis shown to occur antecedent to cancer in the
colon and rectum. Several studies offer evidence that a low fiber intake is involved in
the pathogenesis
of appendicitis. This is in accordance with the occurrence of a right sided fecal
reservoir and the fact that dietary fiber reduces transit time.
Complications of Appendicitis Rupture of the Appendix

The most frequent complication of appendicitis is perforation. Perforation of the
appendix can lead to a peri -appendiceal abscess (a collection of infected pus) or
diffuse peritonitis(infection of the entire lining of the abdomen and the pelvis). The
major reason for appendiceal perforation is delay in diagnosis and treatment. In
general, the longer the delay between diagnosis and surgery, the more likely is
perforation. The risk of perforation 36 hours after the onset of symptoms is at least
15%. Therefore, once appendicitis is diagnosed, surgery should be done without
unnecessary delay.
Peritonitis or Abscess
Peritonitis is a dangerous infection. This complication can occur when bacteria and
other contents of the torn appendix leak into the abdomen (stomach). A ruptured
appendix can lead to peritonitis and abscess. An abscess usually takes the form of a
swollen mass filled with fluid and bacteria.
Blockage or Obstruction of the intestine

A less common complication of appendicitis is blockage or obstruction of the
intestine. Blockage occurs when the inflammation surrounding the appendix causes
the intestinal muscle to stop working, and this prevents the intestinal contents from
passing. If the intestine above the blockage begins to fill with liquid and gas, the
abdomen distends and nausea and vomiting may occur. It then may be necessary to
drain the contents of the intestine through a tube passed through the nose and
esophagus and into the stomach and intestine.
Sepsis
A feared complication of appendicitis is sepsis ,a condition in which infecting bacteria
enter the blood and travel to other parts of the body. This is a very serious, even life-
threatening complication. Fortunately, it occurs infrequently.
Diagnosis
Diagnosis is based on patient history (symptoms) and physical examination backed by
an elevation of neutrophilic, white blood cells. Histories fall into two categories,
typical and atypical. Typical appendicitis usually includes abdominal pain beginning
in the region of the umbilicus for several hours, associated with anorexia, nausea or
vomiting. The pain then "settles" into the right lower quadrant, where tenderness
develops. Atypical histories lack this typical progression and may include pain in the
right lower quadrant as an initial symptom. Atypical histories often require imaging
with ultrasound and/or CT scanning.
A pregnancy test is vital in all women of child bearing age, as ectopic pregnancies nd
appendicitis present with similar symptoms. The consequences of missing an ectopic
pregnancy are serious, and potentially life threatening. Furthermore the general
principles of approaching abdominal pain in women (in so much that it is different
from the approach in men) should be appreciated.
Blood Test
Most patients suspected of having appendicitis would be asked to do a blood test.
50% of the time, the blood test may be normal, so it is not foolproof in diagnosing
appendicitis. Two forms of blood tests are commonly done: FBC (Full blood count) or
CBC (Complete blood count) is an inexpensive and commonly requested blood test. It
involves measuring the blood for its richness in red blood cells as well as the number
of the various white blood cell constituents in it. The number of white cells in the
blood is a usually less than 10,000 cells per cubic millimeter. An abnormal rise in the
number of white blood cells in the blood is a crude indicator of infection or
inflammation going on in the body. Such rise is not specific to appendicitis alone .If it
is abnormally elevated, with a good history and examination findings pointing
towards
appendicitis, the likelihood of having the disease is higher. In pregnancy, there may
be a normal elevation of white blood cells, without any infection present.
CRP
CRP is an acronym for C-reactive protein .It is an acute phase response protein
produced by the liver in response to any infection or inflammatory process in the
body. Again, like the FBC, it is not a specific test. It is another crude marker of
infection or inflammation .Inflammation at ANY site can lead to the CRP to rise. A
significant rise in CRP with corresponding signs and symptoms of appendicitis is a
useful indicator in the diagnosis of appendicitis. It is said that if CRP continues to be
normal after 72 hours of the onset of pain, it is likely that the appendicitis will resolve
on its own without intervention. A worsening CRP with good history is a sure signal
of impending perforation or ruptures and abscess formation.
Urine Test
Urine test in appendicitis is usually normal. It may however show blood if the
appendix is rubbing on the bladder, causing irritation a urine test or urinalysis is
compulsory in women, to rule out pregnancy in appendicitis, as well to help ensure
that the abdominal pain felt and thought to be acute appendicitis is not in fact, due to
ectopic pregnancy.
X– Ray
In 10% of patients with appendicitis, plain abdominal x-ray may demonstrate hard
formed feces in the lumen of the appendix (Fecolith). It is agreed that the finding of
Fecolith in the appendix on X-ray alone is a reason to operate to remove the appendix,
because of the potential to cause worsening symptoms. In this respect, a plain
abdominal X-ray may be useful in the diagnosis of appendicitis, though plain
abdominal x- ray is no longer requested routinely in suspected cases of appendicitis.
An abdominal X– ray may be done with a barium enema contrast to diagnose
appendicitis. Barium enema is whitish toothpaste like material that is passed up into
the rectum to act as a contrast. It will usually fill the whole of the large bowel. In
normal appendix, the lumen will be present and the barium fills it up and is seen when
the x-ray film is shot. In appendicitis, the lumen of the appendix will not be visible on
the barium film.
Ultrasound
Ultrasonography and Doppler sonography provide useful means to detect appendicitis
,especially in children and shows free fluid collection in right iliac fossa along with a
visible appendix without blood flow in color Doppler. In some cases (15%
approximately), however ,ultrasonography of the iliac fossa does not reveal any
abnormalities despite the presence
of appendicitis. This is especially true of early appendicitis before the appendix has
become significantly distended and in adults where larger amounts of fat and bowel
gas make actually seeing the appendix technically difficult. Despite these limitations,
in experienced hand sonographic imaging can often distinguish between appendicitis
and other diseases with very similar symptoms such as inflammation of lymph nodes
near the appendix or pain originating from other pelvic organs such as the ovaries or
fallopian tubes.
Computed tomography
A cat scans demonstrating acute appendicitis (note the appendix has a diameter of
17.1mm and there is surrounding fat stranding.) In places where it is readily available,
CT scan has become frequently used, especially in adults whose diagnosis is not
obvious on history and physical. Concerns about radiation, however, tend to limit use
of CT in pregnant women and children. A properly performed CT scan with modern
equipment has a detection rate (sensitivity)of over 95% and a similar specificity.
Signs of appendicitis on CT scan include lack of oral contrast (oral dye) in the
appendix, direct visualization of appendiceal enlargement (greater than6 mm in cross
sectional diameter), and appendiceal wall enhancement with IV contrast (IV dye).The
inflammation caused by appendicitis in the surrounding peritoneal fat (so called "fat
stranding") can also be observed on CT, providing a mechanism to detect early
appendicitis and a clue that appendicitis may be present even when the appendix is
not well seen. Thus, diagnosis of appendicitis by CT is made more difficult in very
thin patients and in children, both of whom tend to lack significant fat within the
abdomen.
Management
Before surgery
The treatment begins by keeping the patient from eating or drinking in preparation for
surgery. An intravenous drip is used to hydrate the patient. Antibiotics given
intravenously such as cefuroxime and metronidazole may be administered early to
help kill bacteria and thus reduce the spread of infection in the abdomen and
postoperative complications in the abdomen or wound. Equivocal cases may become
more difficult to assess with antibiotic treatment and benefit from serial examinations.
If the stomach is empty (no food in the past six hours) general anaesthesia is usually
used. Other wise, spinal anaesthesia may be used. Once the decision to perform an
appendectomy has been made, the preparation procedure takes more or less one to
two hours. Meanwhile, the surgeon will explain the surgery procedure and will
present the risks that must be considered when performing an appendectomy. With all
surgeries there are certain risks that must be evaluated before performing the
procedures .However, the risks are different depending on the state of the appendix. If
the appendix has not ruptured, the complication rate is only about 3% but if the
appendix has ruptured, the complication rate rises to almost 59%. The most usual
complications that can occur are pneumonia, hernia of the incision, thrombophlebitis,
bleeding or adhesions .Recent evidence indicates that a delay in obtaining surgery
after admission results in no measurable difference inpatient outcomes. The surgeon
will also explain how long the recovery process should take. Abdomen hair is usually
removed in order to avoid complications that may appear regarding the incision.
Inmost of the cases patients experience nausea or vomiting which requires specific
medication before surgery. Antibiotics along with pain medication may also be
administrated prior to appendectomies.
Pain management
Pain from appendicitis can be severe. Strong pain medications (i.e., narcotic pain
medications) are recommended for pain management prior to surgery. Morphine is
generally the standard of care in adults and children in the treatment of pain from
appendicitis prior to surgery .In the past (and in some medical textbooks that are still
published today), it was commonly accepted among the majority of academic sources
that pain medication not be given until the surgeon has the chance to evaluate the
patient, so as to not "corrupt" the findings of the physical examination. This line of
practice, combined with the fact that surgeons may sometimes take hours to come to
evaluate the patient, especially if he or she is in the middle of surgery or has to drive
in from home, often leads to a situation that is ethically questionable at best.
More recently, due to better understanding of the importance of pain control in
patients, it has been shown that the physical examination is actually not that
dramatically disturbed when pain medication is given prior to medical evaluation.
Individual hospitals and clinics have adapted to this new approach of pain
management of appendicitis by developing a compromise of allowing the surgeon a
maximum time to arrive for evaluation, such as 20 to 30 minutes, before active pain
management is initiated. Many surgeons also advocate this new approach of providing
pain management immediately rather than only after surgical evaluation.
Surgery
The surgical procedure for the removal of the appendix is called an
appendicectomy (also known as an appendectomy). Often now the operation can be
performed via ala paroscopic approach, or via three small incisions with a camera to
visualize the area of interest in the abdomen. If the findings reveal supportive
appendicitis with complications such as rupture, abscess, adhesions, etc., conversion
to open laparotomy may be necessary. An open laparotomy incision if required most
often centers on the area of maximum tenderness, Mc Burney's point ,in the right
lower quadrant. A transverse or a gridiron diagonal incision is used most
commonly .According to a meta-analysis from the Cochrane Collaboration comparing
laparoscopic and open procedures, laparoscopic procedures seem to have various
advantages over the open procedure. Wound infections were less likely after
laparoscopic appendicectomy than after open
Complications of Appendectomy
The most common complication of appendectomy is infection of the wound, that is,
of the surgical incision. Such infections vary in severity from mild, with only redness
and perhaps some tenderness over the incision, to moderate, requiring only
antibiotics, to severe, requiring antibiotics and surgical treatment. Occasionally, the
inflammation and infection of appendicitis are so severe that the surgeon will not
close the incision at the end of the surgery because
of concern that the wound is already infected. Instead, the surgical closing is
postponed for several days to allow the infection to subside with antibiotic therapy
and make it less likely for infection to occur within the incision. Another complication
of appendectomy is an abscess, a collection of pus in the area of the appendix.
Although abscesses can be drained of their pus surgically, there are also non-surgical
techniques.
Laparotomy
Laparotomy is the traditional type of surgery used for treating appendicitis. This
procedure consists in the removal of the infected appendix through a single larger
incision in the lower right area of the abdomen. The incision in a laparotomy is
usually 2-3 inches long. This type of surgery is used also for visualizing and
examining structures inside the abdominal cavity and it is called exploratory
laparotomy .During a traditional appendectomy procedure, the patient is placed under
general anesthesia in order to keep his/her muscles completely relaxed and to keep the
patient unconscious. The incision is two to three inches (76 mm) long and it is made
in the right lower abdomen, several inches above the hip bone .Once the incision
opens the abdomen cavity and the appendix is identified, the surgeon removes the
infected tissue and cuts the appendix from the surrounding tissue. After the surgeon
inspects carefully and closely the infected area and there are no signs that surrounding
tissues are damaged or infected, he will start closing the incision. This means sewing
the muscles and using surgical staples or stitches to close the skin up. In order to
prevent infections the incision is covered with a sterile bandage. The entire procedure
does not last longer than an hour if complications do not occur.
Laparoscopic surgery
The newer method to treat appendicitis is the laparoscopic surgery. This surgical
procedure consists of making three to four incisions in the abdomen, each 0.25 to 0.5
inch (6.3 to13 mm) long. This type of appendectomy is made by inserting a special
surgical tool called laparoscope into one of the incisions. The laparoscope is
connected to a monitor outside the patient's body and it is designed to help the
surgeon to inspect the infected area in the abdomen. The other two incisions are made
for the specific removal of the appendix by using surgical instruments .Laparoscopic
surgery also requires general anesthesia and it can last up to two hours. The latest
methods are NOTES appendectomy pioneered in Coimbatore, India where there is no
incision on the external skin and SILS (Single incision laparoscopic Surgery) where
as ingle 2.5 cm incision is made to perform the surgery.
After surgery
Hospital lengths of stay typically range from a few hours to a few days, but can be a
few weeks if complications occur. The recovery process may vary depending on the
severity of the condition, if the appendix had ruptured or not before surgery.
Appendix surgery recovery is generally a lot faster if the appendix did not rupture. It
is important that patients respect their doctor's advice and limit their physical activity
so the tissues can heal faster. Recovery after an appendectomy may not require diet
changes or a lifestyle change .After surgery occurs, the patient will be transferred to a
Post-anesthesia care unit so his or her vital signs can be closely monitored in order to
detect anesthesia and/or surgery related complications. Pain medication may also be
administrated if necessary. After patients are completely awake, they are moved into a
hospital room to recover. Most individuals will be offered clear liquids the day after
the surgery and then progress to a regular diet when the intestines start to function
properly. It is highly recommended that patients sit up on the edge of the bed and
walk short distances for several times a day. Moving is mandatory and pain
medication may be given if necessary. Full recovery from appendectomies takes about
4 to 6weeks but it can prolong to up to 8 weeks if the appendix had rupture
Conclusion
Most appendicitis patients recover easily with surgical treatment, but complications
can occur if treatment is delayed or if peritonitis occurs. Recovery time depends on
age, condition
,complications, and other circumstances, including the amount of alcohol
consumption, but usually is between 10 and 28 days. For young children (around 10
years old), the recovery takes three weeks. The real possibility of life-threatening
peritonitis is the reason why acute appendicitis warrants speedy evaluation and
treatment. The patient may have to undergo a medical evacuation .Appendectomies
have occasionally been performed in emergency conditions (i.e. ,out side of a proper
hospital), when a timely medical evaluation was impossible.
Prevention
Appendicitis is probably not preventable, although there is some indication that a diet
high in green vegetables and tomatoes may help prevent appendicitis.
Textbook References/Primary References :

Assessment: Lippincott; 2007 Edition.
Taber’s Cyclopedic Medical Dictionary: 18th edition
Fundamentals of General surgery: Kozier and Erb; 8th Edition. Medical-Surgical of
General surgery: Bunner and Suddarth; 12th Edition.
CHOLECYSTITIS
ABSTRACT
Background: The treatment of acute cholecystitis has been controversially
discussed in the literature as there are no high-evidence-level data yet for determining the
optimal point in time for surgical intervention. So far, the laparoscopic removal of the
gallbladder within 72 h has been the most preferred approach in acute cholecystitis. Methods:
We conducted a systematic review by including randomized trials of early laparoscopic
cholecystectomy for acute cholecystitis. Results: Based on a few prospective studies and two
meta-analyses, there was consent to prefer an early laparoscopic cholecystectomy for patients
suffering from acute calculous cholecystitis while the term ‘early' has not been consistently
defined yet. So far, there is new level 1b evidence brought forth by the so-called ‘ACDC'
study which has convincingly shown in a prospective randomized setting that immediate
laparoscopic cholecystectomy - within a time frame of 24 h after hospital admission - is the
smartest approach in ASA I-III patients suffering from acute calculous cholecystitis
compared to a more conservative approach with a delayed laparoscopic cholecystectomy
after an initial antibiotic treatment in terms of morbidity, length of hospital stay, and overall
treatment costs. Concerning critically ill patients suffering from acute calculous or acalculous
cholecystitis, there is no consensus in treatment due to missing data in the literature.
Conclusion: Laparoscopic cholecystectomy for acute cholecystitis within 24 h after hospital
admission is a safe procedure and should be the preferred treatment for ASA I-III patients. In
critically ill patients, the intervention should be determined by a narrow interdisciplinary
consent based on the patient's individual comorbidities.
PATIENT’S HISTORY

Reliability: 85%

GENERAL DATA:

This is a case of BJ, a 30 year-old male, widowed,carpenter, Filipino, Roman Catholic, born
on April 14 1988, from Purok 1 , Malilipot, Albay, admitted for the first time at Bicol
Regional Training and Teaching Hospital on October 15, 2017.



1 week prior to admission, patient experienced abdominal pain,right upper quadrant, non
radiating , pain scal was 5/10. No other symptoms was noted ,consultation was not done, no
medication was given.
1 day prior to admission, due to persistence of right upper quadrant pain and now it’s
associated with back pain , pain was radiating to the back side and pain scale was increase to
9/10. Hence consultation was done in private clinic and patient was referred to BMC hospital,
and upon arrival admission was done.

Patient had PTB on 2005, wherein he completed 6-month treatment with Isoniazid and
Rifampicin at the local health center in Malilipot, Albay. Follow-up consultation was done;
allegedly was cured. No other known medical conditions such as HTN, stroke, renal disease,
asthma, DM, cardiac disease, GI disease, thyroid disease, blood dyscrasia, or malignancies.

FAMILY HISTORY:

Paternal grandparents are deceased; age at and cause of death are unrecalled.
Father died at 75 years old due to an apparent Acute Myocardial Infarction. He also had
inguinal hernia.
Mother died at 80 years old. No known medical conditions; death was attributed to old
age.
No heredofamilial disorders such as HTN, stroke, renal disease, gastrointestinal disease,
asthma, PTB, seizures, and malignancies noted among blood relatives.


Patient is a non-smoker and occasional alcoholic beverage drinker for 22 years in moderate
amounts. He denies illicit drug use.
Patient is an elementary graduate and working as a carpenter He had been widowed for 2
years since his wife’s death in 2016 due to pneumonia. They have 5 children. The patient
lives with one of his daughters. The household is composed of 6 members, together in a
concrete house with a water-sealed toilet and 3 bedrooms, which is 15 meters away from the
neighboring house. Garbage disposal is via a compost pit; no waste segregation practiced.
He has a regular diet of rice, fish, meat, vegetables and fruits; prefers vegetables. Drinking
water source is from the local water system, unsterilized.

REVIEW OF SYSTEMS:

Constitutional: No fever, weight gain/loss, chills, fatigue.
HEENT: (+) headache, dizziness, lightheadedness, syncope, trauma, eye pain, redness,
double vision, blurred vision, hear loss, earache, ear discharge, mouth sores, bleeding gums,
sore throat, hoarseness, dysphagia, neck pain, neck stiffness.
Respiratory: (+) cough; no hemoptysis and dyspnea.
nocturnal dyspnea, easy fatigability, hypertension.
Gastrointestinal: No loss of appetite, nausea, vomiting, hematemesis, abdominal pain,
dysphagia, hematochezia, diarrhea, hemorrhoids, constipation.
Renal: No dysuria, polyuria, nocturia, gross hematuria, incontinence, urinary retention,
urinary urgency, hesitancy, dribbling.
Endocrine: No polydypsia, polyphagia, heat/ cold intolerance, excessive sweating.




Skin: Dark complexion, no lesions.

HEENT: Anicteric sclerae, pink palpebral conjunctivae, pupils 2-3 mm, equally reactive and
no mouth ulcers. No tonsillopharyngeal congestion. Supple neck, midline trachea, thyroid
lobes not felt, no cervical lymphadenopathy.

Chest: Flat, no scars, symmetrical chest expansion, no retractions. No palpable mass,
symmetric vocal and tactile fremitus. Resonant on percussion. Clear breath sounds on
bilateral lung fields; no wheeze, no crackles
Heart: Adynamic precordium; no heaves, PMI at 5th L ICS MCL. Cardiac dullness in

the 3rd to 5th left interspaces. Cardiac rate of 88 beats per minute, regular rhythm, no murmurs.

Abdomen: Flabby, no scars or visible veins. Normal active bowel sounds. Soft, non-tender,
no palpable mass. Liver and spleen non-enlarged.

Extremities: No scars or pigmentations, equal length; no edema; no joint swelling; no
limitation of movement. Full and equal pulses. CRT <2s
Neurologic:
Motor: Good muscle tone and bulk
Cranial Nerves:
VIII - Able to hear

R L
Biceps + +
2 2
Triceps + +
2 2
Brachioradial + +
is 2 2
Patellar + +
2 2
Achilles + +
2 2

IMPRESSION: cholecystitis
COURSE IN THE WARD
Secure consent to care and management

• Diet : low fat diet
• Monitor V/S q shift
• Labs : CBC w/pc , urinalysis , liver function test ALT/AST, ultrasound • IV
fluid : PNSS 1L @ 100cc/hr
• Meds : Demerol 50mg IVTT now then prn
• HNBB 20mg 1 amp IVTT now
• Moderate high back rest is to elevate the upper portion of the body to increase
lung
• expansion thus promoting gas exchange. This is also to prevent ascending
infection that
• could be caused by possible rupture of the gallbladder. • Refer accordingly.
Day 2
• c/o : sever abdominal and vomiting
• IVF TF: PNSS 1L @ KVO
• start cefoxitin 1 g IVTT q 8hrs ANST • inform OR
pre-operative
• NPO
• assess V/S prior to OR
• IVF : D5NSS 1L @ 120cc/hr
• Meds :diazepam 10mg/tab OD • Ranitidine 150mg/tab 1 tab OD • Vit k
Post –operative
• To PACU then to ward
• NPO for 4 hrs then may have SD
• Monitor V/S q 15min untill stable then 30 min then q 2 • Meds : Etoricoxib
120mg/tab PO
• Tramadol 100mg/tab OD or prn
• Demerol 50mg IVTT
• Sultamicillin 375mg po TID
• O2 inhalation 2 ml until fully awake
Day 3
• May have DAT • Continue meds • Wound care
• MGH
Discharge meds
• Etoricoxib 90mg PO BID
• Tramadol 100mg 1⁄2 tab PO BID
• Sultamicillin 375 mg PO BID
• Advise pt to follow up after 1 month.
DIAGNOSTIC
CBC
Parameter
Wbc 14.1
HCT 42
HBG 13
Segment 0.70
Lymphocytes 0.21
Platelet 278
Blood chemistry
Parameter
Total bilirubin 8.3
Direct bilirubin 0.9
Indirect bilirubin 7.4
SGPT 60.2
SGOT 55.1
Alkaline phosphate 191
URINALYSIS
· Biliary Colic
· Acute Gastritis
· Acute Pancreatitis
FINAL DIAGNOSIS :- cholecystitis
DISCUSSION
Cholecystitis
Acute calculus cholecystitis is a very common disease with several area of uncertainty. The
World Society of Emergency Surgery developed extensive guidelines in order to cover grey
areas. The diagnostic criteria, the antimicrobial therapy, the evaluation of associated common
bile duct stones, the identification of “high risk” patients, the surgical timing, the type of
surgery, and the alternatives to surgery are discussed. Moreover the algorithm is proposed: as
soon as diagnosis is made and after the evaluation of choledocholithiasis risk, laparoscopic
cholecystectomy should be offered to all patients exception of those with high risk of
morbidity or mortality. These Guidelines must be considered as an adjunctive tool for
decision but they are not substitute of the clinical judgement for the individual patient.
Calculous cholecystitis is the most common, and usually less serious, type of acute
cholecystitis. It accounts for around 95% of all cases. Calculous cholecystitis develops when
the main opening to the gallbladder, called the cystic duct, gets blocked by a gallstone or by a
substance known as biliary sludge. Biliary sludge is a mixture of bile (a liquid produced by
the liver that helps digest fats) and small crystals of cholesterol and salt.
The blockage in the cystic duct results in a build-up of bile in the gallbladder, increasing the
pressure inside it and causing it to become inflamed. In around 1 in every 5 cases, the
inflamed gallbladder also becomes infected by bacteria.
Symptoms
• pain
• abdominal tenderness • nausea
• vomiting
• fever
• chills
• sweating
Pain is one of the most distinctive features of acute cholecystitis. You will usually feel it in
the upper right area of your abdomen. Pain may also occur between your shoulder blades or
radiate from the abdominal area to your right shoulder. The onset of the pain is often sudden
and may be very intense. More often than not, it is a constant pain lasting for a few minutes
or hours. It may become worse after you eat a meal.
Causes :- In about 90 percent of cases, acute cholecystitis is caused by gallstones blocking

your cystic duct. In other cases, it may be caused by tumors or other problems with your bile
duct, such as inflammation, strictures, cysts, trauma, surgery, parasites, or infection. In most
cases, however, the infection is a result of cholecystitis, not the cause.
Risk factors
• gallstones
• high-fat diet
• high-cholesterol diet
• low-fiber diet
• old age
• being female
• obesity
• rapid weight loss
• certain drugs
• pregnancy
• certain ethnicities (e.g., Native American, Mexican-American)
• diabetes
Diagnosis
The following tests may be helpful in diagnosing acute cholecystitis:
Blood Tests
Blood tests will provide your doctor with a complete blood count (CBC) and liver
enzymes levels help them assess your liver function. The results can help them learn
if your bile flow is blocked.
Ultrasonography
This test is usually the first step to reaching an acute cholecystitis diagnosis. It
employs sound waves to create an image of your gallbladder and bile ducts.
X-Ray
X-rays are often performed to rule out other conditions.
Oral Cholecystogram (OCG)

In this test, you will be asked to swallow pills containing a dye before you are X-
rayed. The dye will help your doctor detect any problems with your gallbladder,
including gallstones.
Hepatobiliary Iminodiacetic Acid (HIDA) Scan
This scan can help your doctor track and identify an obstruction in your bile flow.
They will inject a solution into your body and use a special camera to view it.
Computed Tomography (CT)

CT scans can be used to create cross-sectional images of your abdomen. These images
allow your doctor to detect gallstones.
Magnetic Resonance Imaging (MRI)
MRI scans use a magnetic field and radio waves to create an image of your abdomen.
Treatment
The first step of treatment is to control inflammation. Your doctor may prescribe:
• antibiotics to prevent or treat infection
• medications to temporarily control your pain • fasting to relieve the gallbladder from
stress
After your condition has been stabilized, your doctor may recommend surgery to
remove your gallbladder. This is the only guaranteed way to prevent cholecystitis
from happening again. This procedure is known as a cholecystectomy. A
cholecystectomy may be performed laparoscopically or through open surgery.
Laparoscopic surgery is performed by making small incisions in your abdomen. A
small camera and some surgical instruments are then inserted through the incision.
The camera displays theall incisions. The small incision results in faster recovery
times. Patients prefer it as well because it doesn’t leave an unpleasant scar.
Prevention
The majority of cholecystitis cases are caused by gallstones. You may reduce your
chances of developing gallstones by:
• losing weight slowly if you are overweight or obese
• maintaining a healthy diet that is rich in fiber and low in fat • eating more fruits and
vegetables
Conclusion
Although calculous cholecystitis often occurs in the context of the intensive care unit
in patients with major underlying illnesses, it should be recognized that a significant
proportion of patients with this condition present as outpatients with no underlying
risk factors. The incidence of this form of AAC in South Africa has not been
established. Prompt recognition of this condition and
surgical management is necessary to minimise the associated morbidity and mortality.
Reference
1. Parithivel VS, Gerst PH, Banerjee S, Parikh V, Albu E. Acute acalculous
cholecystitis in young patients without predisposing factors. Am Surg 2010.
2. Kalliafas S, Ziegler DW, Flancbaum L, Choban PS. Acute acalculous cholecystitis:
incidence, risk factors, diagnosis, and outcome. Am Surg 2014.
3. Yusuf TE, Baron TH. AIDS cholangiopathy. Curr Treat Options Gastroenterol
2009
4. Ryu JK, Ryu KH, Kim KH. Clinical features of acute acalculous cholecystitis. J
Clin Gastroenterol 2013.
BURN
Abstract
Electrical burns are the third most common cause of burn injuries, after scald and flame
burns. In spite of decreasing mortality rates as advancements are made in treatment
modalities and medical equipment, significant complications and socioeconomic
consequences still accompany electrical burns. Analyzed in the present study were data from
patients hospitalized for electrical burns between 2008 and 2012 in the Samsun Training and
Research Hospital, the only burn care center in the Black Sea region of Turkey. Methods:
Data from 94 patients (84 males, 10 females) hospitalized for electrical burns between 2008
and 2012 were retrospectively evaluated. Patient age, gender, occupation, presence of
coexisting trauma, burn degree, burned percentage of total body surface area (TBSA), voltage
of the electric current (low or high), medical cost (per day and total), and infection rates were
analyzed. Results: Mean patient age was 26.4±13.2 years. Ten patients were female (10.6%)
and 84 were male (89.4%). High-voltage burns were sustained by 47 patients (50%) and low-
voltage burns by 42 (44.7%); the remaining 5 were flash burns. Mean burned TBSA was
21.8±19.8% in high-voltage injuries and 11.9±6.9% in low-voltage injuries. Seven patients
had accompanying soft tissue lacerations, major bone fractures, or epidural hematomas.
Findings of infection were encountered in 31 patients (32.9%), and appropriate treatments
were initiated according to culture results. Mean duration of hospitalization was 21.3±19.8
days in patients with high-voltage burns and 8.6±6.2 days in patients with low-voltage burns.
Mean hospital stay was 2.5-fold longer, and total medical costs were 4-fold higher in patients
with high-voltage burns. Conclusion: Young adult males who were injured in industrial
accidents constituted the majority of high-voltage burn patients. Incidence of these injuries
may be reduced by improvements in training regarding the safe use of electrical devices, and
correct installation and safe maintenance of power grids, as well as by a review of
occupational safety regulations.
GENERAL DATA
THIS IS A CASE OF J.Y 21 YEAR OLD MALE BORN ON 09-26-1998, SINGLE
/FILIPINO, ROMAN CATHOLIC LIVES IN ZONE 2, LERMA NAGA, CAMARINES
SUR.
INFORMANT
Patient
RELAIBILITY
95%
DATE OF ADMISSION
12 February 2020
CHEIF COMPLAINT
ELECTRICAL BURN
HISTORY OF PRESENT ILLNESS

PATIENT SUFFERED FROM ELECTRICAL BURN (220 VOLTS) AT 11 A.M ON DEC
-15- 2019 IN IROSIN, SORSOGON ON A POLE AND FELL FROM ABOUT 40 FTS ON
THE FLOOR WHICH WAS COVERED BY BANANA PEELS AND WAS TAKEN TO
HOSPITAL IN SORSOGON PRIOR TO TRANSFERRING TO OUR INSTITUTION.
PAST MEDICAL HISTORY

PATIENT IS KNOW ALERGIC TO FISH PRODUCTS WHICH CONTAINS SARDINE.
FAMILY HISTORY
PATIENT HAS KNOWN CASE OF CANCER ON METARNAL SIDE.
PERSONAL HISTORY
PATIENT IS AN UNDERGRADUATE, WORKING AS AN LINEMAN. PATIENT
CURRENTLY IS IN RELATIONSHIP AND LIVES WITH HER PARTNER. PATIENT IS
A SMOKER 9 PACKS A YEAR WITH OCCASIONAL ALCOHOL CONSUMPTION.
PHYSICAL EXAMINATION
• GE
NERAL SURVEY : Awake,responsive and not in cardiorespiratory distress.
• VI
TAL SIGNS : BP: 140/90 CR: 81 RR: 26 TEMP: 36.2 02 SAT: 99.
• HE
ENT : (+) bilateral burn on posterior side of ears (+) posterior head neck half of the part of
trapezius, no cervical lymphadenopathy
•
• CH
EST/LUNGS : (+) Superficial burn on chest and back ,symmetric chest expansion, clear
breathsounds, (-) retractions.
• CV
S : adynamic precordium, Tachycardic (-) murmurs
• AB
DOMEN : (+) Superficial burn on left flank , Flat,soft, non tender, normoactive bowel
sounds.
• EX
TREMITIES : (+) left leg avulsed wound exposed to anteriorly tibia and fibula for about
23 cm burn , (+) Avulsed wound on the Right foot, Superficial burn on Left arm, (+)
limited range of motion in left extremities
• NE
UROLOGIC : GCS 15
• Cra
nial Nerves:
I – unable to asses
VIII - Able to hear
REVIEW OF SYSTEM
• SK
IN: (-) rashes (-) itching (+) burn
• HE
AD: (-) headache (-) dizziness
• EY
ES: (-) pain (-) redness (-) excessive tearing
• EA
RS: (-) tinnitus (-) vertigo (-) discharge
• NO
SE AND SINUSES: (-) discharge (-) nosebleed
• M
OUTH: (-) hoarseness (-)dry mouth
• NE
CK: (-) stiffness in the neck
• RESPIRATORY: (-) hemoptysis (-) pleuritic chest pain
• CARDIOVASCULAR: (-) chest pain or discomfort (-) palpitations
• GASTROINTESTINAL: (-) black and tarry stool (+)loss of appetite
• URINARY: (-)dysuria (-) hematuria (-) flank pain
• GENITAL (-) hernias (-) vaginal (-) vulvar
• MUSCOLOSKELETAL: (-) muscle pain (-) chills
• PSYCHIATRIC: (-) nervousness (-) depression
• NEUROLOGIC: (-) changes in mood (-) decrease sensorium
DIAGNOSIS
ELECTRICAL BURN; PARTIAL THICKNESS BURN 28% TOTAL BODY SURFACE
AREA
DISCUSSION
INITIAL EVALUATION
Initial evaluation of the burned patient involves four crucial assessments: airway
management, evaluation of other injuries, estimation of burn size, and diagnosis of CO and
cyanide poisoning. With direct thermal injury to the upper airway or smoke inhalation, rapid
and severe airway edema is a potentially lethal threat. Anticipating the need for intubation
and establishing an early airway are critical. Perioral burns and singed nasal hairs are signs
that the oral cavity and pharynx should be further evaluated for mucosal injury, but these
physical findings alone do not indicate an upper airway injury. Signs of impending respira-
tory compromise may include a hoarse voice, wheezing, or stri- dor; subjective dyspnea is a
particularly concerning symptom and should trigger prompt elective endotracheal intubation.
In patients with combined multiple trauma, especially oral trauma, nasotracheal intubation
may be useful but should be avoided if oral intubation is safe and easy.
Patients with acute burn injuries should never receive prophylactic antibiotics. This
intervention has been clearly demonstrated to promote development of fungal infections and
resistant organism and was abandoned in the mid-1980s. A tetanus booster should be
administered in the emergency room. The importance of pain management for these patients
has been widely recognized over the past 25 years. However, we must also consider treatment
of long-term anxiety. Therefore, it is important to administer an anxiolytic such as a
benzodiaz- epine with the initial narcotics.
An important contributor to early mortality in burn patients is carbon monoxide (CO)

poisoning resulting from smoke inhalation. The affinity of CO for hemoglobin is
approximately 200 to 250 times more than that of oxygen, which decreases the levels of
normal oxygenated hemoglobin and can quickly lead to anoxia and death. Unexpected
neurologic symptoms should raise the level of suspicion, and an arterial carboxyhemoglobin
level must be obtained because pulse oximetry can be falsely elevated. Administration of
100% oxygen is the gold standard for treatment of CO poisoning and reduces the half-life of
CO from 250 minutes in room air to 40 to 60 minutes on 100% oxygen. Some authors have
proposed hyperbaric oxygen as an adjunctive therapy for CO poisoning. However, the data
are mixed regarding the success of hyperbaric oxygen, and its associated logistical
difficulties and complications have limited its usefulness for patients with moderate or large
burns.Patients who sustain a cardiac arrest as a result of their CO poisoning have an
extremely poor prognosis regardless of the success of initial resuscitation attempts.Hydrogen
cyanide toxicity may also be a component of smoke inhalation injury. Afflicted patients may
have a persistent lactic acidosis or ST elevation on electrocardiogram (ECG). Cyanide
inhibits cytochrome oxidase, which is required for oxidative phosphorylation.Treatment
consists of sodium thiosulfate, hydroxocobalamin, and 100% oxygen. Sodium thiosulfate
works by transforming cyanide into a nontoxic thiocyanate derivative, but it works slowly
and is not effective for acute therapy. Hydroxocobalamin quickly complexes with cyanide, is
excreted by the kidney, and is recommended for immediate therapy.In the majority of
patients, the lactic acidosis will resolve with ventilation, and sodium thiosulfate treatment
becomes unnecessary.
CLASSIFICATION OF BURNS
Burns are commonly classified as thermal, electrical, or chemical burns, with thermal burns
consisting of flame, contact, or scald burns. Flame burns are not only the most common cause
for hospital admission of burns, but also have the highest mortality. This is primarily related
to their association with structural fires and the accompanying inhalation injury and/or CO
poisoning.
Electrical burns make up only 4% of U.S. hospital admissions but have special concerns
including the potential for cardiac arrhythmias and compartment syndromes with concurrent
rhabdomyolysis. A baseline ECG is recommended in all patients
with an electrical injury, and a normal ECG in a low-voltage injury may preclude hospital
admission. Because compartment syndrome and rhabdomyolysis are common in high-voltage
electrical injuries, vigilance must be maintained for neurologic or vascular compromise, and
fasciotomies should be performed even in cases of moderate clinical suspicion. Long-term
neurologic and visual symptoms are not uncommon with high-voltage electrical injuries,
and ophthalmologic and neurologic consultation should be obtained to better define a
patient’s baseline function.
COMPLICATIONS IN BURN CARE
There are several complications commonly associated with treatment of burn patients.
Though not always avoidable, maintaining vigilance for typical complications and using
appropriate techniques for prevention may limit the frequency and severity of complications.
Ventilator-associated pneumonia, as in all critically ill patients, is a significant problem in
burned patients. However, it is so common in patients with inhalation injury that a better
nomenclature may be post-injury pneumonia. Unfortunately, commonly used scores in
critical illness such as the Clinical Pulmonary Infection Score (CPIS) have not been shown to
be reliable in burn patients
Massive resuscitation of burned patients may lead to an abdominal compartment syndrome

characterized by increased airway pressures with hypoventilation, and decreased urine output
and hemodynamic compromise. Decompressive laparotomy is the standard of care for
refractory abdominal compartment syndrome but carries an especially poor prognosis in burn
patients.
Deep vein thrombosis (DVT) has been commonly believed to be a rare phenomenon in
burned patients, and there is a paucity of controlled studies regarding heparin prophylaxis in
this population. However, recent data show that up to 25% of burn patients develop DVT,
and fatal pulmonary emboli have been reported in burn patients.
Burn patients often require central venous access for fluid resuscitation and hemodynamic
monitoring. Because of the anatomic relation of their burns to commonly used access sites,
burn patients may be at higher risk for catheter-related bloodstream infections.
TREATMENT
Multitudes of topical therapies exist for the treatment of burn wounds. Silver sulfadiazine is
one of the most widely used in clinical practice. Silver sulfadiazine has a wide range of
antimicrobial activity, primarily as prophylaxis against burn wound infections rather than
treatment of existing infections. It has the added benefits of being inexpensive and easily
applied and has soothing qualities. It is not significantly absorbed systemically and thus has
minimal metabolic derangements. Silver sulfadiazine has a reputation for causing
neutropenia, but this association is more likely due to neutrophil margination from the
inflammatory response. True allergic reactions to the sulfa component of silver sulfadiazine
are rare, and at-risk patients can have a small test patch applied to identify a burning
sensation or rash. Silver sulfadiazine destroys skin grafts and is contraindicated on burns or
donor sites in proximity to newly grafted areas. Also, silver sulfadiazine may retard epithelial
migration in healing partial-thickness wounds.
Mafenide acetate, either in cream or solution form, is an effective topical antimicrobial. It is
effective even in the presence of eschar and can be used in both treating and preventing
wound infections; the solution formulation is an excellent anti-microbial for fresh skin grafts.
Use of mafenide acetate may be limited by pain with application to partial-thickness burns.
Mafenide is absorbed systemically, and a major side effect is metabolic acidosis resulting
from carbonic anhydrase inhibition.
Silver nitrate has broad-spectrum antimicrobial activity as a topical solution. The solution
used must be dilute (0.5%), and prolonged topical application leads to electrolyte
extravasation with resulting hyponatremia. A rare complication is methemoglobinemia.
Although inexpensive, silver nitrate solution causes black stains, and laundry costs may offset
any fiscal benefit to the hospital. Increasingly, Dakin’s solution (0.5% sodium hypochlorite
solution) is being used as an inexpensive topical antimicrobial.
For smaller burns or larger burns that are nearly healed, topical ointments such as bacitracin,
neomycin, and polymyxin B can be used. These are also useful for superficial partial-
thickness facial burns as they can be applied and left open to air without dressing coverage.
Meshed skin grafts in which the interstices are nearly closed are another indication for use of
these agents, preferably with greasy gauze to help retain the ointment in the affected area. All
three have been reported to cause nephrotoxicity and should be used sparingly in large burns.
The recent media fascination with methicillin-resistant Staphylococcus aureus (MRSA) has
led to widespread use by community practitioners of mupirocin for new burns. Unless the
patient has known risk factors for MRSA, mupirocin should only be used in culture-positive
burn wound infections to prevent emergence of further resistance.
Silver-impregnated dressings such as Acticoat (Smith & Nephew, London, United Kingdom),
Aquacel Ag (Convatec, Princeton, NJ), and Mepilex Ag (Mölnlycke Health Care US, LLC,
Norcross, GA) are increasingly being used for donor sites, skin grafts, and partial-thickness
burns. These may be more comfortable for the patient, reduce the number of dressing
changes, and shorten hospital length of stay, but they do limit serial wound examinations.
Biologic membranes such as Biobrane (Dow- Hickham, Sugarland, TX) provide a prolonged
barrier under which wounds may heal. Because of the occlusive nature of these dressings,
these are typically used only on fresh superficial partial-thickness burns that are clearly not
contaminated.
OBSTETRICS -GYNAECOLOGY DEPARTMENTAL
OVARIAN DERMATOID CYST
ABSTRACT
The term dermoid cyst does not appear to be restricted to a single kind of lesion nor
is it used in only a single medical discipline. The term dermoid cyst can be found in
the vocabulary of dermatologists, dermatopathologists, general pathologists,
gynecologists, neurosurgeons, or pediatricians. If asked, all of these clinicians would
most probably define and describe dermoid cysts differently. For example,
gynecologists and general pathologists might say that a dermoid cyst is a cystic
tumor of the ovary. In contrast, neurosurgeons tend to view a dermoid cyst is
associated with a congenital cyst of the spine or an intracranial congenital cyst. For
pediatricians and dermatologists, dermoid cyst means subcutaneous cysts, which
are usually congenital.
In all disciplines, however, the common factor is the presence of a solitary, or
occasionally multiple, hamartomatous tumor. The tumor is covered by a thick
dermislike wall that contains multiple sebaceous glands and almost all skin adnexa.
Hairs and large amounts of fatty masses cover poorly to fully differentiated structures
derived from the ectoderm.
Depending on the location of the lesion, dermoid cysts may contain substances such
as nails and dental, cartilagelike, and bonelike structures. If limited to the skin or
subcutaneous tissue, dermoid cysts are thin-walled tumors that contain different
amounts of fatty masses; occasionally, they contain horny masses and hairs.
PATIENT HISTORY
Reliability: 90%
GENERAL DATA:
This is a case of GL, a 28 year-old female, married, Filipino, born on January 12,
1991, Roman Catholic, housekeeper, high school graduate, from Ipil, San Fernando,
Masbate, admitted for the first time at Bicol Regional Training and Teaching Hospital
on August 25, 2017.
1 year PTA , patient noticed a palpable lump in her abdomen, she can not
determine the size but it was most marked on the right side below the level of the
navel and is movable. It is gradually increasing but she never felt any abdominal
pain. Patient start to consult a private physican when she noticed an unusual
discharge, as she described, a tapioca like material during her menstrual period with
associated foul smelly odor. No other associated symptoms were noted like
abdominal pain, fever, vaginal itchiness, achange in bowel habits, dysuria and
frequency. She was advised to have an abdominal U/S which revealed mass
measuring 10 cm in the right hypogastric area. Surgical intervention was suggested
but instead patient is lost to follow up.
2 month PTA, patient got pregnant with her first baby and due to her existing
condition she was advised again for an U/S . so U/S trasvaginal done which revealed
a single live fetus in a transverse lie position and a thin walled cystic mass. A right
adnexal mass measuring about 16.2 cm /14cm/11.6cm and left adnexial mass
measuring about 4.5cm/4.2cm/3.9cm. an impression of probable bilateral teratoma
was seen . she was advised again for surgical intervention due to the risk that it
might affect her baby but still patient is lost to follow up.Patient came because of
abdominal pain hence admission was done.
No other known medical conditions such as HTN, stroke, renal disease, asthma,
PTB, cardiac disease, GI disease, thyroid disease, blood dyscrasia, or malignancies.
No previous accident.
FAMILY HISTORY:
Paternal grandparents are deceased;

Maternal grandfather’s age at and cause of death are unrecalled. Maternal
grandmother died to 86 years old due to Pneumonia.
78 year-old father had stroke in 2011 and has hypertension.
77 year-old mother is also hypertensive, 4 Siblings are otherwise well.
No heredofamilial disorders such as malignancies, cardiac disease, asthma, PTB,
seizures, renal disease and gastrointestinal disease noted among blood relatives.
Patient used to be a smoker at 19 pack-years. Since 30 years old, she used to take
alcoholic beverages once a month, then quitting at age 40. She is a high school
graduate and housekeeper. She is married for 30 years since age 16. She is living
with her 50 year-old husband and the family of her son. The household is composed
of 6 members, together in an owned house made of mixed concrete and light
materials with a water-sealed toilet and 2 bedrooms, which is 10 meters away from
the neighboring house. Garbage disposal is via a compost pit; waste segregation is
practiced.
She has a regular diet of rice, fish, meat, vegetables and fruits; prefers vegetables.
OBSTETRIC HISTORY:
Patient is currently pregnant on her first baby at 12 weeks. Her OB score was G1P0.
GYNECOLOGIC HISTORY:
Patient had her menarche at 14 years old that lasted for 7 day, consuming 4
pads/day,moderately soaked and associated with dysmenorrheal. Subsequently
menses were regular with an interval of 27-32 days, lasting for 3-5 days, consuming
3-4 pads/day, moderately to fully soaked associated with dysmenorrheal.
REVIEW OF SYSTEMS:
Constitutional: No weight loss/gain, fatigue, fever.

HEENT: No headache, dizziness, lightheadedness, syncope, trauma, eye pain,
redness, double vision, blurred vision, hear loss, earache, ear discharge, mouth
sores, bleeding gums, sore throat, hoarseness, dysphagia, neck pain, neck stiffness.
Cardiovascular: No chest pain, edema, orthopnea, palpitations, cyanosis,
paroxysmal nocturnal dyspnea, easy fatigability.
Gastrointestinal: No nausea, vomiting, hematemesis, abdominal pain, dysphagia,
hematochezia, diarrhea, hemorrhoids, constipation.
Hematologic: No easy bruising.
Endocrine: No polyuria, heat/ cold intolerance, excessive sweating.
General Survey: Ambulatory, conscious, coherent, not in cardiorespiratory distress,

afebrile.
Skin: Fair complexion, no pigmentation, no rashes. Good turgor, warm.
HEENT: Anicteric sclerae, pink palpebral conjunctivae, pupils 2-3 mm equally

reactive and responsive to light and accommodation. No ear discharge. No nasal
discharge. Pinkish lips, no mouth ulcers. No tonsillopharyngeal congestion. Supple
neck, midline trachea, thyroid lobes not felt, no cervical lymphadenopathy.
Chest: No scars, symmetrical chest expansion, no retractions. No palpable mass,

symmetric vocal and tactile fremitus. Resonant lungs. Clear breath sounds on
bilateral lung fields; no wheeze, no crackles.
Breast: Pendulous, symmetric, nipples without discharge; no mass.
Heart: Adynamic precordium; no heaves, no thrills, PMI at 5th L ICS MCL. Normal
rate, regular rhythm, no murmurs.
Abdomen: Globular,no visible veins. Normal active bowel sounds. Soft, non-tender,
(+) tenderness on hypo gastric area. Liver and spleen non-enlarged.
Extremities: Equal length, no edema, no cyanosis, no limitation of movement, no

joint swelling; full and equal pulses, CRT <2s.
Neurologic:
Motor: Good muscle tone and bulkSensory: no sensory deficits
Cranial Nerves:
I - Not tested
VIII - Able to hear
IMPRESSION: PU 14 weeks AOG,NIL,G1P0, dermoid cyst right.
COURS IN THE WARD:-
Secure consent for admission and management

▪ Diet as tolerated
▪ IVF : D5LR 1L at 15-20 uggt/min replace to maintenance fluid D5W 500cc+4
amp(duvadilan) or isoxsuprine HCL at 30 gtt/min.
▪ Labs : CBC w/pc, Bloodtyping, urinalysis, HBsAg, RPR ▪ Meds :
paracetamol 600mg iv every 6 hrs
Omeprazole 40mg vial iv
DAY 2 ( pre operative ):
▪ Anesthesia notes
▪ NPO
▪ Secure consent for procedure
▪ Meds : omeprazole 40mg TIV 2 6 am
▪ To OR on call
▪ Surgery started at 10 am procedure S/P pelvic lap, unilateral oophorectomy
right done.
(post –op) :
▪ Transfer patient to PACU. For monitor
S q 15 mins till stable
▪ Oxygen inhalation at 2ml
▪ NPO
▪ IVF : D5LRS 1L 25 gtt/min
▪ TF : D5LRS 1L and D5W 1L * 20-25 gtt/min
▪ Meds : dynastat 40mg TIV (-) ANST q 12 hrs * doses
Ketorolac 30 mg TIV q 6 hrs *4 doses Paracetamol 600mg TIV q 6hrs
Omeprazole 40mg TIV
Cefixime 750mg TIV q 12 hrs Continue duvadilan drip Monitor I&O every shift
Watch out for bleeding
Day 3
Patient has flatus and may have clear liquids, gelatin,soft boiled eggs and
cracker at sitting postion. Indwelling catheter was ordered to be removed at
1;30 pm and insertion of 2 dulcolax suppository per anus. Duvadilan was
ordered to be discontinued and to continue IV pain medications for another 24
hrs. repeat CBC was ordered continue IVF.
In the afternoon, patients med was shift to oral meds : ▪ Cefuroxime
500mg/tab BID
▪ Paracetamol 500mg/tab as prn
▪ Folic acid 5 mg OD
▪ Isoxsuprine HCL 10mg/tab TID
Discharged plan :
Diet plan : high fiber , more iron contain and low salt deit.
Exercise: encourage to patient to do some stretching exercises so flow of
extrimities is good and no vein thrombosis
Meds : cefuroxime 500mg/tab BID for 5 days, mefenamic acid 500mg/tab BID
for 2 days, folic acid 5 mg OD for 1 month, and vit B complex 500 mg/tab for
10 days.
DIAGNOSTIC:-
CBC
Parameter
Wbc 7.9
Hct 41
Hbg 14
Segmenter 0.68
Lymphocyte 0.34
Platelet 348
URINALYSIS
Blood typing : ‘’O’’ +ve Miscellaneous result
RPR/VDRL : non-reactive
HBsAg Screening ; non-reactive
Hepatitis B (HVB) : negative
Ultrasound report :
Presentation - cephalic , single live fetus, with amniotic fluid : AFI 11.1cm , placental
location : posterior , with grade 2, AOG : 12wk, EDD: 07-30-2017, FHR: 134bpm ,
estimate fetal weight :
1133g , normohydramnios;
DIFFERENTIAL DIAGNOSIS:-
1. Dermatologic Manifestations of Metastatic Carcinomas
2. Metastatic Neoplasms to the Oral Cavity
3. Pilomatrixoma
4. Steatocystoma Multiplex
5. Trichilemmal Cyst (Pilar Cyst)
FINAL DIAGNOSIS:- PU 14 weeks AOG,NIL,G1P0, dermoid cyst right S/P unilateral

salpingo – oopherectomy right.
DISCUSSION:-
The occurrence of an adnexal mass during pregnancy is uncommon. The incidence

of Dermoid with pregnancy is approximately 37 %.Most of them are benign and
usually disappear by the 16 week of gestation. Their persistence represents a major
concern related to the obstetrical management and possibility of malignancy.
Diagnosis th would include pelvic examination in the first trimester, an initial
ultrasound and a careful evaluation at the time of operative intervention. One should
consider an ovarian mass in any woman who experiences abdominal pain. Torsion,
rupture, infection and hemorrhage of ovarian tumor should be included in the
differential diagnosis of any catastrophic abdominal obstetric event. Delaying surgery
into the mid second trimester allows for a substantial reduction in the incidence of
functional adnexal masses. Only 6% of adnexal masses excised during pregnancy to
be malignant. During pregnancy, the risk of torsion for an adnexal mass is reported
to be approximately 3 to 15%.
Ovarian cysts are fluid-filled sacs or pockets in an ovary or on its surface. Women
have two ovaries — each about the size and shape of an almond — on each side of
the uterus. Eggs (ova), which develop and mature in the ovaries, are released in
monthly cycles during the childbearing years.Many women have ovarian cysts at
some time. Most ovarian cysts present little or no discomfort and are harmless. The
majority disappears without treatment within a few months.
However, ovarian cysts — especially those that have ruptured — can cause serious
symptoms. To protect your health, get regular pelvic exams and know the symptoms
that can signal a potentially serious problem.
Symptoms
Most cysts don't cause symptoms and go away on their own. However, a
large ovarian cyst can cause:
• Pelvic pain — a dull or sharp ache in the lower abdomen on the side of the
cyst • Fullness or heaviness in your abdomen
• Bloating
Causes
Most ovarian cysts develop as a result of your menstrual cycle (functional
cysts). Other types of cysts are much less common.
Functional cysts
Your ovaries normally grow cyst-like structures called follicles each month.
Follicles produce the hormones estrogen and progesterone and release an
egg when you ovulate.If a normal monthly follicle keeps growing, it's known as
a functional cyst. There are two types of
functional cysts;
1. Follicular cyst. Around the midpoint of your menstrual cycle, an egg
bursts out of its follicle and travels down the fallopian tube. A follicular
cyst begins when the follicle doesn't rupture or release its egg, but
continues to grow.
2. Corpus luteum cyst. When a follicle releases its egg, it begins
producing estrogen and progesterone for conception. This follicle is
now called the corpus luteum. Sometimes, fluid accumulates inside the
follicle, causing the corpus luteum to grow into a cyst.
Functional cysts are usually harmless, rarely cause pain, and often disappear
on their own within two or three menstrual cycles;
Other cysts
Types of cysts not related to the normal function of your menstrual cycle
include:
1. Dermoid cysts. Also called teratomas, these can contain tissue, such
as hair, skin or teeth, because they form from embryonic cells. They're
rarely cancerous.
2. Cystadenomas. These develop on the surface of an ovary and might
be filled with a watery or a mucous material.
3. Endometriomas. These develop as a result of a condition in which
uterine endometrial cells grow outside your uterus (endometriosis).
Some of the tissue can attach to your ovary and form a growth.
Dermoid cysts and cystadenomas can become large, causing the ovary to
move out of position. This increases the chance of painful twisting of your
ovary, called ovarian torsion. Ovarian torsion may also result in decreasing or
stopping blood flow to the ovary.
Risk factors:
Your risk of developing an ovarian cyst is heightened by:
Hormonal problems. These include taking the fertility drug clomiphene
(Clomid), which is used to cause you to ovulate.
• Pregnancy. Sometimes, the cyst that forms when you ovulate stays on your
ovary throughout your pregnancy.
• Endometriosis. This condition causes uterine endometrial cells to grow
outside your uterus. Some of the tissue can attach to your ovary and form a
growth.
• A severe pelvic infection. If the infection spreads to the ovaries, it can cause
cysts.
• A previous ovarian cyst. If you've had one, you're likely to develop more.
Complications ; Some women develop less common types of cysts that a
doctor finds during a pelvic exam. Cystic ovarian masses that develop after
menopause might be cancerous (malignant). That's why it's important to have
regular pelvic exams.
Infrequent complications associated with ovarian cysts include:
• Ovarian torsion. Cysts that enlarge can cause the ovary to move, increasing
the chance of painful twisting of your ovary (ovarian torsion). Symptoms can
include an abrupt onset of severe pelvic pain, nausea and vomiting. Ovarian
torsion can also decrease or stop blood flow to the ovaries.
• Rupture. A cyst that ruptures can cause severe pain and internal bleeding.
The larger the cyst, the greater the risk of rupture. Vigorous activity that
affects the pelvis, such as vaginal intercourse, also increases the risk.
Diagnosis
A cyst on your ovary can be found during a pelvic exam. Depending on its
size and whether it's fluid filled, solid or mixed, your doctor likely will
recommend tests to determine its type and whether you need treatment.
Possible tests include:
• Pregnancy test. A positive test might suggest that you have a corpus luteum
cyst.
• Pelvic ultrasound. A wandlike device (transducer) sends and receives high-
frequency sound waves (ultrasound) to create an image of your uterus and
ovaries on a video screen. Your doctor analyzes the image to confirm the
presence of a cyst, help identify its location and determine whether it's solid,
filled with fluid or mixed.
• Laparoscopy. Using a laparoscope — a slim, lighted instrument inserted into
your abdomen through a small incision — your doctor can see your ovaries
and remove the ovarian cyst. This is a surgical procedure that requires
anesthesia.
• CA 125 blood test. Blood levels of a protein called cancer antigen 125 (CA
125) often are elevated in women with ovarian cancer. If your cyst is partially
solid and you're at high risk of ovarian cancer, your doctor might order this
test.
Elevated CA 125 levels can also occur in noncancerous conditions, such as
endometriosis, uterine fibroids and pelvic inflammatory disease.
Treatment
Treatment depends on your age, the type and size of your cyst, and your
symptoms. Your doctor might suggest:
• Watchful waiting. In many cases you can wait and be re-examined to see if
the cyst goes away within a few months. This is typically an option —
regardless of your age — if you have no symptoms and an ultrasound shows
you have a simple, small, fluid-filled cyst.
Your doctor will likely recommend that you get follow-up pelvic ultrasounds at
intervals to see if your cyst changes in size.
• Medication. Your doctor might recommend hormonal contraceptives, such
as birth control pills, to keep ovarian cysts from recurring. However, birth
control pills won't shrink an existing cyst.
• Surgery. Your doctor might suggest removing a cyst that is large, doesn't
look like a functional cyst, is growing, continues through two or three
menstrual cycles, or causes pain.
Some cysts can be removed without removing the ovary (ovarian
cystectomy). In some cases, your doctor might suggest removing the affected
ovary and leaving the other intact (oophorectomy).
If a cystic mass is cancerous, your doctor will likely refer you to a gynecologic
cancer specialist. You might need to have your uterus, ovaries and fallopian
tubes removed (total hysterectomy) and possibly chemotherapy or radiation.
Your doctor is also likely to recommend surgery when an ovarian cyst
develops after menopause.
Prevention
Although there's no way to prevent ovarian cysts, regular pelvic examinations
help ensure that changes in your ovaries are diagnosed as early as possible.
Be alert to changes in your monthly cycle, including unusual menstrual
symptoms, especially ones that persist for more than a few cycles. Talk to
your doctor about changes that concern you.
CONCLUSION :
This paper describes 3 cases of unusual presentations of ovarian teratoma,
as well as the current clinical features and therapy of ovarian teratomas,
including proper evaluation by
ultrasonography and tumour marker studies in selected cases. Surgical
therapy for symptomatic women or solid tumours may involve laparoscopy by
experienced surgeons, or laparotomy, particularly for suspected malignant
variants.
References :
1. Peterson WF, Prevost EC, Edmunds FT et al: Benign cystic teratomas of the
ovary. A clinico-statistical study of 1,007 cases with a review of the literature. Am J
Obstr Gynecol 2010
2. Ein SH, Darte JMM, Stephen CA: Cystic and solid ovarian tumors in children. A
44- year review. J Pediatr Surg 2011
3. Blackwell WJ, Dockerty MB, Masson JC, et al: Dermoid cysts of the ovary: their
clinical and pathologic significance. Am J Obstr Gynecol 2015
. 4. Marcial-Rojas RA, Medina R: Cystic teratoma of the ovary. A clinical and
pathological analysis of two hundred sixty-eight tumors. Arch Pathol 2011
OBSTETRICS - GYNECOLOGIST DEPARTMENT
NORMAL LABOR DELIVERY
ABSTRACT
Labor is a physiologic process during which the products of conception (ie, the
fetus, membranes, umbilical cord, and placenta) are expelled outside of the uterus.
Labor is achieved with changes in the biochemical connective tissue and with
gradual effacement and dilatation of the uterine cervix as a result of rhythmic uterine
contractions of sufficient frequency, intensity, and duration. Labor is a clinical
diagnosis. The onset of labor is defined as regular, painful uterine contractions
resulting in progressive cervical effacement and dilatation. Cervical dilatation in the
absence of uterine contraction suggests cervical insufficiency, whereas uterine
contraction without cervical change does not meet the definition of labor.
PATIENT HISTORY
Reliability: 90%
GENERAL DATA:
This is a case of ARR, a 24 year-old female, married, Filipino, born on July 10, 1993, Roman
Catholic, housewife, from Liebmann, Camarines Sur, admitted for the first time at Bicol
Medical Center on February 10, 2018.
CHIEF COMPLAINT: labor pain
Patient is a Gravida 1 Para 0 at 39 6/7 weeks AOG. LMP was on May 7, 2017;. EDC is on
February 11, 2018.
o G1: present pregnancy
She had prenatal check-up at the local health center 5x during her 3rdto 9th month AOG.
Vitamin supplementation include Ferrous sulfate and Multivitamin tablets taken one tablet
each daily for 1 month. She had no ultrasound, blood tests and urinalysis done.
Few hours prior to admission, patient experienced labor pain with abnormal uterine
contractions, hence consulted and was admitted.
MENSTRUAL HISTORY:
Patient had menarche at 13 years old. Her normal menstruation is regular monthly with an
interval of 28-31 days, lasting 4 days. Flow is moderate, in which she consumes 4 regular
sanitary pads per day, moderately soaked. No accompanying dysmenorrhea.
GYNECOLOGIC HISTORY:
She had coitarche at age 18, and had only 1 sexual partner. No history of dyspareunia,
postcoital bleeding or pelvic infection. No contraceptive use.
No known medical conditions such as HTN, DM, cardiac disease, stroke, renal disease,
asthma, PTB, GI disease, thyroid disease, blood dyscrasias, and malignancies.
FAMILY HISTORY:
Paternal grandparents are deceased;Maternal grandparents are deceased;

Parents, both 59 years old, and siblings aged 39, 35, 32, 30 and 29 are otherwise well.
No heredofamilial disorders such as HTN, stroke, cardiac disease, DM, malignancies, asthma,
PTB, seizures, renal disease and gastrointestinal disease noted among blood relatives.
Patient is a nonsmoker, non-alcoholic and non-user of illicit drugs. She is a high school
graduate and housekeeper. She is married for 2 years to a now 26-year old laborer. She lives
with her husband in an owned house made of light materials with a water-sealed toilet and
2 bedrooms, which is 10 meters away from the neighboring house. Garbage disposal is via a
compost pit; waste segregation not practiced.
She has a regular diet of rice, fish, meat, vegetables and fruits; prefers vegetables.
REVIEW OF SYSTEMS:
Constitutional: (+) weight gain, no fatigue, no fever.

Respiratory: No cough, hemoptysis and dyspnea.
Gastrointestinal: No nausea, vomiting, hematemesis, abdominal pain, dysphagia,
hematochezia, diarrhea, hemorrhoids, constipation.
Genitalia: No pain, swelling, discharge and ulcers.
Hematologic: No easy bruising.
Endocrine: No polyuria, heat/ cold intolerance, excessive sweating.
Skin: No pallor or jaundice, no pigmentation, no rashes. Good turgor, warm.
no mouth ulcers. No tonsillopharyngeal congestion.
Neck: Supple, midline trachea, thyroid lobes not felt, no cervical lymphadenopathy.

vocal and tactile fremitus. Resonant lungs. Clear breath sounds on bilateral lung fields.
Breast: Pendulous, symmetric, nipples without discharge; no mass.
Heart: Adynamic precordium; no heaves, no thrills, PMI at 5th L ICS MCL.Cardiac rate at 82
beats per minute, regular rhythm, no murmurs.
Abdomen: Gravid, symmetric, (+) linea nigra, (+) striae gravidarum, no scar or visible veins.
Fundic height 30 cm
Leopold’s 1st maneuver: cephalic presentation
Leopold’s 2nd maneuver: longitudinal lie, fetal back at the right side
Leopold’s 3rd maneuver: floating, unengaged
Leopold’s 4th maneuver: vertex
Fetal Heart Tone 150 bpm
Pelvic Examination: External genitalia without lesions
Internal exam: Parous introitus, vagina admits 2 fingers with ease; cervix is closed and soft

swelling; full and equal pulses, CRT <2s.
Neurologic:
Motor: Good muscle tone and bulk,
Cranial Nerves:
I – Can smell the scent of orange peel

VIII - Able to hear
IMPRESSION: Gravida 1 Para 0 Pregnancy Uterine 39 6/7 weeks AOG Cephalic In Labor

Patient was admitted in delivery room, upon admission intravenous fluids was infused,
and laboratory was requested. Upon admission NST was done and result was noted, patient
is for vital sign monitoring and also FHT monitoring,IE was done every 4 hours and result
was noted. After 10 hours of labor patient delivered baby girl via normal spontaneous
vaginal delivery, AS 8-9 , BW- 2.990 . Baby care was done and patient was transferred to OB
ward for further treatment. Regularly medications was given and vital sign monitoring was
done in Obward , improvement was noted and patient was discharged on day 3. Upon
discharged following due medication was given- Cefuroxime 500mg/cap for 7days ,
mefenamic acid 500mg/cap TID for 3 more days, feso4 tab once a day with advice and
instructed for follow up check up after 2 weeks.
DIAGNOSTIC:-
CBC-
Red blood cell 4.13
Hemoglobin 131
Hematocrit 0.39
Platelet count 308
Neutrophils 46
Lymphocytes 36
Blood chem:-
Sodium 138 mmol/l
Potassium 4.4 mg/dl
Creatinine 99mmol/l
URINALYSIS- normal
HBSAG and RPR - non reactive
FINAL DIAGNOSIS:- Gravida 1 Para 1 (1001) Pregnancy Uterine delivered to a live term
cephalic baby girl as 8-9, AGA via spontaneous vaginal delivery.
DISCUSSION:-
Practice Essentials
Labor is a physiologic process during which the fetus, membranes, umbilical cord,
and placenta are expelled from the uterus.
· Stages of labor
o Obstetricians have divided labor into 3 stages that delineate milestones

in a continuous process.
· First stage of labor
o Begins with regular uterine contractions and ends with complete
cervical dilatation at 10 cm
o Divided into a latent phase and an active phase
o The latent phase begins with mild, irregular uterine contractions that
soften and shorten the cervix
o Contractions become progressively more rhythmic and stronger
o The active phase usually begins at about 3-4 cm of cervical dilation
and is characterized by rapid cervical dilation and descent of the
presenting fetal part
· Second stage of labor
o Begins with complete cervical dilatation and ends with the delivery of
the fetus
o In nulliparous women, the second stage should be considered
prolonged if it exceeds 3 hours if regional anesthesia is administered or
2 hours in the absence of regional anesthesia
o In multiparous women, the second stage should be considered
prolonged if it exceeds 2 hours with regional anesthesia or 1 hour
without it [1]
· Third stage of labor
o The period between the delivery of the fetus and the delivery of the
placenta and fetal membranes
o Delivery of the placenta often takes less than 10 minutes, but the third
stage may last as long as 30 minutes
o Expectant management involves spontaneous delivery of the placenta
o The third stage of labor is considered prolonged after 30 minutes, and
active intervention is commonly considered [2]
o Active management often involves prophylactic administration of
oxytocin or other uterotonics (prostaglandins or ergot alkaloids), cord
clamping/cutting, and controlled traction of the umbilical cord
· Mechanism of labor
o The mechanisms of labor, also known as the cardinal movements,

involve changes in the position of the fetus’s head during its passage in
labor. These are described in relation to a vertex presentation.
Although labor and delivery occurs in a continuous fashion, the cardinal
movements are described as the following 7 discrete sequences [2] :
o Engagement
o Descent
o Flexion
o Internal rotation
o Extension
o Restitution and external rotation
o Expulsion
· History
o The initial assessment of labor should include a review of the patient's

prenatal care, including confirmation of the estimated date of delivery.
Focused history taking should elicit the following information:
o Frequency and time of onset of contractions
o Status of the amniotic membranes (whether spontaneous rupture of the
membranes has occurred, and if so, whether the amniotic fluid is clear
or meconium stained)
o Fetal movements
o Presence or absence of vaginal bleeding.
o Braxton-Hicks contractions must be differentiated from true
contractions. Typical features of Braxton-Hicks contractions are as
follows:
o Usually occur no more often than once or twice per hour, and often just
a few times per day
o Irregular and do not increase in frequency with increasing intensity
o Resolve with ambulation or a change in activity
o Contractions that lead to labor have the following characteristics:
o May start as infrequently as every 10-15 minutes, but usually
accelerate over time, increasing to contractions that occur every 2-3
minutes
o Tend to last longer and are more intense than Braxton-Hicks
contractions
o Lead to cervical change
· Physical examination
o The physical examination should include documentation of the
following:
o Maternal vital signs
o Fetal presentation
o Assessment of fetal well-being
o Frequency, duration, and intensity of uterine contractions
o Abdominal examination with Leopold maneuvers
o Pelvic examination with sterile gloves
o Digital examination allows the clinician to determine the following
aspects of the cervix:
o Degree of dilatation, which ranges from 0 cm (closed or fingertip) to 10
cm (complete or fully dilated)
o Effacement (assessment of the cervical length, which can be reported
as a percentage of the normal 3- to 4-cm–long cervix or described as
the actual cervical length)
o Position (ie, anterior or posterior)
o Consistency (ie, soft or firm)
o Palpation of the presenting part of the fetus allows the examiner to
establish its station, by quantifying the distance of the body (-5 to +5
cm) that is presenting relative to the maternal ischial spines, where 0
station is in line with the plane of the maternal ischial spines. [2]
· Intrapartum management of labor
o First stage of labor

o On admission to the Labor and Delivery suite, a woman having normal
labor should be encouraged to assume the position that she finds most
comfortable. Possibilities including the following:
o Walking
o Lying supine
o Sitting
o Resting in a left lateral decubitus position
o Management includes the following:
o Periodic assessment of the frequency and strength of uterine
contractions and changes in cervix and in the fetus' station and position
o Monitoring the fetal heart rate at least every 15 minutes, particularly
during and immediately after uterine contractions; in most obstetric
units, the fetal heart rate is assessed continuously [3]
Second stage of labor
o With complete cervical dilatation, the fetal heart rate should be
monitored or auscultated at least every 5 minutes and after each
contraction. [3] Prolonged duration of the second stage alone does not
mandate operative delivery if progress is being made, but management
options for second-stage arrest include the following:
o Continuing observation/expectant management
o Operative vaginal delivery by forceps or vacuum-assisted vaginal
delivery, or cesarean delivery.
Delivery of the fetus
o Positioning of the mother for delivery can be any of the following [2] :
o Supine with her knees bent (ie, dorsal lithotomy position; the usual
choice)
o Lateral (Sims) position
o Partial sitting or squatting position
o On her hands and knees
o Episiotomy used to be routinely performed at this time, but current
recommendations restrict its use to maternal or fetal indications
Delivery maneuvers are as follows:
o The head is held in mid position until it is delivered, followed by
suctioning of the oropharynx and nares
o Check the fetus's neck for a wrapped umbilical cord, and promptly
reduce it if possible
o If the cord is wrapped too tightly to be removed, the cord can be double
clamped and cut
o The fetus's anterior shoulder is delivered with gentle downward traction
on its head and chin
o Subsequent upward pressure in the opposite direction facilitates
delivery of the posterior shoulder
o The rest of the fetus should now be easily delivered with gentle traction
away from the mother
o If not done previously, the cord is clamped and cut
o The baby is vigorously stimulated and dried and then transferred to the
care of the waiting attendants or placed on the mother's abdomen
Third stage of labor
o The following 3 classic signs indicate that the placenta has separated
from the uterus [2] :
o The uterus contracts and rises
o The umbilical cord suddenly lengthens
o A gush of blood occurs
o Delivery of the placenta usually happens within 5-10 minutes after
delivery of the fetus, but it is considered normal up to 30 minutes after
delivery of the fetus.
· Pain control
o Agents given in intermittent doses for systemic pain control include the
following [4] :
o Meperidine, 25-50 mg IV every 1-2 hours or 50-100 mg IM every 2-4
hours
o Fentanyl, 50-100 mcg IV every hour
o Nalbuphine, 10 mg IV or IM every 3 hours
o Butorphanol, 1-2 mg IV or IM every 4 hours
o Morphine, 2-5 mg IV or 10 mg IM every 4 hours
o As an alternative, regional anesthesia may be given. Anesthesia
options include the following:
o Epidural
o Spinal
o Combined spinal-epidural
REFERENCE:-
1. ACOG. American College of Obstetricians and Gynecologists Practice Bulletin.
Dystocia and augmentation of labor. Clinical management guidelines for
obstetricians-gynecologists. No 49. American College of Obstetricians and
Gynecologists: Washington, DC; December 2003.
1. 2. Norwitz ER, Robinson JN, Repke JT. Labor and delivery. Gabbe SG,
Niebyl JR, Simpson JL, eds. Obstetrics: Normal and problem pregnancies.
3rd ed. New York: Churchill Livingstone; 2003.
2. 3. ACOG. American College of Obstetricians and Gynecologists Practice
Bulletin. Intrapartum Fetal Heart Rate Monitoring. Clinical Management
Guidelines for Obstetricians-Gynecologists. No 36. American College of
Obstetricians and Gynecologists;: Washington, DC; December 2005.
2. ACOG. American College of Obstetricians and Gynecologists Practice Bulletin.
Obstetric Analgesia and Anesthesia. Clinical Management Guidelines for
Obstetricians-Gynecologists. No 36. American College of Obstetricians and
Gynecologists;: Washington, DC; July 2002.
3. Friedman EA. Primigravid labor; a graphicostatistical analysis. Obstet Gynecol. 1955

Dec. 6(6):567-89. [Medline].
4. Friedman EA, Sachtleben MR. Dysfunctional labor. I. Prolonged latent phase in the
nullipara. Obstet Gynecol. 1961 Feb. 17:135-48. [Medline].
5. Friedman EA, Sachtleben MR. Dysfunctional labor. II. Protracted active-phase

dilatation in the nullipara. Obstet Gynecol. 1961 May. 17:566-78. [Medline].
6. Kilpatrick SJ, Laros RK Jr. Characteristics of normal labor. Obstet Gynecol. 1989 Jul.
74(1):85-7. [Medline].

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AGO MEDICAL AND EDUCATION CENTER

BICOL CRISTIAN COLLAGE OF MEDICINE

In partial fulfillment of the

A Compilation of clinical histories in my one year clinical rotation in Bicol

OBSTETRICS AND GYNAECOLOGIST

Skin: No pallor, jaundice or pigmentation, good turgor, no lesions.

COURSE IN THE WARD

BLOOD C/S- no growth after 72 hr

Rule in Rule out

FINAL DIAGNOSIS :- enteric fever

Enteric Fever (Typhoid Fever)

Human volunteer experiments established an infecting dose of about 10 5 -10 9 organisms,

components of the heteropentameric B subunit of pertussis toxin. Although the cellular

The propensity to become a carrier follows the epidemiology of gallbladder disease,

In addition to antibiotics, the importance of supportive treatment and maintenance of

REFERENCE:- Nelson book of Pediatric

Skin: No pallor, jaundice or pigmentation, good turgor, no lesions.

Chest x-ray – Pneumonia in both lungs

Rule in Rule out

Although most cases of pneumonia are caused by microorganisms, noninfectious causes

Pneumonia is frequently preceded by several days of symptoms of an upper respiratory tract

Point-of-care use of portable or handheld ultrasonography is highly sensitive and specific in

The empiric treatment of suspected bacterial pneumonia in a hospitalized child requires an

If viral pneumonia is suspected, it is reasonable to withhold antibiotic therapy, especially for

Typically, patients with uncomplicated community-acquired bacterial pneumonia show

Mortality from community-acquired pneumonia in developed nations is rare, and most

H. influenzae type b infection.

REFERENCE — NELSONE BOOK OF PEDIATRIC

Informant: Auntie & Uncle

HISTORY OF PRESENT ILLNESS:

Deep Tendon Reflexes:

Babinski Negati Negati

INTUBATION PERIOD: Uncertain. Probably 6 days to 10 days

MODE OF TRANSMISSION: Dengue viruses are transmitted to humans through the

GRADING THE SEVERITY OF DENGUE FEVER:

SUSCEPTABILITY, RESISTANCE, AND OCCURRENCE:

>all persons are susceptible

Dengue haemorrhagic fever (DHF), a potentially lethal complication, was firstrecognized in

DENGUE PREVENTION: There is no vaccine to prevent dengue. Prevention centers on

when traveling in tropical areas:

Use mosquito repellents on skin and clothing.

No other known medical conditions such as stroke, hypertension ,renal

Course in the ward:

CHEST XRAY- TB in both lungs.

SPUTUM EXAMINATION- POSITIVE

Community-acquired Signs of lobar or atypical Sputum examination with

Nontuberculous Mycobacterium avium If sputum AFB culture is

FINAL DIAGNOSIS:- Pulmonary tuberculosis

FROM EXPOSURE TO INFECTION

NATURAL HISTORY OF DISEASE

PATHOGENESIS and IMMUNITY

THE HOST RESPONSE, GRANULOMA FORMATION and LATENCY

TB OF THE UPPER AIRWAYS

while preventing the emergency of drug resistance o To interrupt transmission by

adverse reaction of significance is hepatitis Baseline assessment of liver

Babinski Negati Negati

COURSE IN THE WARD:-

FINAL DIAGNOSIS:- Dengue with Warning Signs

DISCUSSION ABOUT THE CASE:-

INTUBATION PERIOD: Uncertain. Probably 6 days to 10 days

MODE OF TRANSMISSION: Dengue viruses are transmitted to humans through the

1.Severe, frank type