Enteric Fever Paediatrics CPC

1. ENTERIC FEVER
PRESENTED BY:
Syed Zain Gilani 23957
Ahsan Khalid 19532
Fasi Ur Rehman 19719
Ahsan Imran 31123

2. HISTORY

3. Personal
Profile
• Name : Muhammad Shahmeer
• Father name: Muhammad Zaheer
• Age: 7 years old
• Residence : Pir Wadai, Rawalpindi
• Mode of Admission: Emergency
• Date of Admission: 15th Feb 2024
• Informant: Mother

4. Presenting
Complaint
• Fever / 3 weeks
• Abdominal Pain / 2 weeks
• Diarrhea / 5 days
• Vomiting / 1 Episode

5. History of Present illness
• The informant of history is patient’s mother who is well aware of
disease.
• My patient was in usual state of health 3 weeks back when he
developed fever.
• Fever was gradual in onset, continuous, high grade, documented
to be 103oF with diurnal variation, more in evening, associated
with rigors and chills.
• Fever was relieved after taking antipyretics and Syrup
Paracetamol.

6. History of Present illness
• The patient had diarrhea, 8 to 9 episodes per day, containing no blood or
mucous, watery in nature, associated with lower abdominal pain, which was
sudden in onset and non progressive in nature.
• Patient was admitted in Paeds ward, 5 days back, and administered IV
antibiotics and Syrup Paracetamol. Now he is afebrile and pain free.

7. Systemic Review
• General: There is history of decreased appetite and weight loss.
• CNS: No history of fits, headache, neck stiffness.
• CVS: No history of Cyanosis, Night Sweats
• Respiratory: No history of cough, sore throat.
• GIT: There is history of Diarrhoea and Lower Abdominal Pain.
• GUS: No history of incontinence, dysuria, hematuria, burning
micturition.
• MSK: No history of joint swelling and rash.

8. Past Medical History
History of Pneumonia at age of one year and was
admitted to the Hospital for treatment

9. Treatment History
Patient took:
• Syrup Panadol
• Augementin
• Nebulization.

10. Birth
History
Antenatal
• Booking was done
• Injection Tetanus was administered
• Anomaly scan was not done
• Hypertension was present, but no
history pre-eclampsia/eclampsia
• Hepatitis C history

11. Birth
History
Natal
• Gestational age  40 Weeks
• Mode of delivery  SVD
• Complications  None
• Place of delivery  Hospital
Postnatal
• Immediate Cry after birth
• No NICU admission

12. Feeding History
• The child was breastfed till the age of 5 months
• The child was started cow milk at 1 year of age
• Weaning started by 8 months
• Before illness, caloric intake: 880kcal/day.
• Current caloric intake: 540kcal/day
• Required calories: 1250kcal/day

13. Immunization History
Immunizations was done according to EPI schedule at
age.

14. Developmental History
He has achieved developmental milestones according to
his age.

15. Personal/Schooling
History
My patient left school in one class due to financial
reasons

16. Family History
• Patient’s is a product of non-consanguineous marriage. He is 3rd
among the siblings of four. There are no similar complaints in other
family members. There is no family history of DM, TB and
Thalassemia. Mother is only Hypertensive. Other siblings are healthy
and alive.

17. Family History
8
year
s
11
years
7
year
s
3.5
years

18. Socioeconomic History
• He belongs to a lower class family. His father is Railway
employee, lives in his own house comprising of 3 rooms along
with 8 family members. They use unboiled water for drinking
purpose.

19. EXAMINATION

20. General
physical
examination
My patient was comfortably lying in bed, active and alert, with
cannula intact on dorsum of right hand.
•BP=100/70 mm Hg
•R/R = 22/min
•Temp = 98.1°F
•Pulse= 102/min
•SpaO2= 98% at room air
•Height=100cm
•Weight =18kg
•OFC =49cm
•MUAC= 15cm
•GCS= 15/15

21. General
physical
examination
• Patient is not dysmorphic and is well
hydrated
• BCG scar is present on Right arm
• Lymph nodes are not palpable
• There are no signs of the following:
• Jaundice
• Pallor
• Edema
• Clubbing

22. CVS examination
• Patient has a pulse of 102 beats per minute with normal rate,
rhythm, volume and character.
• On inspection there are no visible veins, scar marks or
pulsations.
• Apex beat is palpable in left fifth intercostal space.
• On Auscultation, Normal S1 and S2 heart sounds can be heard
with no murmurs.

23. Respiratory examination
• ENT examination is unremarkable
• Symmetrical and B/L clear chest with no added sounds and
equal air entry. No visible pigmentation or veins and intercostal
retraction.

24. GIT examination
• Symmetrical and flat abdomen with no scar marks, bruises or
striae and had centrally inverted umbilicus.
• Soft –tender abdomen with hepatomegaly 2.5cm below costal
margin.
• Spleen 4cm palpable
• No masses felt
• Hernial orifices are intact, and Genitalia are normal looking

25. CNS examination
• There’s normal power and tone in all limbs with intact reflexes
• No signs of Meningeal irritation
• Pupillary reflex is also positive (Pupils are constricted)

26. INVESTIGATIONS

27. INVESTIGATIONS
• CBC
• Blood Culture
• Urine RE
• LFTs (ALT)

28. MANAGEMENT

29. MANAGEMENT
• Supportive  Proper Hydration and Nutrition
• Specific:
1. IV Celfrixone
2. Oral Cefexime
3. Flouroquinolones
4. Azithromycin for 7 to 14 days

30. PROVISIONAL
DIAGNOSIS
ENTERIC FEVER

31. Differential diagnosis:
Meningitis
Malaria

32. ENTERIC FEVER

33. Definition:
• It is a bacterial disease caused by typhoid
bacillus.
• It is characterized by prolonged fever,
abdominal pain, diarrhea, delirium, rose
spots, and splenomegaly and complicated
sometimes by intestinal bleeding and
perforation.

34. Etiology:
• Typhoid fever is caused by salmonella
typhi.
• Paratyphoid fever is caused by
salmonella paratyphoid A,B, and C.
• Salmonella organisms are gram –ve
bacilli.
• They contain 3 types of antigens:
 O antigen (somatic or lipopolysaccharide
antigen)
 H antigen (flagellar antigen)
 Vi antigen (capsular or polysaccharide
virulence antigen)

35. Transmission:
• Infection is transmitted by ingestion of
contaminated food, milk, water, or
contact with an infected animal.
• Person-to-person spread occurs by the
Oro-fecal transmission.

36. Pathogenesis:
If the inflammation is severe, these inflammatory lesions may erode the intestinal wall leading to the intestinal
perforation.
There is necrosis of the Peyer's patches, which causes sloughing of the overlying epithelium leading to the ulcers,
which may bleed. These ulcers heal without scarring.
After ingestion, S. typhi, survives the acidity of the stomach and enters the small intestine, where bacteria
penetrate the mucosa and enter mononuclear phagocytes of ileal Peyer's patches and mesenteric lymph nodes.
Bacteria enter the body mostly by ingestion of contaminated food or water.

37. Via the intestinal lymphatics, the organisms not
destroyed by the monocytes reach the liver,
spleen, mesenteric lymph nodes, and bone
marrow and proliferate there.
At the end of the incubation period, they
pass into the blood stream and produce
bacteremia and its associated symptoms.
Pathogenesis:

38. Pathogenesis:
The bacteria then infect the gallbladder via bacteremia. The
result is that the organism re-enters the gastrointestinal tract in
the bile and reinfects Peyer patches.
Bacteria that do not reinfect the host are shed in the stool and so
become available to infect others.
Chronic carriers are responsible for much of the
transmission of the organism.

39. Clinical
features:
Disease period Sign and symptoms
First week Fever and chills gradually
increasing and persisting,
headache, abdominal
tenderness.
Second week Rash, abdominal pain,
diarrhea or constipation,
delirium, rose spots,
splenomegaly and
hepatomegaly
Third week Complications of intestinal
bleeding and perforation,
shock, melena, rigid
abdomen, coma
Fourth week and
onwards
Restoration of symptoms,
relapse, weight loss, cachexia.

41. Complications:
Intestinal
perforation
Intestinal
hemorrhage
Toxic
encephalopathy
Acute
cholecystitis or
hepatitis
Pneumonia
(superinfection)
Pyelonephritis Meningitis Osteomyelitis Septic arthritis Sepsis
Toxic
myocarditis
Fatal bone
marrow
suppression

42. Investigations
• Culture
• Blood culture (positive during the first 2 weeks)
• Urine and stool culture
• Culture of bone marrow (positive during the later stages)
• Serological tests
• Widal test: O antibody greater than 1:160 are suggestive while H
antibody titers signifies previous infection or immunization
• PCR: more specific and sensitive than blood culture
• CBC (leukopenia, normochromic normocytic anemia,
thrombocytopenia)
• Liver function Tests

43. Management
Specific

44. Supportive
• Corticosteroids in severe toxemia or prolonged
symptoms, initial dose of dexamethasone is 3mg/kg,
followed by 1 mg/kg every 6 hours for 48 hours
• Blood transfusion (anemia or severe intestinal
bleeding)
• Adequate nutrition, hydration and electrolyte
balance
• If intestinal perforation, surgical intervention with
broad spectrum antibiotics
• For thrombocytopenia, platelet transfusion to avoid
bleeding.

45. Prognosis
• Mortality rate higher than 10%
• Relapse may also occur in treated
patient after 2 weeks of stopping
antibiotics with mild symptoms
• 1-5% of enteric patients become a
carrier, chronic carriers are at
increased risk to get biliary tract
disease

46. THANK YOU!