CASE REPORT

HIDROCEPHALUS
WITH
BRONCOPNEUMONIA +
TB
 Name : Rajib

Patients Overview
7 Years Old Kid was brought by his Mother to Nganjuk Hospital
Emergency Room, after experiencing shortness of breath, cough, and
fever.

Past Medical History

3 Years ago, the patient was diagnosed with hidrocephalus.
Because of the Hidrocephalus, the patient had operated twice in Dr
Sutomo Hospital Surabaya.
3 Years ago, the patient also experienced spasms, one day could be 3
times spasms.

Social History
patient lives with the parents and from the middle class family.
Physical Examination

-Mental Status: Patient compos mentis
-Vital Signs = Respiration Rate: 28x/min, HR: 100x/min, T: 38
- Head, Face, and Neck Examination= A/I/C/D = - / - / - / -
-Chest Examination = Auscultation : Pulmo : Ronkhi (+)
-Abdominal Examination = Bowel Sound (+) normal
-Extremities = Normal

Laboratory Monitoring
Daily Blood Test
Hematocrit 29.0 L
Trombosit 172 L
THORAX PHOTO
 THE RESULTS
PULMO : -The bronchovasculer patterns
of lungs are rough and there is triangle-
shape coating at suprahilus dextra.
There are infiltrates in right and left lungs.

DIAGNOSE: TUBERCULOSIS
 ASSESMENT
HIDROCEPHALUS + VP SHUNT WITH
BRONKOPNEUMONIA AND TB
PROGRESS NOTE
PROGRESS NOTE
PROGRESS NOTE
 HIDROCEPHALUS
Hydrocephalus can be defined broadly as
a disturbance of cerebrospinal fluid (CSF)
formation, flow, or absorption, leading to
an increase in volume occupied by this
fluid in the central nervous system (CNS).
 SYMPTOMS
Symptoms in infants include abnormal enlargement of the head, poor feeding, irritability,
reduced activity, and vomiting.

Symptoms in children and adults include the following:

Headaches (initially in the morning)
Vomiting, more significant in the morning
Blurred vision: A consequence of papilledema and, later, of optic atrophy
Double vision: Related to unilateral or bilateral sixth nerve palsy
Drowsiness
 PATHOPHYSIOLOGY
Normal route of CSF from production to clearance is the following: From the
choroid plexus, the CSF flows to the lateral ventricle, then to the
interventricular foramen of Monro, the third ventricle, the cerebral aqueduct
of Sylvius, the fourth ventricle, the 2 lateral foramina of Luschka and 1
medial foramen of Magendie, the subarachnoid space, the arachnoid
.
granulations, the dural sinus, and finally into the venous drainage
 PATHOPHISIOLOGY
ICP rises if production of CSF exceeds absorption. This occurs if CSF is
overproduced, resistance to CSF flow is increased, or venous sinus
pressure is increased. CSF production falls as ICP rises. Compensation
may occur through transventricular absorption of CSF and also by
absorption along nerve root sleeves. Temporal and frontal horns dilate first,
often asymmetrically. This may result in elevation of the corpus callosum,
stretching or perforation of the septum pellucidum, thinning of the cerebral
mantle, or enlargement of the third ventricle downward into the pituitary
fossa (which may cause pituitary dysfunction).
 PATHOPHISIOLOGY
The mechanism of NPH has not been elucidated completely. Current
theories include increased resistance to flow of CSF within the ventricular
system or subarachnoid villi; intermittently elevated CSF pressure, usually
at night; and ventricular enlargement caused by an initial rise in CSF
pressure; the enlargement is maintained despite normal pressure because
of the Laplace law. Although pressure is normal, the enlarged ventricular
area reflects increased force on the ventricular wall.
 BRONCHOPNEUMONIA
Pneumonia is acute inflammatory disease
on lung caused by infection
microorganisms that will lead to the
consolidation of lung tissue and disorders
local gas exchange
 SYMPTOMS
Cough is the most common symptom of
pneumonia in infants, along with
tachypnea, retractions, and hypoxemia.
These may be accompanied by
congestion, fever, irritability, and
decreased feeding. Streptococcus
pneumoniae is by far the most common
bacterial pathogen in infants aged 1-3
months
 PATHOPHISIOLOGY
Pneumonia is characterized by inflammation of
the alveoli and terminal airspaces in response to
invasion by an infectious agent introduced into
the lungs through hematogenous spread or
inhalation. The inflammatory cascade triggers
the leakage of plasma and the loss of surfactant,
resulting in air loss and consolidation.
 TUBERCULOSIS
Tuberculosis is an infectious disease
caused by bacteria mycobacterium
tuberculosa .
 SYMPTOMS
Classic clinical features associated with active pulmonary TB are as
follows (elderly individuals with TB may not display typical signs and
symptoms):
Cough
Weight loss/anorexia
Fever
Night sweats
Hemoptysis
Chest pain
Fatigue
 PATHOPHISIOLOGY
Infection with M tuberculosis results most
commonly through exposure of the lungs or
mucous membranes to infected aerosols.
Droplets in these aerosols are 1-5 m in
diameter; in a person with active pulmonary TB,
a single cough can generate 3000 infective
droplets, with as few as 10 bacilli needed to
initiate infection.
 PATHOPHISIOLOGY
When inhaled, droplet nuclei are deposited
within the terminal airspaces of the lung.
The organisms grow for 2-12 weeks, until
they reach 1000-10,000 in number, which
is sufficient to elicit a cellular immune
response that can be detected by a
reaction to the tuberculin skin test.
 PATHOPHISIOLOGY
Mycobacteria are highly antigenic, and
they promote a vigorous, nonspecific
immune response. Their antigenicity is
due to multiple cell wall constituents,
including glycoproteins, phospholipids,
and wax D, which activate Langerhans
cells, lymphocytes, and
polymorphonuclear leukocytes
 PATHOPHISIOLOGY
When a person is infected with M tuberculosis,
the infection can take 1 of a variety of paths,
most of which do not lead to actual TB. The
infection may be cleared by the host immune
system or suppressed into an inactive form
called latent tuberculosis infection (LTBI), with
resistant hosts controlling mycobacterial growth
at distant foci before the development of active
disease. Patients with LTBI cannot spread TB.
 PATHOPHISIOLOGY
The lungs are the most common site for
the development of TB; 85% of patients
with TB present with pulmonary
complaints. Extrapulmonary TB can occur
as part of a primary or late, generalized
infection. An extrapulmonary location may
also serve as a reactivation site;
extrapulmonary reactivation may coexist
with pulmonary reactivation