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Showing posts with label pediatric Top-ups. Show all posts
Showing posts with label pediatric Top-ups. Show all posts

Tuesday, April 14, 2020

Prolonged Fever: 07 Essential steps to reach the diagnosis? Blind empirical drug therapy when indicated?

Prolonged Fever


STEP # 01: Keep in mind the causes of prolonged fever

These are infections & non-infectious causes

Infections causes:

Bacterial infections 
Systemic infections: Salmonellosis, brucellosis, listeriosis, leptospirosis, tularemia, tuberculosis 
Hidden focal infections: Abscess (liver, perinephric, pelvic), endocarditis, pericarditis, pyelonephritis, osteomyelitis 

Viral infections 
Infectious mononucleosis, cytomegalovirus infection, Human immunodeficiency virus (HIV), hepatitis 

Parasitic infestations 
Malaria, toxoplasmosis, visceral larva migrans

Non-infectious causes:

Rheumatic diseases
Rheumatic fever, systemic rheumatoid arthritis, polyarteritis nodosa, systemic lupus erythematosus, kawasaki disease, mixed connective tissue disease

Malignancies
Leukemia, lymphoma, neuroblastoma

Immune reactions
Drug fever, serum sickness

Other causes
Factitious fever or false fever, Crohn disease, Diabetes insipidus, Anhydrotic ectodermal dysplasia, Familial Mediterranean fever

STEP # 02: Is it  prolonged fever?

Prolonged fever is a fever with duration of more than 10 - 14 days. Although it is not as common as short febrile illness, it causes greater concern of both parents and doctors.
Fortunately, unlike adults, most cases of prolonged fever in children are caused by benign infections and the prognosis for ultimate recovery is generally good.

STEP # 03: Is it  true prolonged fever?

Is it truly a prolonged fever?
• Is there an evident cause?
• Unexplained prolonged fever... What is the cause?

Is it truly a prolonged fever?
The complaint of prolonged fever, as any other prolonged complaint, should not be accepted without careful analysis. Parents may misinterpret normal temperature as a mild fever. Careful history may reveal that the condition represents 2 short febrile illnesses rather than a prolonged one. Documentation of fever is important in accepting the complaint as a true prolonged fever.

STEP # 04: Is there an evident cause for prolonged fever?

With documented prolonged fever, detailed history and meticulous examination may
reveal an evident cause or at least suggest a specific disease.

History and examination in children with prolonged fever

Nonspecific findings denoting significant illness

Symptoms: Anorexia, weight loss.
Signs: Toxic look, pallor, cachexia, lymphadenopathy or Hepatosplenomegaly.

Specific findings suggesting a particular disease

Symptoms related to a specific system: CNS, chest, heart, GIT, urinary.

History of contact to an adult with chronic chest disease: ? Tuberculosis.

History of eating rabbit meat: ? Tularemia.

History of medications: ? Drug fever.

Rigors: Septicemia, pyelonephritis or malaria.

Pharyngitis: Infectious mononucleosis, cytomeglovirus, tularemia, toxoplasmosis.

CNS examination May suggest meningitis.

Chest examination: May reveal pneumonia or empyema.

Cardiac examination: May reveal endocarditis or pericarditis.

Abdominal examination: Liver (hepatitis, abscess) or loin tenderness (perinephric abscess).

Skeletal examination: Arthritis or osteomyelitis (focal tenderness).

Rectal examination: Focal tenderness suggests pelvic abscess.

STEP # 05: After history and examination, did you find any cause for prolonged fever?

With clinical suspicion of any disease, investigations should be directed to confirm or exclude the suspected disease.

Unexplained prolonged fever... What is the cause?
When history and physical examination fail to reveal an evident cause or to suggest a specific disease, the term “unexplained prolonged fever” or “fever of unknown origin
(FUO)” can be used. These terms should be restricted to cases of documented fever with duration of at least 10-14 days.

STEP # 06: Whether to admit or not?

In patients with good general condition and a rather short history, simple investigations (CBC, ESR, CRP, urine analysis) can be made on an outpatient basis.
Normal laboratory findings in this group indicate that the illness is mostly a benign viral infection. Reassurance and follow-up are important.

Patients with clinical findings indicating that the illness is significant should be hospitalized and further investigated. Hospitalization is also indicated in those with abnormal results of initial simple investigations.

Hospitalization is useful for several reasons:
a. Documentation of fever: Temperature should be regularly measured by a reliable person to exclude the possibility of “factitious or false fever”.
b. Drugs should be avoided as much as possible to exclude the possibility of drug fever. In this case, fever will subside within 1-3 days of discontinuation of the responsible drug.
c. Close observation for the general condition (appetite, activity, reaction to stimulation), presence of rigors (septicemia, malaria) or appearance of new symptoms or signs. Frequently, the fever may subside spontaneously without any specific therapy and even before completing the investigations.

STEP # 06: Investigations in children with unexplained prolonged fever

Nonspecific Investigations to confirm the presence of significant illness
Complete blood count (CBC): Leukocytosis, leukopenia or eosinophilia (larva migrans).
Erythrocyte sedimentation rate (ESR): Above 30 mm (first hour).
C-reactive protein (CRP): Above 20 - 30 mg/liter.
Chest X-ray: Pneumonic consolidation or pulmonary infiltrate.

Specific investigations to identify the causative disease
Initial investigations
Blood culture (aerobic and anaerobic): May be repeated.
Urine culture.
Tuberculin test and culture of gastric washing.
Blood film for malaria.
Common serological tests: Typhoid, infectious mononucleosis (monospot), brucella.

When the above specific initial investigations are negative
Specific blood culture for listeriosis, leptospirosis, tularemia.
Specific serological tests for leptospirosis, tularemia, toxoplasmosis.
Bone marrow examination (for leukemic blast cells) and culture (bacteria).
Abdominal ultrasonography: For liver abscess, epinephric abscess.
Echocardiography: In patients with preexisting cardiac disease (infective endocarditis).

When all of above are negative
Lymph node biopsy: May reveal lymphoma.
Radioactive scanning: May reveal osteomyelitis.
Total body CT scanning or MRI: May reveal hidden tumors.

Remember: International studies showed that in 25% of cases, the cause remains unknown even after exhaustive investigations.

STEP # 07: Blind empirical drug therapy may or may not be started? When indicated?

Blind empirical drug therapy should be generally avoided as it may mask the condition and makes the diagnosis more difficult. Exceptions to this rule are:
a. Blind antibiotic therapy in patients with the clinical diagnosis of septicemia but the organism could not be isolated.
b. Blind antituberculous therapy in sick patients with cachexia and weight loss and when the possibility of tuberculosis is strongly standing in spite of the negative laboratory investigations.



Sunday, April 12, 2020

Causes of recurrent pneumonia in Pediatrics: Pediatrics Top-ups

What are the causes of recurrent pneumonia in Pediatrics?

• Aspiration susceptibility: Oropharyngeal incoordination,   vocal cord paralysis, gastroesophageal reflux, tracheoesophageal fistula

• Immunodeficiency: Congenital, acquired

• Congenital cardiac defects: Atrial septal defect, ventricular septal defect, patent ductus arteriosus

• Abnormal secretions or reduced clearance of secretions: Asthma, cystic fibrosis, ciliary dyskinesia

• Pulmonary anomalies: Sequestration, cystic adenomatoid malformation

• Airway compression or obstruction: Foreign body, vascular ring, enlarged lymph node, malignancy

• Miscellaneous: For example, sickle cell disease, sarcoidosis

Can a chest radiograph reliably distinguish between viral and bacterial pneumonia?

Can a chest radiograph reliably distinguish between viral and bacterial pneumonia?


No. Viral infections more commonly have multifocal interstitial, perihilar, or peribronchial infiltrates; hyperinflation; segmental atelectasis; and hilar adenopathy. Effusions are uncommon. However, there can be considerable overlap in features with bacterial (and chlamydophilal and mycoplasmal) pneumonia. Bacterial pneumonia more commonly results in lobar and alveolar infiltrates, but the sensitivity and specificity of this finding are not very high.

But most children with alveolar pneumonia, especially those with lobar infiltrates, have laboratory evidence of a bacterial infection. Interstitial infiltrates are seen in both viral and bacterial pneumonias.


For detail study, you can visit at 

What is the risk for epilepsy after a simple febrile seizure?

What is the risk for epilepsy after a simple febrile seizure?



The risk depends on several variables. In otherwise normal children with a simple febrile seizure, the risk for later epilepsy is about 2%. The risk for epilepsy is higher if any of the following is present:
• There is a close family history of nonfebrile seizures.
• Prior neurologic or developmental abnormalities exist.
• The patient had an atypical or complex febrile seizure, defined as focal seizures, seizures lasting at least 15 minutes, and/or multiple attacks within 24 hours.
One risk factor increases the risk to 3%. If all three risk factors are present, the likelihood of later epilepsy increases to 5% to 10%.

Thursday, April 9, 2020

INFANTILE SPASM and INFANTILE SPASM TREATMENT

INFANTILE SPASM and INFANTILE SPASM TREATMENT


INFANTILE SPASM (WEST syndrome):

  • Steroids and Vigabatrin are considered as the first line medications for infantile spasms and ACTH injections are not considered superior to oral prednisolone in treatment of infantile spasms.

  • For tuberous sclerosis, Vigabatrin should be used as first line, without steroids
  • If not tuberous sclerosis: Combination therapy with steroids and vigabatrin has been shown to produce quicker spasm resolution


HIGH DOSE ACTH PROTOCOL IN INFANTILE SPASM:

Schedule
Dose IM
Day 1-14 (week 1 and 2)
75 Units/m2/dose twice a day, may receive only 1 dose on day1
Taper over 2 weeks (weeks 3 and 4)
Day 15-17
30 Units/m2/dose every morning
Day 18-20
15 Units/m2/dose every morning
Day 21-23
10 Units/m2/dose every morning
Day 24-30
10 Units/m2/dose every other morning

Treatment failure: If ACTH treatment has failed after 2 weeks
Then what to do?
  • Consider switching to an alternative agent with a different mechanism of action (i.e. vigabatrin). Taper ACTH according to the protocol above, while simultaneously beginning an alternative agent.
  • Gastrointestinal prophylaxis: H2 blocker or proton pump inhibitor is required during the full course of ACTH treatment (e.g. ranitidine, omeprazole, or lansoprazole). GI prophylaxis can be stopped when ACTH is stopped.
  • PJP prophylaxis: Patients will be immunosuppressed while on ACTH and for weeks after ACTH treatment. PJP prophylaxis is needed with Bactrim 2.5 mg/kg/dose two times a day or BID on three consecutive days each week (preferred practice is Monday, Tuesday and Wednesday) during ACTH treatment and for an additional 4 weeks after ACTH treatment is stopped.
  • Immunizations: In general, children receiving high dose systemic corticosteroids (such as ACTH or prednisolone) should NOT receive LIVE-virus vaccines until 4 weeks after discontinuation of steroids. Inactivated vaccines may be temporarily deferred until corticosteroids are discontinued or may be given during corticosteroid treatment if caregiver adherence with follow-up is not likely.
  • Stress dose steroids: At the cessation of steroids or with illness, there may be a need for stress dose steroids. Patients will have adrenal insufficiency after the course of ACTH for as long as they received the medication, (e.g. a patient treated with 4 weeks of ACTH will have adrenal insufficiency for 4 weeks following cessation of therapy). They should be evaluated by a physician for any signs of illness including fever, vomiting, diarrhea, or with trauma to assess for hypoglycemia and hypotension.


Monitoring:
  • Common side effects from ACTH include hypertension, hyperglycemia, irritability, immunosuppression, stomach irritation, increased appetite, and adrenal crisis (especially if stopped abruptly).
  • Hypertension: Blood pressure monitoring is required 2-3 times per week.
  • Sustained hypertension is defined as systolic blood pressure (SBP) greater than 95th% (in children 100 is >95th %) on 3 consecutive days.
  • Sustained hypertension can be a sign of steroid-induced endocrine dysfunction or cardiomyopathy (septal hypertrophy), which can develop after 5+ days of ACTH treatment. BP monitoring and prompt attention to hypertension is critical.
  • Hyperglycemia: Weekly glucose monitoring is required.
  • If hyperglycemia occurs (glucose is >200), ensure the patient’s PCP is involved. Draw a BMP to check for hypokalemia. Insulin treatment may be required.


ORAL PREDNISOLONE PROTOCOL:
Low dose 4mg/day vs high dose 8mg/day (max: 60mg/day)

Days
Dose
1-14
2.6mg/kg/day 3 times a day (8mg/kg/day) Maximum dose 60mg/day
15-21
2.6mg/kg/day 2 times a day
22-28
2.6mg/kg/day 1 time a day
29
Stop

Treatment failure: If ACTH treatment has failed after 2 weeks
Then what to do?
Consider switching to an alternative agent with a different mechanism of action (i.e. vigabatrin). Taper ACTH according to the protocol above, while simultaneously beginning an alternative agent.

FOLLOW-UP FOR ALL THERAPIES:
  • Following the initiation of any first-line treatment, efficacy of therapy should be assessed by 2 weeks.
  • Short-term outcomes include cessation of spasms and EEG confirmation of treatment response showing resolution of hypsarhythmia.
  • §  EEG should be used to assess for resolution of spasms and hypsarhythmia at 12-16 days. EEG should be of sufficient duration to include wake and sleep.

If spasms or hypsarhythmia persist at 2 weeks then:
  • Many children will respond to an alternative first-line therapy. Consider switching treatment to an alternative first-line treatment with a different mechanism of action. Follow the weaning protocols outlined for the specific first-line agent.
  • Efficacy of the alternative therapy should also be assessed at 2 weeks, as above.
  • In patients without a clear etiology for IS, consider vitamin B6 diagnostic challenge.
  • If spasms or hypsarhythmia persists or recur 2 weeks after treatment with an alternative first-line medication, consider prompt referral to an epileptologist to pursue additional treatment options.
  • Consider repeat EEG 1-4 weeks after completion of treatment to confirm sustained efficacy. Also consider repeat EEG if there is concern for developmental plateau/regression or clinical seizures.
  • If spasms or hypsarhythmia abnormalities persist or recur in the absence of an established etiology, or if the child does not follow the expected treatment course based on the established etiology, the etiology should be further investigated, to include at least 1 of the following: repeat video EEG monitoring, MRI, or genetic/metabolic studies.
  • Neuropsychological testing is recommended within the first two years of life.



VIGABATRIN
Dosing (Infants and children 1 month – 2 years):
  • 25 mg/kg/dose twice a day – increase by 25-50 mg/kg/DAY increments every 3 days for spasm control, to max of 75mg/kg/dose twice a day.
  • At conclusion of treatment, vigabatrin should be tapered off by 25-50 mg/kg/DAY every 3-4 days.
  • Treatment failure: If vigabatrin treatment has failed after 2 weeks, consider switching to an alternative agent with a different mechanism of action (i.e. ACTH or prednisolone).
  • Vigabatrin should be weaned by 25-50 mg/kg/DAY every 3-4 days while simultaneously beginning an alternative agent.
  • Duration of therapy, if vigabatrin is successful, optimal duration of treatment is unknown. Common practice is 6 months.

Monitoring: 
  • Baseline eye exams within 4 weeks of vigabatrin initiation, every 3 months during therapy, and at 3-6 months following discontinuation of therapy are recommended for vigabatrin therapy. Pre-existing visual impairment is not a contraindication for vigabatrin treatment
  • Baseline MRI is encouraged due to vigabatrin-associated changes on MRI.

Second line treatment may include (in no recommended order as this will depend on the infant’s presentation and possible underlying aetiology):
  • Trial of Pyridoxine
  • Topiramate or zonisamide
  • Sodium valproate
  • Nitrazepam
  • Ketogenic diet ,
  • Evaluation for epilepsy Surgery
  • Where prednisolone has been used but ineffective or partially effective, there are occasional children who appear to respond to ACTH 

Wednesday, November 20, 2019

PEDIATRICS TOP-UP: Preauricular Pits/Sinus (PPS)


Preauricular Pits/Sinus (PPS)
• Small indentations located anterior to the helix and superior to the tragus

• Can occur unilaterally (~50%) or bilaterally (~50%)

• Prevalence ranges between 1% and 10% depending on ethnicity

• Can occur in isolation with no increased risk of hearing impairment or renal         issues

• Can be associated with hearing impairment and organ malformations

• Branchio-oto-renal (BOR) syndrome:
–– Most common inherited syndrome causing hearing loss (autosomal dominant)
–– Clinical presentation: preauricular pits, sensorineural hearing loss (SNHL), branchial cysts (may present as holes/pits in the side of the neck or as tags/pits in front of the ear), renal anomalies

• Beckwith-Wiedemann syndrome:
–– Clinical presentation: macroglossia, asymmetric ear lobules or creases, omphalocele, Wilms tumor, hepatoblastoma.
–– Hearing loss can present later in childhood as conductive or mixed hearing loss

• PPS do not require surgical excision unless they are frequently draining or infected
• Passing of prenatal hearing screen should be confirmed in all patients
• Audiogram should be performed if there are other outer ear deformities or any evidence of genetic syndromes

When to suggest renal ultrasound in children with ear anomalies when accompanied by any of the following:
–– Other known organ malformations
–– Family history of deafness and auricular and/or renal malformation
–– Maternal history of gestational diabetes mellitus

Tuesday, October 1, 2019

PEDIATRIC TOP_UPS: SIMPLE QUESTIONS AND SIMPLE ANSWERS

SIMPLE QUESTIONS AND SIMPLE ANSWERS


QUESTION#01
A diabetic child receives regular and NPH insulin twice daily.Blood glucose in 4 AM is elevated (250) and is normal in 12 MN (120 mg/dL).

WHAT TO DO?

QUESTION#02

4.0 kg weight of newborn whose present hemoglobin is 5.0 m g/100 cc. Child needs transfusion of packed RBC to increase hemoglobin up to 12. 

HOW MUCH BLOOD IS REQUIRED?
Click here for 

QUESTION#03
RASH: MENTION ONLY ONE DISEASE
  RASH 

 Erythema marginatum

 Erythema migrans 

 Erythema multiforme exudativum

 Erythema multiforme, maculopapular or scarliniform

 Erythema nodosum


A 8-year-old boy cam e for a routine physical examination. Physical examination: height (75th percentile), weight (above 95th percentile), and Tanner stage I (genitalia).



QUESTION#05
A patient appears with Kawasaki disease and abdominal pain: 

WHAT MAY BE THE CAUSE? 




Sunday, September 22, 2019

INFANTILE SPASM and INFANTILE SPASM TREATMENT


INFANTILE SPASM (WEST syndrome):

  • Steroids and Vigabatrin are considered as the first line medications for infantile spasms and ACTH injections are not considered superior to oral prednisolone in treatment of infantile spasms.

  • For tuberous sclerosis, Vigabatrin should be used as first line, without steroids
  • If not tuberous sclerosis: Combination therapy with steroids and vigabatrin has been shown to produce quicker spasm resolution


HIGH DOSE ACTH PROTOCOL IN INFANTILE SPASM:

Schedule
Dose IM
Day 1-14 (week 1 and 2)
75 Units/m2/dose twice a day, may receive only 1 dose on day1
Taper over 2 weeks (weeks 3 and 4)
Day 15-17
30 Units/m2/dose every morning
Day 18-20
15 Units/m2/dose every morning
Day 21-23
10 Units/m2/dose every morning
Day 24-30
10 Units/m2/dose every other morning

Treatment failure: If ACTH treatment has failed after 2 weeks
Then what to do?
  • Consider switching to an alternative agent with a different mechanism of action (i.e. vigabatrin). Taper ACTH according to the protocol above, while simultaneously beginning an alternative agent.
  • Gastrointestinal prophylaxis: H2 blocker or proton pump inhibitor is required during the full course of ACTH treatment (e.g. ranitidine, omeprazole, or lansoprazole). GI prophylaxis can be stopped when ACTH is stopped.
  • PJP prophylaxis: Patients will be immunosuppressed while on ACTH and for weeks after ACTH treatment. PJP prophylaxis is needed with Bactrim 2.5 mg/kg/dose two times a day or BID on three consecutive days each week (preferred practice is Monday, Tuesday and Wednesday) during ACTH treatment and for an additional 4 weeks after ACTH treatment is stopped.
  • Immunizations: In general, children receiving high dose systemic corticosteroids (such as ACTH or prednisolone) should NOT receive LIVE-virus vaccines until 4 weeks after discontinuation of steroids. Inactivated vaccines may be temporarily deferred until corticosteroids are discontinued or may be given during corticosteroid treatment if caregiver adherence with follow-up is not likely.
  • Stress dose steroids: At the cessation of steroids or with illness, there may be a need for stress dose steroids. Patients will have adrenal insufficiency after the course of ACTH for as long as they received the medication, (e.g. a patient treated with 4 weeks of ACTH will have adrenal insufficiency for 4 weeks following cessation of therapy). They should be evaluated by a physician for any signs of illness including fever, vomiting, diarrhea, or with trauma to assess for hypoglycemia and hypotension.


Monitoring:
  • Common side effects from ACTH include hypertension, hyperglycemia, irritability, immunosuppression, stomach irritation, increased appetite, and adrenal crisis (especially if stopped abruptly).
  • Hypertension: Blood pressure monitoring is required 2-3 times per week.
  • Sustained hypertension is defined as systolic blood pressure (SBP) greater than 95th% (in children 100 is >95th %) on 3 consecutive days.
  • Sustained hypertension can be a sign of steroid-induced endocrine dysfunction or cardiomyopathy (septal hypertrophy), which can develop after 5+ days of ACTH treatment. BP monitoring and prompt attention to hypertension is critical.
  • Hyperglycemia: Weekly glucose monitoring is required.
  • If hyperglycemia occurs (glucose is >200), ensure the patient’s PCP is involved. Draw a BMP to check for hypokalemia. Insulin treatment may be required.


ORAL PREDNISOLONE PROTOCOL:
Low dose 4mg/day vs high dose 8mg/day (max: 60mg/day)

Days
Dose
1-14
2.6mg/kg/day 3 times a day (8mg/kg/day) Maximum dose 60mg/day
15-21
2.6mg/kg/day 2 times a day
22-28
2.6mg/kg/day 1 time a day
29
Stop

Treatment failure: If ACTH treatment has failed after 2 weeks
Then what to do?
Consider switching to an alternative agent with a different mechanism of action (i.e. vigabatrin). Taper ACTH according to the protocol above, while simultaneously beginning an alternative agent.

FOLLOW-UP FOR ALL THERAPIES:
  • Following the initiation of any first-line treatment, efficacy of therapy should be assessed by 2 weeks.
  • Short-term outcomes include cessation of spasms and EEG confirmation of treatment response showing resolution of hypsarhythmia.
  • §  EEG should be used to assess for resolution of spasms and hypsarhythmia at 12-16 days. EEG should be of sufficient duration to include wake and sleep.

If spasms or hypsarhythmia persist at 2 weeks then:
  • Many children will respond to an alternative first-line therapy. Consider switching treatment to an alternative first-line treatment with a different mechanism of action. Follow the weaning protocols outlined for the specific first-line agent.
  • Efficacy of the alternative therapy should also be assessed at 2 weeks, as above.
  • In patients without a clear etiology for IS, consider vitamin B6 diagnostic challenge.
  • If spasms or hypsarhythmia persists or recur 2 weeks after treatment with an alternative first-line medication, consider prompt referral to an epileptologist to pursue additional treatment options.
  • Consider repeat EEG 1-4 weeks after completion of treatment to confirm sustained efficacy. Also consider repeat EEG if there is concern for developmental plateau/regression or clinical seizures.
  • If spasms or hypsarhythmia abnormalities persist or recur in the absence of an established etiology, or if the child does not follow the expected treatment course based on the established etiology, the etiology should be further investigated, to include at least 1 of the following: repeat video EEG monitoring, MRI, or genetic/metabolic studies.
  • Neuropsychological testing is recommended within the first two years of life.



VIGABATRIN
Dosing (Infants and children 1 month – 2 years):
  • 25 mg/kg/dose twice a day – increase by 25-50 mg/kg/DAY increments every 3 days for spasm control, to max of 75mg/kg/dose twice a day.
  • At conclusion of treatment, vigabatrin should be tapered off by 25-50 mg/kg/DAY every 3-4 days.
  • Treatment failure: If vigabatrin treatment has failed after 2 weeks, consider switching to an alternative agent with a different mechanism of action (i.e. ACTH or prednisolone).
  • Vigabatrin should be weaned by 25-50 mg/kg/DAY every 3-4 days while simultaneously beginning an alternative agent.
  • Duration of therapy, if vigabatrin is successful, optimal duration of treatment is unknown. Common practice is 6 months.

Monitoring: 
  • Baseline eye exams within 4 weeks of vigabatrin initiation, every 3 months during therapy, and at 3-6 months following discontinuation of therapy are recommended for vigabatrin therapy. Pre-existing visual impairment is not a contraindication for vigabatrin treatment
  • Baseline MRI is encouraged due to vigabatrin-associated changes on MRI.

Second line treatment may include (in no recommended order as this will depend on the infant’s presentation and possible underlying aetiology):
  • Trial of Pyridoxine
  • Topiramate or zonisamide
  • Sodium valproate
  • Nitrazepam
  • Ketogenic diet ,
  • Evaluation for epilepsy Surgery
  • Where prednisolone has been used but ineffective or partially effective, there are occasional children who appear to respond to ACTH