medicine

1. Dr Henok PCHR ll
Dr Rodas PCHR lll
Moderator Dr Turegne pediatric ID fellow

2.  History
 Physical examination
 Pertinent investigations
 Discussion
 Management

3. Name:B.Y
Age:5 months
Sex:Female
Address:Gojjam , Debre Markos
Religion of the parents:Orthodox christian

4.  Father is a 40 years old Government worker
 Mother is a 32 years old House wife
 Date of clerking : 5/2/16
 Source of history: The Mother,chart review
 Place – C7 ward
 Age at admission: 3 months
 Date of admission:23/11/15

5. Progressive increment of head size of 1
week duration

6.  This is a 5 months old female infant born from a 30 years old para ll
mother after 8 months of amenorrhea the mother had regular ANC
follow up at health center with baseline investigations told to be
normal
 The delivery was via SVD to effect an outcome of 2k.g female
neonate with Unknown APGAR score
 Immediately after delivery she was admitted to NICU and unspecified
IV medication given for 2 weeks and discharged with improvement

7.  At the age of 3 months She presented with failure to suck of 1 week
duration associated with this she has hx of LGIF,non projectile non
bilious vomiting twice per day ,ABM characterized by twitching of left
eye lid and left lower extremities ,the family noticed increment of
head size
 For the above complain she was taken to Debre Markos hospital and
referred to this hospital where Trans fontanel ultrasound was done
referred to this hospital with an impression of Severe hydrocephalus
for Neuro surgical intervention

8.  Otherwise she has no hx of
 Generalized body rash
 Yellowish discoloration of eyes or skin
 Whitish discoloration at the center of the eyes
 Bleeding from any site
 Abdominal distention

9. At presentation -
 General appearance- ASL
 V/S- PR- 152 RR- 34 T-37.1 SPO2- 95 % with atm air
 ANTHROPOMETRY
Wt – 4.7kg WFA= b/n 0 & -2 Z score
Length –54 cm LFA= at -2 Z score
Hc – 45.5 cm Hc for Age = above 3 Z score
WFL= b/n 1 & 2 Z score

10.  HEENT= Anterior fontanel was bulged and tense
 No cataract , has Sun set eyes
 Pink and moist buccal mucosa
 No nasal discharge
 LGS= No palpable LAP.
 Chest = SC/IC retraction
Clear and good air entry on both side
 Abdomen= full moves with respiration , No palpable organomegaly

11. GUS: NEFG
Int : No edema or Rash
MSK: No deformities
CNS – alert
Tone _ normotonic

12.  After admission she was started on Ceftriaxone , vancomycin and
metronidazole iv , first MRI suggesting abscess + basal leptomeningitis for
which she was taken to OR and Rt Kocher EVD + left Temporal
craniotomy +abscess evacuation was done and continued antibiotics
,EVD was removed 10 days after the procedure and 2 days after removal
she started to have increment in head size , 2 -3 episodes of projectile
vomiting per day , for these complaint MRI was repeated and planned to
operate the patient at Zewditu , meanwhile Vancomycin was
discontinued at Meskerem 15 after she took for 58 days and ceftriaxone
was changed to cefotaxime at Meskerem 22 after she took for 65 days
and metronidazole discontinued after taking for 81 days in total
currently she is referred to Zewditu for possible surgical intervention.

13. CBC 11/8/23 14/8/23 22/8/23 26/8/23 02/9/23 21/9/23
WBC 10.01 15.07 12.48 12.36 9.71 7.7
N 12.9 % 9.8% 12.7% 16.4 %
L 72.8 % 65.4% 65.5% 82.3% 82.4% 69
Hgb 10.2 11.0 10.0 10.8 10.8 10.9
Hct 30.4 27.6 24.9 32.8 32.6 32.6
MCV 85.4 83.1 82.2 82.2 78.2 69
Plt 433 K 658 K 543 K 406 K 326 K 524 K

14. Chemistry 11/8/23 14/8/23 26/8/23 2/9/23 22/9/23
Na+ 138 140 137 123 133.7
K+ 6.58 5.23 5.29 5.71 5.42
Cl+ 106.8 108.8 106.6 93
Urea 7.5 3.3 7
Cr 0.18 0.04 0.33 0.16
10/10/23
8
0.2
CSf Analysis
Csf Glucose 34
Csf Protein 80.7
Csf Gram Stain No bacteria cell seen
Csf Cell Count No cell seen

15. Brain MRI Aug 3 / 2023 Sep /14 /2023 Oct /13/2023
Findings Left Periventricular
rim contrast enhancing
lesion with intra
ventricular extension
and bilateral lateral
ventricle dilation
suggesting abscess +
basal leptomeningitis
Complex hydrocephalus
and left frontal lobe
and basal ganglia
abscess as well as sign
of right posterior
lateral ventricle and
fourth ventriculitis as
well as right frontal and
bilateral temporal lobes
cystic
encephalomalacia likely
sequala of Meningitis
.There is slight
reduction in the size of
the left basal ganglia
abscess otherwise
interval radiologic
worsening of their
complex
Hydrocephalus.
Left periventricular
abscesses- pyogenic
with obstructive
hydrocephalus
+ Bilateral cerebral
gliosis

17.  P1 – 47th Post procedure day after EVD,left temporal craniotomy &
abscess drainage was done for an indication of communicating
hydrocephalus 2ry to complicated neonatal meningitis with
ventriculitis & brain abscess

18. Neonatal meningitis
Complication of neonatal meningitis
-Brain abscess
-Hydrocephalus
Ventriculitis

19.  Bacterial meningitis is more common in the 1st month than at any
other time of life.
 Incidence:0.25-0.32/1000 live births
-declined since the 1970s due to
*prevention of early-onset GBS
*intrapartum antibiotic prophylaxis
*prompt evaluation of neonate with risk factor

20.  Bacterial meningitis occur in 15% of neonate with bacteremia.
 5-10% with EONS & 25-30% of those with LONS have meningitis.
 During 2nd month incidence of meningitis declines by 50%.

21.  Low birth weight (our pt was 2 k.g)
 Preterm birth (our patient 36wk:late preterm)
 Premature/prolonged PROM
 Maternal intra-amniotic infection

22.  GBS
 E.coli
 Gram negative bacilli
 Gram positiveorg.(enterococcus,CONS,S.aureus,Listeria
monocytogenes,group A streptococcus &alpha-hemolytic
streptococci)
 Anaerobic pathogens(esp.bacteroides fragilis);negative culture
results
 Pasteurella multocida:licking with companion animals

23.  Temperature instability
 Neurologic finding
-irritability:60%
-seizure:20-50%
-bulging fontanel:25%
 Poor feeding/vomiting:50%
 Decreased activity:50%
 RD
 Apnea

24.  Hx & P/E
 Ix -CBC
-Blood culture
-Urine culture
-LP

25.  Supportive care
-management of cardiovascular instability
-provision of oxygen and additional respiratory support
-careful fluid therapy
-prevention & management of hypoglycemia
-control of seizures
-nutritional support

26.  Empiric therapy
-based on timing of onset(early Vs late)
-local susceptibility patterns

28.  Serial neurologic evaluation
 Overall clinical status
 Repeat blood culture
 Repeat CSF examination
 Neuroimaging
Long term follow up
-monitoring of hearing(auditory brainstem response)
-vision,and developmental status

30.  Cerebral edema(vasogenic & cytotoxic)
 ICP
 Ventriculitis
 Cerebritis
 Hydrocephalus
 Brain abscess
 Cerebral infarction
 Cerebral venous thrombosis
 Arterial stroke
 Subdural effusion/empyema

31.  Occurs in approximately 10% of patients with neonatal meningitis
 11-19% of patients with gram negative N.meningitis
 Risk increased in meningitis caused by:
-citrobacter koseri,serratia marcescens,proteus mirabilis & cronobacter
sakazakii

32.  The incidence of brain abscess is between 0.3 and 1.3 cases per 100,000 people
per year.
 Development of brain abscess is most often associated with an underlying
etiology, including:
-contiguous spread from an associated infection (meningitis, otitis media,
mastoiditis, sinusitis, soft tissue infection of the face or scalp, orbital cellulitis,
or dental infections)
-direct compromise of the blood– brain barrier due to penetrating head injuries
or surgical procedures

33.  embolic phenomena (endocarditis2-5%); right-to-left shunts
(congenital heart disease or pulmonary arteriovenous malformation)
 immunodeficiency
 infection of foreign material inserted into the central nervous
system (CNS), including ventriculoperitoneal shunts.

34.  Cerebral abscesses occur in both hemispheres in children, but in
adults, left sided abscesses are more common, likely due to
penetrating injuries from right handed assailants.
 Nearly 80% of abscesses occur in the frontal, parietal, and temporal
lobes, while abscesses in the occipital lobe, cerebellum, and
brainstem account for the remainder of cases.
 In 18% of cases, multiple brain abscesses are present, and in nearly
20% of cases, no predisposing risk factor can be identified.

35.  Abscesses in the frontal lobe are often caused by extension from
sinusitis or orbital cellulitis
 Whereas abscesses located in the temporal lobe or cerebellum are
frequently associated with otitis media and mastoiditis.

36.  Direct extension – single
 Hematogenous –multiple
 These locations in the brain in order of decreasing frequency are:
 Frontal or temporal lobes
 Frontal-parietal
 Parietal
 Cerebellar
 Occipital

37.  The predominant organisms that cause brain abscesses are streptococci,
which account for one third of all cases in children
 Streptococcus anginosus group (S. anginosus, Streptococcus constellatus,
and Streptococcus intermedius) being the most common streptococci.
Other important streptococci include Streptococcus pneumoniae,
Enterococcus spp., and other viridans streptococci.

38.  Staphylococcus aureus is the second most common organism in pediatric brain
abscesses, accounting for 11% of cases, and is most often associated with
penetrating injuries.
 Other bacteria isolated from brain abscesses include Gram-negative aerobic
organisms (Haemophilus spp., Escherichia coli, Klebsiella pneumoniae, Proteus
spp., and other Enterobacteriaceae)

39.  Anaerobic bacteria (Gram-positive spp., Bacteroides spp.,
Fusobacterium spp., Prevotella spp., and Actinomyces spp.).

40.  In up to 27% of cases, more than one organismis cultured.
 Abscesses associated with mucosal infections (sinusitis or dental infections)
frequently are polymicrobial and include anaerobic organisms.
 Atypical bacteria, including Nocardia, Mycobacterium, and Listeria spp., and
 Fungi (Aspergillus, Candida, Cryptococcus) are more common in children with
impaired host defenses.

41.  Endocarditis – Viridans streptococci, S. aureus
 Congenital cardiac malformations (especially right-to-left shunts) –
Streptococcus spp
 Klebsiella pneumoniae brain abscess with or without meningitis can
occur as a manifestation of metastatic infection that is associated
with community-acquired primary liver abscess.

42.  Often the early stages of cerebritis and abscess formation are asymptomatic or
associated with nonspecific symptoms, including low-grade fever, headache,
and lethargy.
 As the inflammatory process proceeds, vomiting, severe headache, seizures,
papilledema, focal neurologic signs (hemiparesis), and coma may develop.

43.  The diagnosis is made at a mean of 13 to 14 days after the onset of
symptoms
 Headache most common symptom
 Fever is not a reliable indicator of brain abscess since only 45 to 50
percent of patients have this sign
 Focal neurologic deficits are observed in 50 percent of patients and
generally occur days to weeks after the onset of headache

44.  Seizures develop in 25 percent of cases and can be the first
manifestation of brain abscess
 Grand mal seizures are particularly common in frontal abscesses.
 Neck stiffness occurs in 15 percent of patients with brain abscess.
 This complaint is most commonly associated with occipital lobe
abscess or an abscess that has leaked into a lateral ventricle

45.  A cerebellar abscess is characterized by nystagmus, ipsilateral ataxia
and dysmetria, vomiting, and headache.
 If the abscess ruptures into the ventricular cavity, overwhelming
shock and death occur in 27–85% of cases.

46.  In neonate/early infant :finding can be subtle & include
-vomiting,bulging fontanelle,increased head cirumfrence,separation of
the cranial sutures,hemiparesis,focal seizures,and increased peripheral
WBC.

47.  Prompt imaging of the CNS.
 Brain MRI with contrast is the diagnostic test of choice because it can
aid in differentiating abscesses from cysts and necrotic tumor,better
brain stem visualization ,early cerebritis,satellite lesions
 Both MRI and CT scans with contrast can demonstrate a ring-
enhancing abscess cavity.
 The CT findings of cerebritis are characterized by a parenchymal low-
density lesion, whereas T2-weighted MRI images feature increased
signal intensity

48.  Early cerebritis appears as an irregular area of low density that does
not enhance following contrast injection
 The area of decreased attenuation is often of greater extent than the
abscess itself because of the presence of cerebritis with surrounding
edema
 The ring of contrast enhancement represents breakdown of the blood
brain barrier and the development of an inflammatory capsule

50.  The peripheral white blood cell count is elevated in 60% of cases, and
blood cultures are positive in 28% of cases.
 Lumbar puncture is not routinely recommended in cases of brain
abscesses, because the procedure could cause brain herniation from
elevated intracranial pressure

51.  When tested, the cerebrospinal fluid (CSF) is normal in 16% of cases, 71% of
cases exhibit CSF pleocytosis, and 58% will have an elevated CSF protein level.
 CSF cultures are positive in only 24% of cases
 An electroencephalogram (EEG) may identify corresponding focal slowing.

52.  Empiric therapy consists of a combination of a 3rd-generation
cephalosporin and metronidazole, often with vancomycin to provide
coverage of methicillin resistant S. aureus and cephalosporin-
resistant strains of S. pneumoniae.
 If resistant Gram-negative organisms are suspected, as in cases of
infected ventriculo peritoneal shunts, cefepime or meropenem may
be used as the β- lactam in the initial regimen.

53.  Listeria monocytogenes may cause a brain abscess in the neonate and
if suspected, penicillin G or ampicillin with gentamicin is
recommended.
 In immunocompromised patients, broad-spectrum antibiotic coverage
is used, and amphotericin B therapy should be considered for activity
against fungi

54.  Small abscesses under 2.5 cm in diameter or multiple abscesses, no
raised ICP may be treated with antibiotics in the absence of
drainage, with follow-up neuroimaging studies to ensure a decrease
in abscess size.
 The duration of parenteral antibiotic therapy depends on the
organism and response to treatment but is most typically 6 wk

55.  Abscesses secondary to an infected ventriculo peritoneal shunt may
be initially treated with vancomycin and ceftazidime

56.  >2.5 cm in diameter
 Gas is present in the abscess
 The lesion is multiloculated
 The lesion is located in the posterior fossa
 A fungus is identified

57.  More recent mortality rates, range from 5–10%.
 Factors associated with high mortality rates at the time of admission
include
Delayed administration of antimicrobials
Age < 1 yr
Multiple abscesses
Coma
 Long-term sequelae occur in about one third of the survivors and
include hemiparesis, seizures, hydrocephalus, cranial nerve
abnormalities, and behavioral and learning difficulties

58.  Ventriculitis refers to inflammation of the ventricular fluid & lining of
the ventricles & is sometimes associated with obstruction to CSF
flow.
 It is common complication of neonatal meningitis, occuring in up to
20% of cases.

59.  Cerebrospinal fluid (CSF) shunting is required for the treatment of
many children with hydrocephalus .
 The usual procedure uses a silicone rubber device with a proximal
portion inserted into the ventricle, a unidirectional valve, and a
distal segment that diverts the CSF from the ventricles to either the
peritoneal cavity (ventriculoperitoneal [VP] shunt) or right atrium
(ventriculoatrial [VA] shunt).

60.  The incidence of shunt infection ranges from 1–20% (average, 10%).
 The highest rates are reported in young infants, patients with prior
shunt infections,and certain etiologies of hydrocephalus.
Most infections result from intraoperative contamination of the surgical
wound by skin flora.

61. Patient factor Procedural factors
 Premature birth
 Younger age
 Previous shunt infection
 Certain cause of hydrocephalus
purulentmeningitis,hemorrhage,
MMC
 Experience of the neurosurgeon
 Duration of procedure
 Skin preparation
 Shunt revision
 Gastrostomy tube placement

62.  Shunt infection most frequently develop via colonization of the shunt
with skin flora.
 This may occur at the time of shunt placement or post operatively via
breakdown of the wound or overlying skin.

63.  coagulase-negative staphylococci are isolated in more than half the
cases.
 S.aureus is isolated in approximately 20% and gram-negative bacilli
in 15% of cases.

64.  Shunt infection may also develop via direct contamination of the
distal end of the shunt or via hematogenous seeding.
 These infection account for about 10 to 15% and tend to occur
months after shunt placement
 They may be due to avariety of organisms including
streptococci,gramnegative(p.aeruginosa),anaerobes,mycobacteria&
fungi

65.  Four distinct clinical syndromes have been described:
- colonization of the shunt
- infection associated with wound infection,
- distal infection with peritonitis,
-infection associated with meningitis.

66.  Symptoms associated with colonized VP shunts include
-lethargy, headache, vomiting, a full fontanel, and abdominal pain.
-Fever is common but may be <39°C (102.2°F).
Symptoms usually occur within months of the surgical procedure.
Colonization of a VA shunt results in more severe systemic symptoms,
and specific symptoms of shunt malfunction are often absent

67.  Septic pulmonary emboli, pulmonary hypertension, and infective
endocarditis are frequently reported complications of VA shunt
colonization.
 Chronic VA shunt colonization may cause hypocomplementemic
glomerulonephritis from antigen-antibody complex deposition in the
glomeruli:
commonly called “shunt nephritis”; clinical findings include
hypertension, microscopic hematuria, elevated blood urea nitrogen and
serum creatinine levels,and anemia

68.  Diagnosis is by Gram stain, microscopy, biochemistry, and culture of
CSF.
 It is unusual to observe signs of ventriculitis, and CSF findings can be
only minimally abnormal.
 Blood culture results are usually positive in VA shunt colonization but
negative in cases of VP colonization.

69.  Neuroimaging
-cranial US (intraventricular strands attached to ventricular
surface,echogenic ependyma,dilated ventricles)
-MRI:enhancement of the lining of the ventricles

70.  Wound infection presents with obvious erythema, swelling,
discharge, or dehiscence along the shunt tract and most often occurs
within days to weeks of the surgical procedure.
 S. aureus is the most common isolate.
 In addition to the physical findings, fever is common, and signs of
shunt malfunction eventually ensue in most cases.

71.  Distal infection of VP shunts with peritonitis presents with abdominal
symptoms, usually without evidence of shunt malfunction.
 The pathogenesis is likely related to perforation of bowel at VP shunt
placement or translocation of bacteria across the bowel wall.
 Thus, gram-negative isolates predominate, and mixed infection is
common.
 The infecting organisms are often isolated from only the distal
portion of the shunt.

72. Treatment of shunt colonization includes:
- removal of the shunt and systemic antibiotic therapy directed against
the isolated organisms.
-Treatment without removal of the shunt is rarely successful and should
not be routinely attempted.
-Definitive therapy should be directed toward the isolate and should
account for poor penetration of most antibiotics into the CSF across
noninflamed meninges. Accordingly

73.  Device removal
 Antibiotics therapy
-Empiric therapy After collection of appropriate samples for culture,
empirical therapy is usually with vancomycin plus an antipseudomonal
agent with relatively good CSF penetration, such as ceftazidime or
meropenem.
-Targeted therapy:tailred to culture and sensitivity result

74.  Staphylococci:vancomycin(MRSA,CONS)
Methicilline sensitive:nafcilline/oxacilline
MRSA isolates with a vancomycin MIC >=1linozolid,daptomycin,TMP-SMX
Cutibacterium acnes-penicillin G
Gram negatives

75.  Intraventricular Abs:
-For infection that are refractory to appropriate systemic antibiotic
therapy
-Highly resistent organisms susceptible only to antimicrobials with poor
CSF penetration
-Infections in which shunt cannot be removed

76. Daily CSF cultures should be collected until clearance has been
documented on 2-3 consecutive specimens, and antibiotics should be
continued for at least 10 days after documented sterilization of the
CSF.

77.  In accordance with IDSA 2017
-Infection caused by CONS/C.acne with no or minimal CSF pleocytosis
txed for
-Infection caused by CONS/C.acne with significant CSF pleocytosis t low
CSF glucose,clinical sx txed for 10-14days
-Infection caused by S.aureus or gram negative with/without
significant CSF pleocytosis txed for 10-14 days ,gram –ve 21 days
-For patients with repeatedly positive CSF cultures on appropriate
Abs,tx 10-14 days following the last positive culture

78.  Timing of new shunt placement should be individualized based upon
-the isolated organism,
-the severity of infection
-the improvement of CSF parameters,CSF sterilization

79.  Prevention of shunt infection includes meticulous cutaneous
preparation and surgical technique.
 Systemic and intraventricular antibiotics, antibiotic impregnated
shunts, and soaking the shunt tubing in antibiotics are used to reduce
the incidence of infection, with varying success.

80.  Systemic prophylactic antibiotics given before and during shunt
insertion can reduce the risk for infection and should be used
routinely but should not be continued for more than 24 hr
postoperatively.
 Antibiotic-impregnated catheters also appear to reduce the risk of
infection and may be used in high-risk patients where the devices are
available.

81.  Hydrocephalus occurs in approximately 25% of infants with neontal
meningitis.
 30-44% of cases of gram-negative neonatal meningitis
 More common in meningitis caused by GBS type lll & K1 E.coli then
non K1 E.coli

82.  Hydrocephalus can occur as an acute complication of bacterial
meningitis because it is often caused by adhesive thickening of the
arachnoid villi around the cisterns at the base of the brain.
 Thus, this thickening leads to interference with the normal resorption
of CSF and development of hydrocephalus.
 Less often, obstructive hydrocephalus develops after fibrosis and
gliosis of the cerebral aqueduct or the foramina of Magendie and
Luschka.

83.  Sign of ICP
 Dx :neuroimaging
-neonate:cranial US

84.  Hydrocephalus
 Multicystic encephalomalacia
 Porencephaly
 Cerebral cortical and white matter atrophy
*GDD
*Late onset seizure
*CP
*Hearing loss
*Cortical blindness

86.  Nelson textbook of pediatrics 21st edition
 Uptodate online
 2017 IDSA