Pediatric Flashcards
incidence of AKI
varies from 2–5% of all hospitalizations to > 25% in critically ill infants and children.
Laboratory findings of aki
Anemia due to 1- hemolytic(SLE, RVT, HUS) 2- delutional Leucopenia(SLE) Thrombocytopenia((SLE, RVT, HUS) Hyponatremia(delutional) Metabolic acidosis BUN, S.Cre increase Uric acid , K+, Ph++, increase CA++ low C3 level low in(SLE, PSGN, radiation GN, membarenoprolefrative) Abs in PSGN GUA 1- RBC, protienurea, granuler cast, internsic cause 2- WBC, WBC cast, low grade protienurea, RBC, tubulointerstesial disease CXR cardiomegaly, pulmonary edema.
Renal U/S hydronephrosis, hydroureter, obstruction Renal biopsy may needed.
Ttt of aki
Infant and children with obstruction or non ambulatory bladder catheter, to collect UOP
- fluid therapy according to volume status
A- in case of Hypovolemia, N/S 20 CC/kg within 30 min may repeated 2 or 3 times and watch the UOP in 2 hour , if possible of internsic or post renal.
Diuretics indicated provided that good volume status Frusamide
-4 mg/kg+MANITOL 0.5 g/kg , if no UOP within 30 min consider diuretic infusion , if no UOP, consider Dopamin
-3Mg/kg/min with diuretic , if no UOP, stop diuretic and should be restricted.
-in case of normal volemia consider(insensible water loss) cc/m2 /day + the fluid equal to the UOP.
child
fluid
- In case of Hypervolemia
insensible water loss and
UOP
should be omitted.
Type of the fluid is glucose-containing solution maintaince .
10-30%
Input, output, UOP, chemistry should be checked daily
3- Hyperkalemia >6mg/dl
may lead to cardiac arrythemia
and
g/kg
PH
,
with
If
If
4 <
5 and Ca
(ECG=tent T wave , widing QRS, ST depression, arrest).
Indication of withholding of K+(fluid, diet)+Resin 1 orally or rectally by enema every 2-4 hour.
> 7mg/dl give the flowing
➢ Ca.gluconate 10% 1cc/kg within 3-5min
➢ NACO3 1-2cc/kg over 5-10min
➢ Reguler insulin 0.1U/kg with glucose 50% 1
over 1hour.
in spite of all these measure , still persistent hyperkalemia consider dialysis.
- Acidosis if mild rarely need treatment , if sever
cc/kg
7.15
NAHCO3 <8
with hyperkalemia
need
NAHCO3 infusion (desire PH 7.2, NAHCO3 12).
- Hypocalcemia primarily treated by lowering S.PH++ Ca++ sh be not given I-V unless with tetany to . deposition in tissue, use Ca. carbonate 1 -3 tab
ovoid
meal. 6- Hyponatremia delutional need fluid restriction , if <120 or symptomatic(seizure, lethargy )need 3%NACL .
NACL in m.ag required=0.6XBwt X (125- s.NA) 7- Bleeding due to platelet dysfunction, stress, heparin(dialysis), need oral or I.V H2 blocker ranitidine 8- HT in GN, HUS, need salt and water restriction, Nefidipine 0,25-0,5mg/kg every 2-6hour(max 10mg), B.blocker,long acting Ca.cannel blocker., if sever crisis need NA nitropruside or Labetalol infusion.
9- Anemia mild, delutional , packed RBC, 10 cc/kg within 4-6hour if Hb <7g/dl(better fresh) 10- nutrition NA, PH, K, should be restricted in most cases, protein should be moderately decrease, increase calorie intake.
Indications of dialysis in aki
- -Volume over load +evidence of HT, and /or pulmonary edema refractory to treatment
- Persistent hyperkalemia
- Sever acidosis unresponsive to treatment
- Neurological symptoms(alter mental state , seizure)
- BUN >100-150mg/dl or lower if rapidly rising.
- Ca/Ph imbalance with hypocalcemia tetany .
- Inability to provide adequate nutritional intake because of need for sever fluid restriction.
Intermittent hemodialysis
Pertonial daylsis
Crrt
In aki
Intermittent hemodialysis ➢ Is useful in patients with relatively stable hemodynamic status.
➢
➢
This highly efficient process accomplishes both fluid and electrolyte removal in 3-4 hr sessions using a pump -drive nextracorporeal circuit and large central venous catheter.
3-7 times per week based on the patient’s fluid and electrolyte balance. Peritoneal dialysis
➢ Is most commonly employed in neonates and infants with AKI
➢ Hyperosmolar dialysate is infused into the peritoneal cavity via a surgically or percutaneous placed peritoneal dialysis catheter.
➢ The fluid is allowed to dwell for 45-60 min and is then
drained from the patient by gravity (manually or with
the use of machine-driven Cycling.
➢ Cycles are repeated for 8-24 hr/day based on the
patient’s fluid and electrolyte balance.
➢ Anticoagulation is not necessary.
➢ Contraindicated in patients with significant abdominal
pathology. Continuous renal replacement therapy (CRRT)
➢ ➢ ➢ ➢
➢
Is useful in patients with unstable hemodynamic status Concomitant sepsis Multi organ failure in the intensive care setting.
CRRT is an extracorporeal therapy in which fluid, electrolytes, and small- and medium-size solutes are
continuously removed from the blood (24 hr/day) using a specialized pump-driven machine. Usually, a doublelumen catheter is placed into the subclavian, internal jugular, or femoral vein
Micronutrient deficiency
Ida
common in childhood either from low iron intakes or poor absorption, or as a result of illness or parasite infestation . Hemoglobin cutoffs to define anemia are 110 g/L for children 6-59 mo, 115 g/L for children 5-11 yr, and 120 g/L for children 12-14 yr. Cutoffs to define anemia for nonpreg-nant women are 120 g/L, 110 g/L for pregnant women, and 130 g/L for men.
Epiglottis
Ttt
1-Epiglottitis is a medical emergency and warrants immediate treatment with an artificial airway placed under controlled conditions, either in an operating room or intensive care unit. Establishing an airway by endotracheal or nasotracheal intubation or, less often, by tracheostomy is indicated in patients with epiglottitis.
The duration of intubation depends on the clinical course of the patient and • the duration of epiglottic swelling, as determined by frequent examination using direct laryngoscopy or flexible fiberoptic laryngoscopy. In general, children with acute epiglottitis are intubated for 2-3 days, because the response to antibiotics is usually rapid.
2-Ceftriaxone, cefepime, or meropenem should be given parenterally, pending • culture and susceptibility reports, because 10–40% of H. influenzae type b cases are resistant to ampicillin.
3-Epiglottitis resolves after a few days of antibiotics, and the patient may be • extubated; antibiotics should be continued for at least 10 days.
Croup
Cf
Oe
Dx
Ttt
Complications
Resolved from er
The term laryngotracheobronchitis refers to viral infection of the glottic and subglottic regions 1-Most patients have an upper respiratory tract infection with some combination of rhinorrhea, pharyngitis, mild cough, and low-grade fever for 1-3 days before the signs and symptoms of upper airway obstruction become apparent.
2-The child then develops the characteristic barking cough, hoarseness, and inspiratory stridor. The low-grade fever can persist, although temperatures may occasionally reach 39-40°C (102.2-104°F); some children are afebrile.
is
-
3- Symptoms are characteristically worse at night and often recur with decreasing intensity for several days and resolve completely within a week.
4-Agitation and crying greatly aggravate the symptoms and signs. The child may prefer to sit up in bed or be held upright.
5-Other family members might have mild respiratory illnesses with laryngitis.
Physical examination
1-reveal a hoarse voice, coryza, normal to moderately inflamed pharynx, and a slightly increased respiratory rate.
2-Rarely, the upper airway obstruction progresses and is accompanied by an n increasing respiratory rate; nasal flaring; suprasternal, infrasternal, and intercostal retractions; and continuous stridor.
3-Croup is a disease of the upper airway, and alveolar gas exchange is usually normal.
4-Hypoxia and low oxygen saturation are seen only when complete airway obstruction is imminent.
The child who is hypoxic, cyanotic, pale, or obtunded needs immediate airway management. G Diagnosis
Croup is a clinical diagnosis and does not require a radiograph of the neck.
Radiographs of the neck can show the typical subglottic narrowing, or steeple sign, of croup on the posteroanterior view.
However, the steeple sign may be absent in patients with croup, may be present in patients without croup as a normal variant, and may rarely be present in patients with epiglottitis. TREATMENT
1- The mainstay of treatment for children with croup is airway management and treatment of hypoxia. Treatment of the respiratory distress should take priority over any testing. of
Hx
allergy 2- Most children with either acute spasmodic croup or infectious croup can & recurrent be managed safely at home.
3-Despite the observation that cold night air is beneficial, a Cochrane review 3 % s has found no evidence supporting the use of cool mist in the emergency department for the treatment of croup. 4-Nebulized racemic epinephrine is the established treatment for moderate or severe croup.
~
-
Vasoconstriction
The mechanism of action is believed to decrease the laryngeal mucosal edema.
Traditionally, racemic epinephrine, a 1 : 1 mixture of the D- and L-
isomers of epinephrine, has been administered. A dose of 0.25-0.5 mL of
2.25% racemic epinephrine in 3 mL of normal saline can be used as often as every 20 min.
Racemic epinephrine was initially chosen over the more active and more readily available -epinephrine to minimize anticipated cardiovascular side effects such as tachycardia and hypertension. Current evidence does not favor racemic epinephrine over L-epinephrine (5 mL of 1 : 1,000 solution) in terms of efficacy or safety. &
L
En The indications for the administration of nebulized epinephrine include
0 >moderate to severe stridor at rest, ②
> the possible need for intubation,
use Children with croup should be hospitalized for any of the following:
> progressive stridor,
> severe stridor at rest, respiratory distress, >hypoxia, cyanosis,
> depressed mental status,
> poor oral intake, or the need for reliable observation 5-The effectiveness of oral corticosteroids in viral croup is well established.
Corticosteroids decrease the edema in the laryngeal mucosa through their antiinflammatory action.
Oral steroids are beneficial, even in mild croup, as measured by reduced hospitalization, shorter duration of hospitalization, and reduced need for subsequent interventions such as epinephrine administration.
Most studies that demonstrated the efficacy of oral dexamethasone used a single dose of 0.6 mg/kg.
Intramuscular dexamethasone and nebulized budesonide have an equivalent clinical effect; oral dosing of dexamethasone is as effective as intramuscular administration. Indication for discharge from ER Patients can be safely discharged home after a 2-3 hr period of observation provided they have
> no stridor at rest;
> have normal air entry,
> normal pulse oximetry,
> and normal level of consciousness;
> and have received steroids. most likely
=>
no
progression. COMPLICATIONS
Complications occur in approximately 15% of patients with viral croup. The most common is
> extension of the infectious process to involve other regions of the respiratory tract, such as the middle ear, the terminal bronchioles, or the pulmonary parenchyma.
> Bacterial tracheitis may be a complication of viral croup rather than a distinct disease.
> Pneumomediastinum and pneumothorax are the most common complications of tracheotomy.
Bacterial tracheitis
Bacterial tracheitis is an acute bacterial infection of the upper airway that is potentially life-threatening.
> S. aureus is the most commonly isolated pathogen, with isolated reports of methicillin-resistant S. aureus. S. pneumoniae, S. pyogenes, Moraxella catarrhalis, nontypeable H. influenzae; anaerobic organisms have also been implicated.
> The mean age is between 5 and 7 yr. There is a slight male predominance.
> Bacterial tracheitis often follows a viral respiratory infection (especially laryngotracheitis), so it may be considered a bacterial complication of a viral disease, rather than a primary bacterial illness.
This life-threatening entity is more common than epiglottitis in vaccinated populations CLINICAL MANIFESTATIONS
Typically the child has a brassy cough, apparently as part of a viral
laryngotracheobronchitis.
1-High fever and toxicity with respiratory distress can occur immediately or after a few days of apparent improvement.
2-The patient can lie flat, does not drool, and does not have the dysphagia associated with epiglottitis. The usual treatment for croup (racemic epinephrine) is ineffective. DIAGNOSIS
The diagnosis is based on evidence of bacterial upper airway disease, which includes high fever, purulent airway secretions, and an absence of the classic findings of epiglottitis. X-rays are not needed but can show the 1`purulent material is noted below the cords during classic findings ; endotracheal intubation
TREATMENT
Appropriate antimicrobial therapy, which usually includes antistaphylococcal agents, should be instituted in any patient whose course suggests bacterial tracheitis.
1-Empiric therapy recommendations for bacterial tracheitis include vancomycin or clindamycin and a 3rd -generation cephalosporin (e.g., ceftriaxone or cefepime).
2-When bacterial tracheitis is diagnosed by direct laryngoscopy or is strongly suspected on clinical grounds, an artificial airway should be strongly considered. Supplemental oxygen is usually necessary. Intubation or tracheostomy may be necessary, but only 50–60% of patients require intubation for management; younger patients are more likely to need intubation.
Fate of asthma
in general , the prognosis is good in young children : –
1- 50% of all patients are virtually free of symptoms within 1020years but recurrence are common in adulthood .
2- children who have mild asthma with onset between 2year & puberty , the remission rate is about 50% & only 5% experience sever asthma .
3- children with sever asthma characterized by steroid dependent with frequent hospitalization rarely improved & about 95% become adult asthma .
Asthma
Exercise test
running for 1-2 minutes causing bronchdilator , while prolong strenous exercise leading
to bronchconstriction .
Before test doing : bronchodilator and cromolyn withhold for at least 6-8 hour , while slow releasing theophylin should not be administered at least 12 -24 hr prior the test .
The test done by treadmill through running 3-4 mile / hr up to 15% grade while breathing through mouth for at least 6 minute leading to air way obstruction .
PFT ( pulmonary function test ) done immediately before and after test , 5 , 10 minute Showing decreased PEFR or FEV in one second of at least 15% without premedication . Note :– if no air way obstruction , it is best to repeat the test in other day when relative humidity is low .
UTI
Introduction & aetiology
UTIs) commonly occur in children of all ages, UTIs are most common in children under age 1 yr
➢ 1-3% of girls and 1% in boys ➢ In girls, Peak via infancy and toilet training, after the 1st
attack of girls, 60-80% will develop 2nd attack of UTI, within
18 months ➢ In boys, more common in 1st year and much more common
in uncircumcised, ➢ In 1st year M/F 2.8:5.4, beyond infancy , the ratio is 1:10
▪Atiology ➢ Mainly by colonic bacteria, in female, 54–67% due to E-coli
followed by proteus and Kliebsiella .
➢ In male, older than 4 year , proteus common as E-coli,
reported G+ve in male ➢ Staph-saprophyticus is a pathogen in both sex ➢ Virus(adeno) 11,21 cystitis ➢ UTI have been consider as imported cause in development of
renal insufficiency and end stage renal disease
UTI
Cf
Dx
➢ Abd pain(flank) ➢ Fever(may be the only manifestation), particular consideration
~
un
=>
bilateral flank pain
usually
related
to
muscle
not
to renal
Cause
.
should occur for a temperature > 39°C without another source lasting more than 24 hr for males and more than 48 hr for females => Considered UTI With exclusion of other causes of fever such CNS and .
as
➢ Malaise
as
respiratory
➢ Nausea ➢ Vomiting ➢ Accasionlly diarrhea ➢ In newborn and infant, nonspecific (irritability, jaundice, poor
=>
due
to
irritation
of bladder
.
feeding, weight loss).
➢ Pyelonephritis is the most common serious bacterial infection in
infants <24 mo of age who have fever without an obvious focus ➢ Involvement of renal parenchyma is termed acute pyelonephritis whereas if there is no parenchymal involvement, the condition maybe termed pyelitis.
➢ Renal abscess typically occurs following hematogenous spread with S. aureus or can occur following a pyelonephritic infection caused by the usual uropathogens
➢ Acute pyelonephritis can result in renal injury, termed pyelonephritic scarring.
2- Cystitis
➢ Bladder involvement, dysuria, frequency, urgency, suprapubic pain, incontinence, malodorous urine (is not specific for a UTI), no renal damage, no fever
not
specific and
malodorousurine
&_ &201
*
➢ Acute hemorrhagic cystitis, though uncommon in children, is often caused by E . coli; it also has been attributed to adenovirus types 11 and 21. ➢ Adenovirus cystitis is more common in boys; it is self-limiting, with hematuria lasting approximately 4 days. ➢ Patients receiving immunosuppressive therapy are at higher risk for hemorrhagic cystitis So before Chemotherapy patient
the
of
well
/
3- Asymptomatic bacteruria
hydrated
to
avoid
damage
the bladder .
➢ +ve urine culture · but no manifestation, benign condition , no treatment require ⑧ except in pregnancy Diagnosis ➢ Suspected from symptoms and/or finding of urine
analysis or both.
➢ +culture is necessary for confirmation and
appropriate treatment ➢ the Dx of UTI, depend on proper sampling of urine(4
ways) ➢ 1- Midstream urine = in child having toilet training
(in uncircumcised boy, the prepuce should be
retracted).
➢ +ve if the colony count more than 100,000 colony –
forming units(CFU) of single MO ➢ or child is symptomatic, and 10,000 CFU is consider
UTI, 2- Adhesive , sealed , sterile collecting urine bag in infant, after disinfection of skin of genitalia.
false-positive rate too high to be suitable for diagnosing UTI; false-positive S ** however, a negative culture is strong evidence that 15 3 Y UTI is absent. Negative
1
-
%
Contaminated
,
& !
dr
,
·
-
/
*
·
+ve if the colony count more than 100,000 CFU of single MO and child is symptamatic, and +ve urine analysis
however if any of this criteria are not met , we may need next way 3. Catheterized sample= proper skin preparation , gentle technique of catheter is important, feeding tube poly thene nu 5 or 8 nu with lubricant in older child to decrease risk of trauma,
+ve if more than 10 000 CFU 4- Suprapubic puncture = +ve if any MO best method
NOTE Prompt plating of urine sample is important (stay in room temp for 60 min, lead to over growth of minor contamination the may suggest UTI), put it in refrigerator.
single MO
Other indications of uti
A- pyuria (pus cell in urine A WBC count on urinalysis above 3-6 WBCs/high-powerfield) suggest UTI, this finding is more confirmatory than diagnostic.
Conversely, pyuria can be present without UTI., so its absence does not exclude UTI(sterile pyuria) Sterile pyuria (positive leukocytes, negative culture) occurs in 1- partially treated bacterial UTIs 2-viral infections 3-renal tuberculosis 4- renal abscess 5- UTI in the presence of urinary obstruction, 6- urethritis due to a sexually transmitted infection 7-inflammation near the ureter or bladder (appendicitis, Crohn disease), 8- interstitial nephritis (eosinophils)
If a child asymptomatic, GUA normal, it is unlikely UTI, however, if child B- Nitrite and leukocytestrase +ve in urine C- Microscopic hematuria is common in acute cystitis, but microhematuria alone does not suggest UTI.
D- Blood (neutrophilia, increase ESR, CRP, in renal abscess, WBC 20,000 -25,000, blood culture is indicated sepsis in infant
E-Renal Scanning with Techneutiaium- labeled DMSA(DiMarcoptoSuccinic Acid) Is the most sensitive and accurate way to detect the renal scaring. F- Urogram less sensitive than DMSA in detecting the renal scaring, and need 1-2 year to detect the pathology , risk of radiation G- CT of abdomin to detect the scaring in some time.
UTI
Ttt
1- Acute Cystitis should be treated to prevent pyelonephritis A- if symptomatic (sever), urine culture should be obtained, a 3- to 5day course of therapy with Trimethoprim-sulfamethoxazole (TMP-SMX) (6-12 mg TMP/kg/day in 2 divided doses) or trimethoprim is effective against many strains of E. coli.
Nitrofurantoin (5-7 mg/kg/24 hr in 3-4 divided doses) also is effective and has the advantage of being active against Klebsiella and Enterobacter organisms.
Amoxicillin (50 mg/kg/24 hr in 2 divided doses) also may be effective as initial treatment but has a high rate of bacterial resistance.
B- if symptomatic (less sever ),treatment started till result of urine culture. 2- Pyelonephritis
14 days course of broad spectrum of AB (Ampicillin 100 mg/kg+Gentamycin 3 -5 mg/kg, cefotaxime 100 mg/kg/24 hr, or Ceftriaxone 50-75mg/kg not exceed 2 gram)is preferable (less ototoxicity and nephrrotoxicity).
serum Cr and level of Gentamycin should be obtained before and during treatment if prolonged.
Indications of hospitalisation in uti
A- dehydration B- unable to drink C-possipble sepsis D-age less than 1month
➢ Alkalization of urine is valuable in treatment of proteus with Gentamycin.
➢ Oral 3rd generation cephalosporin (Cefixim) is effective in G-ve other than
Pseudomonas ➢ quinolone derivative is effective(contraindicated below age of 17years, effect
the growing cartilage ), occasion for short-course therapy in younger children with Pseudomonas UTI Levofloxacin is an alternative quinolone with a good safety profile in children
➢ Some outhers suggest loading dose of Ceftriaxone then oral 3rd generation cephalosporin(cefixim).
➢ In abscess percutaneous drainage +parental AB ➢ Urine culture should be obtained 1week after complete the treatment (should
be sterile)
Recurrent uti
In recurrent UTI and in absence of risk factor , periodic urine culture every 3months for 2 years (if child asymptomatic) is indicated.
In recurrent UTI , identify the risk factor and treat it and give AB prophylactic(1/3 of therapeutic dose) , Trimetheprime, Nitrofurantuine , Nalidixic acid., indicated in 1- neurogenic bladder 2- stasis due to obustruction 3- VUR 4- stone Amoxil, Keflex is effective but increase risk of breaking through UTI(become resistant)
Probiotic, cranberry juice
Recurrent UTI:
➢ Two or more episodes of UTI with acute pyelonephritis/upper
urinary tract infection, or ➢ One episode of UTI with acute pyelonephritis/upper urinary tract
infection plus one or more episode of UTI with cystitis/lower
urinary tract infection, or ➢ Three or more episodes of UTI with cystitis/lower urinary tract
infection.
Imagining in uti
Imaging Study
1-1st episode of clinical pyelonephritis 2-Those with a febrile UTI 3- In infants, those with systemic illness 4-A positive urine culture, irrespective of temperature,
a sonogram of kidneys and bladder should be performed to assess 1- Kidney size 2-Detect hydronephrosis 3- Ureteral dilation, 4- Identify the duplicated urinary tract 5- Evaluate bladder anatomy.
Next, a DMSA scan is performed to identify whether the child has acute pyelonephritis. If the DMSA scan is positive and shows either acute pyelonephritis or renal scarring,
. a voiding cystourethrogram performed in(AAP) 1-Ultrasound study is abnormal.
2-Atypical features.
(VCUG)
is
3- Recurrent febrile UTI . If reflux is identified, clinician needs to decide on whether to send the child to a facility with DMSA capability(if available) or instead do a VCUG VCUR Time= 2-6 week after infection 2types 1- Radionucltide less radiation, less anatomical differentiation 2- Contrast more radiation , good differentiation
Definitions of atypical and recurrent UTI
Atypical UTI UTI associated with sepsis or bacteraemia Concern regarding obstructive uropathy Failure to respond to antibiotics within 48 hours Associated impaired renal function (elevated creatinine level) Infection with a non E. coli organism .
Recurrent UTI:
➢ Two or more episodes of UTI with acute pyelonephritis/upper
urinary tract infection, or ➢ One episode of UTI with acute pyelonephritis/upper urinary tract
infection plus one or more episode of UTI with cystitis/lower
urinary tract infection, or ➢ Three or more episodes of UTI with cystitis/lower urinary tract
infection.
Atypical uti
UTI associated with sepsis or bacteraemia
Concern regarding obstructive uropathy
Failure to respond to antibiotics within 48 hours
Associated impaired renal function (elevated creatinine level)
Infection with a non E. coli organism
UTI
Vur
retrograde flow of urine from the bladder to the ureter renal pelvis
Normally , ureter is attached to the bladder in oblique
direction perforating between the bladder mucosa
and
detroser muscle , creating a flap-valve mechanisim that prevent reflux.
Reflux occur when the tunnel between the mucosa and detroser muscle is short or obliterated. ➢ ➢ ➢ ➢ ➢ ➢ ➢ ➢
Affecting 1–2% of children VUR usually is congenital and often is familial. 35% of sibling of a child with reflux also have a reflux VUR in 50% in boy with posterior urethral valve, 25% in neuropathic bladder, 15% in renal agenasis VUR is present in approximately 30% of females who had a urinary tract infection in 5–15% of infants with antenatal hydronephrosis.
20% of ESRD, gave a history of reflux VUR is important cause of HT in children
Clinical feature Usually discovered during evaluation of UTI, 80% in female , average age is 2-3 year Renal insufficiency, HT DIAGNOSIS 1- VCUG, reflux occurring during bladder filling is called (low pressure)or passive and less likely to show spontaneous resolution, high pressure or active more likely to show spontaneous resolution, 2- Renal U/S 3- DMSA 4- Check the Bpr , ht, wt, urine culture Natural History 1- Grade 1 and 2 ,whether uni or bilateral spontenous resolution 2- Grade 3 younger age and unilateral high rate of resolution 3- Grade 4 bilateral less likely to resolve than unilateral 4- Grade 5 rarely resolve The main age of spontaneous resolution is 6 years ▪Treatment The goal are to 1- prevent pyelonephritis 2- renal insufficiency 3- others reflux complication Treatment contain the following ➢ AB prophylaxis , urine culture ➢ VCUG every 12-18 month ➢ Check the Bpr , ht, wt frequently The above medical treatment is successful when ❖ No infection.
❖ No scar .
❖ Reflux resolve Surgical treatment indicated in ➢ New scar ➢ Breakthrough UTI ➢ Not resolve at the age more than 7 year(failure of medical treatment) ➢ Grade 4 and 5
Hereditary spherocytosis
Resulting from abnormalities of (spectrin , ankyrin and protein 4.2 , band 3 )which are major components of cytoskelton responsible of shape RBC causing loss of membrane surface without loss of volume cell shape
changed from normal biconcave disc to spherocyte of RBC( and increasing in
cation permeability , cation transport leading to spherocyte cell resulting in destructing prematurely in spleen ) which considered less deformable when passing through narrow passage in the spleen .
IS AD & less AR , 25% of all patients from mutation
C|F:—IS variable from no symptoms to sever H.A with growth failure , splenomegally & chronic transfusion requirement in infancy necessitating early splenectomy .
In neonate may presents as anemia & hyperbilirubinemia After infancy , the spleen is usually enlarge & pigmentry gall stone as early as 4-5 years Liable of aplastic crisis as result from parvo virus
Note :– hemolysis may be more prominent in neonate because HbF bind poorly with 2,3DPG causing more free 2,3DFG which destabilize interaction of spectrin, ankyrin and protein 4.2 in RBC membrane . Lab. Finding
1-
feature of hemolysis ( anemia Hb is usually 6-10gm/dl & increase retic count which
usually 6-20% with mean 10% ) 2- MCV is normal & MCHC often is increased(36-38) 3- presence of spherocyte ( more than 15-20 % ) 4- erythroroid hyperplasia .
5- gall stone Diagnosis :–
1- clinical examination .
2-lab. Finding .
3-incubated osmotic fragility test . D.D ;—other causes of spherocyte ;–
a- iso & auto immune H.A.
b- rare causes like thermal injury , clostredia infection, wilson dis.
+incubated osmotic fragility test :– RBC are incubated in progressive dilution of an iso-osmotic buffered salt solution and when exposed to hypotonic saline cause the RBC to swell called spherocyte which lyse more readily than biconcave and this is accentuated by depriving the cells of glucose over night at 37c so called incubated osmotic fragility test . Osmotic fragility test in cong. spherocytosis treatment
-
Depend on severity of anemia :–A- factor important in treatment (Hb, retic count, age , growth .
B- Folic acid 1 mg daily C- prior splenectomy should immune against pneumo coccal , meningo coccal & H. Influenza .
Should kept on pencillin as 125 mg twice daily for those of less
than 5 years of age and 250 mg for above 5years of age .
Scoring of asthma
zero
1
2
1- mental state normal 2-cynosis non 3-accessory muscle none 4-air entry good 5- pulsus paradoxus < 10 6-PaO2 70-100 7-PaCO2 <40%
agitated or depressed in room air moderate fair 10-25 < 70% in room air 40-65
coma in 40% o2 marked poor
> 25
< 70% in 40% o2
> 65
Classification of asthma
S&S 1-altertness
2- color
3-resp rate
Mild Moderate normal &may be agitated N or usual agitated
normal
pale
normal to 30%
30-50%above normal -
severe usually agitated
cyanosis
more than 50%
4-dyspnea
above normal mild dyspnea on walking
moderate sever at rest with stop feeding while at rest , softer cry & difficulty of feeding talking speak in normal speak in phrases in single word , partial phrases sentences or partial sentences Sitting can lie down prefer sitting sit upright 5-accessory no to mild moderate retraction sever with nasal flaring muscle retraction intercostal, sternal used hyperinflation of chest 6-auscultation expiratory expiratory + inspiratory silent chest 7-PEFR 70-90% above normal 40-69% less than 40% 8-Pco2 less than 42% less than 42% more than 42% 9-O2 saturation more than 95% 90-95% less than 90% `10- pao2 normal > 60% < 60% usually cyanosed
mild form : 1- shortness of breath or dyspnea 2- tachypnea ( up to 30% above normal)
moderate form :– 1- tachypnea ( from 30-50 % above normal ) 2- minimal chest wall retraction 3- flaring of alae nasi
severe form :- 1-marked tachypnea > 70 breath /min ( above 50% of normal ) 2- apneic episode / irreqular breathing / bradypnea 3- lower chest wall retractions 4- head bobbing ( used sternocleidomastoid muscle ) 5- cyanosis —————————————–Normal pulse rate :–2-12 month : 160 beat/min , 1-2 year : 120 beat/ min 2-8 years : 110 beat/min
Ttt of acute asthma
Home mgx
Written home plan can reduce the death rate by 70%
1-PEFR :- done every 2-3 times per day ( if PEFR is decreased
needs medical intervention & if decreased between 50-80%
needs change in medical therapy & if below 50% needs acute
intervention
2-inhalation therapy by ventolin inhaler up to 3 time /hour( good response characterized by resolution of symptoms within 1 hour , no further symptoms over next 4 hrs and improvement in PEF peak expiratory flow value to at least 80% ).
3-incomplete response ( persistent symptoms , PEF < 80%) :–needs short course of oral cortico steriod like prednisolone 1-2mg/kg/day for 4 days plus inhaled B agonist therapy . .
4- medical attention:-should be looking for or sought for :1- sever exacerbation & persistent respiratory distress , 2- lack of expected response or lack of sustained improvement after initial therapy 3-further deterioration or high risk factors of asthma morbidity or mortality ..
Ttt of acute asthma
Er
1-correction of hypoxia , 2- rapid improvement of air way obstruction , 3-prevention of
progression or recurrence of symptoms .
Intervention or treatment depend on clinical severity on arrival , response to initial therapy, and risk factors associated with increased morbidity and mortality .
1-O2 therapy :-to improve oxygenation which given by mask or nasal
prongs 2-3/ min.( hypoxia caused by acute episode of asthma and drugs used in treatment like B-agonist , aminophylin ( as result in VPM through pulmonary vasodilator and increased cardiac output . Mist tent should not be used as resulting in irritation leading to coughing and worsening
wheezing . .
2-ventolin or albuterol nebulizer 0.15mglkg every 20 minutes for one hour.
Inhaled iprotropium bromide ( given if no significant response is seen within first inhaled B agonist & given every 6 hr in a dose o.25 mg for 6 years of age and 0.5 mg for those 12 years of age 3-may need systemic Cortico.Steriod either orally or I.V 4-in sever case , used intra muscular or subcutaneous adrenalin 0.01ml/kg given once or twice at interval 20 minutes to obtain optimum relief ( 0.05 ml is often effectively in infant and young children ) after one hr —re-asses :1-if sustained improvement of symptoms , normal physical finding & O2 saturation of more than 92% , PEF of more than 70% for 3 hr home discharge .
if discharge , on 1-ventolin inhaler for above 5 years or oral salbutamol 2-.3-7 day course of C.S 3- if no response ( persistent symptoms ) —asses & hospital admission :
—a- if moderate distress needs ward admission b- if sever distress needs I.C.U
Indications of hospital for acute asthma
1-moderate to sever exacerbation that not improved within 1-2hr from intensive therapy in emergency ward .
2-has risk factors for morbidity & mortality ( risk factors for sever asthma ) :–A- biological – 1-previous sever asthma exacerbation 2-sever air way obstruction 3- rapid attack 4- sever air way hyper-responsiveness 5-poor response to systemic C.S ⑤ Case form) 6-repeated visit to emergency ward in last 48 hrs * leven in mild 7-2 or more hospital admission of the past year or 3-4 emergency visit in last year . .
B-economic & psycho-social :-1- poverty 2- crowding 3-mother less than 20 years 4- poor education 5-family dysfunction Ji & 6- psychopath in parent & children C-environment :- 1- allergen exposure 2-smoking 3-air pollution 4-urban environment
Status asthmatics
Def
Mgx
A-admission to I.C.U & doing chart for observation for PR,RR, BP & decrease , send for CBP, S.electrolyte , cardiac monitor & blood gas return to infections & Nat(SIADA) ↳ arrhythmia due hypoxia or drugs analysis ( PO2, PCO2, PH 2 hypokalemia ) kt ↑ if there (due to
normal
when
hypoxia
subside.
->
to
2
BP in normal
hypoxia
when
hypoxia
hypoxia
Subside
-
->
decrease intake
of It
is
due monitor to B-start therapy :- aminophylin) 1- O2 therapy to maintain PO2 70-90% or O2 saturation above 92%
response to
or
TX
.
drugs
return to
such
as
nubiulizer
or
normal
when
hypoxia
Subside
z G
①
&
2- correction of dehydration: from insensible water loss , decreased intake of fluid & and duiretic effect of aminophylin ( should be given 2/3 of maintainance ) 3- bronch-dilator by a-continuous or frequent Nebulizer with O2 b- aminophylin( 5mg/kg ) or continuous in a dose 0.75-1.25 mglkg /hr ↳ every hrs c- anti muscurine like atropin sulfate should not used as first line but added with B agonist ( 0.05- 0.1mglkg atropin sulfate in a dose of not more than o.25mg ( S.E like mental confusion , tachycardia ) prednisolone rapid action but mineralo corticoid effect
-
4-6
.
- *
-
.
dexamethasone
effect but
iprotropium bromide has fewer S.E than atropin best Steroid asthma rapid action meneralo coid effect 4- C.S ( methyl prednisolone in a dose ofcorte 1-2 mg /kg /every 12 hr for 3-7 days
meneralocorticoid
-> No
&
slow
action
use
in
->
+
no
.
best
11
Mid
5-mechanical ventilation for sever hypoxia o2 saturation of < 90% 6- sedation is Contra indication .
7-chest x-ray should be done in all patients & repeated as indicated to detect complication .
Mettyl prednisolone
↳
L
increase
patencyof
hirways
8-other therapy like Mg sulfate in a dose 25-75 mg/kg with maximum dose 2.5 gm , inhaled heliox ( has adjuvent therapy ) ,
Classification of chronic asthma
severity of asthma Day with symptom night sym FEV1 1-mild intermittent <2episode per wk <2 per month >80% 2-mild persistent 3-6 episode per wk 3-4 per moth >80% 3-moderate persistent daily symptoms >5night per month 60-80% 4-Sever persistent Continuous Sym. Frequent <60%
Prevent chronic asthma
Mild intermittent :– 1-no daily medication needed 2-used short acting inhaled B2 agonist ( salbutamol , albuterol ) as needed ( 1-3 puff every 4 hr ) Mild persistent :- one daily medication like ( low dose inhaled C.S 40micro-gram 1-4 puff per day ), intal ( cromolyn) ,nedocromil & leukotrin antagonist like montolukast , zafirlukast Lipo-oxygenase inhibition like zileuton which given above 12 years
Moderate persistent:–either:-A-one daily medication by medium
dose inhaled C.S ( 80micro-gram 2-4 puff / twice a day Or B-two daily medication like low to medium dose inhaled c.s + long
acting bronch-dilator especially for night time symptoms ( salmetrol )
,
sustained released theophylin or long acting B2 agonist
Sever persistent :–3 daily medication :-
1- high dose inhaled c.s 80 micro gram puff l twice a day + 2-long acting brncho-dilator( salmetrol )or B2 agonist + 3-oral c.s in a dose 1 mg /kg l day of not exceed 60 mg l day then
gradually reduce dose to lowest dose which control symptoms
4- correction comborbid condition & emotional disturbances. Exercise induced asthma :–prevented by :–
1- inhalation adrenerhic drug immediately before exercise like inhaled albuterol which give protection for 4 hr . OR inhaled salmetrol given halve hr before exercise .
2-inhaled cromolyn or nedocromil shortly before exercise
Heliox
is a helium/ O2 ( 80/20 or 70/30) mixture that may provide dramatic benefit for
emergency department patients with severe asthma exacerbation , it is dense as room air and consequently travel more easily down narrow passage , which lead to quickly decreasing the work of breathing ., .
The gas mixture is used to drive the nebulizer ,by better delivery of the inhaled bronchodilator .
Briefly , heliox driven nebulizer treatment should have the gas set at rate of 8-10 L/min .and with double usual amount of albuterol .
Inhaled budesonide
Severity Low Medium Highly
0-4 years
0.25-0.5 mg
0.5 1mg
4-11 years 0.5 mg 1 mg 2 mg
Asthma
Ttt in emergency ward
In mild to moderate distress :– 1- O2 therapy to achieve o2 saturation ≥ 92% 2- nebulized ventoline 0.15 mg/kg/dose for 5-7 minute / every 20 minute for three time with o2 therapy . or used inhaled ventoline, Albuterol or through metered dose inhaler 3- oral systemic cortico steroid if no immediate response or recently taken oral steroid ( oral prednisolone 1-2 mg/kg ).
Severe respiratory distress : 1- O2 therapy 2- high dose ventolin or albuterol with ipratropium through inhaler or nebulizer or metered dose Every 20 minute or continuous for one hour with O2 .
3- oral or I.V or I.M corticosteroid 4- chest x ray 5- may need sub cutaneous adrenaline
6- may need adjuvant therapy (Mg sulfate and heliox )
Folate deficiency vs. Vitamin B12 deficiency
features folate def
1- absorption in small intestine
2- anemia earlier within 4-7 month of age
3- intrinsic factors no needed absorption
4- FTT( failure to thrive) yes
B12 deficiency small intestine later 3-4 years
needed for
yes strict vegetarian
5- risk factors goat milk , chronic hemolysis drugs ( anti convulsant phenytoin , phenobarb primodin , methotrexate ,TM 6-MCV increased increased 7-MCHC normal normal
8- hypersedmented neutrophile yes yes
9- serum folate decreased normal
10- vit B12 level normal decreased
11- platelets &neutrophil decreased decreased in advance case in advance case
Folate deficiency
Vitamin B12deficiency
Folic acid def.:—
Folic acid absorbed through out small intestine and human can not synthesis folate & depend on dietary sources including 1/3 from green vegetable & fruit , 1/3 from animal organ like liver and kidney and 1/3 from cereals and grain.
-
Body O store of folate are limited and Anemia occurs after 2—3 month folate free diet
of C|F
1- peak age 4—7 month ( is earlier than IDA) 2-may FTT, chronic diarrhea , irritability.
3- hemorrhage may occur in advance age Causes ;–1-inadeguate intake ( poor nutrition , chronic hemolysis , goat milk ) 2-decrease absorption(Anticonvulsant like phenytoin, phenobarbital, primodin ) 3-drug induced folate metabolism(Methotrexate , Tm/SM, pyrimethamine)
4- cong. Abnormality of folate metabolism Lab. Finding :—-
1- macrocytosis( MCVof more than 100 ) .
2-neutropenia & thrombocytopenia . 3– hypersegmented neutrophil
4- S. folate is decresed & LDH is elevated Treatment ;–Folate 0.5 -1 mg \ day for 3-4 wk until definite hematological response has occurred Maintaince therapy 0.2 mg is adequate Vit. B12 def
Is derived from cobalamine in food of animal source( which is commonly meat and fish ) secondary to production by micro-organism (human can not synthesis B12 ) , it is in contrast to folate store , older children and adult have sufficient V.B12 store at least 3-5 years unless infant born to mother with low V.B12 store where clinical sign appeared in first 4-5 month of life .
Causes :—
1- inadequate intake as in strict vegetarian
2- lack of intrinsic factor as in pernicious anemia or gastric surgery .
3- impaired absorption as in dis. of terminal illeum , IBD ,over growth of bacteria , duplication of small intestine 4-absence of vit 12 transport protein .
C\F:–Non specific manifestation like weakness, FTT, irritability , pallor, glossitis , vomiting , diarrhea, parasthesia, numbness, development delay.
Lab. Finding :–Macrocytosis, hypersegmented neutrophil, neutropenia & thrompocytopenia in advance case , s.iron & folic acid are normal, LDH is elevated Treatment :—1mg paranterally ( increase retic count within 2-4 days Treatment of precipitated factors If neurological involvement — 1mg of B12 I.M for 2 wks then maintained on dose 1-5 microgram\day
Ida
Is most common hematological dis. of infancy & childhood , its frequency related to certain basic aspects of iron metabolism , resulting from lack of sufficient iron for synthesis of Hb .
New born infants contains 0.5gm of iron, where in adult contains 5gmof iron ( to normal body (make up this discrepancy needed 1 mg daily as 0.8 absorbed need daily and 0.2 mg to replace shedding of blood cell Note : only absorbed 10% of iron therefore needed daily10 mg 0f iron within food .
Etiology :—
1- inadequate iron intake , cow milk intolerance when younger 1 year of age or toddlers when ingest large amount of cow milk
2- blood loss as in peptic ulcer, polyp, IBD, occult blood, milk allergy , meckles diverticulum.
3- defect in iron absorption as in malabsorption syndrome .
C\F:—-
1- pallor . 2- pagophagia . 3-if Hb bellow 5gm\dl developed irritability, anorexia , tachycardia & cardiac dilatation .
4- may associated with impaired alertness & learning
Note : IDA is rare before age of 6 month in term infant in the absence of blood loss or before doubling birth weight in preterm infant . .
. • Lab. Finding
1-decrease s. iron , increase IBC(iron binding capacity), decrease s. ferritin 2- hypochromic microcytic in blood film.
3- WBC is normal , platelets count is increased ( however , platelets may be decreased in sever IDA).
DD:—
1- other causes of hypochromic microcytic 2-anemia of chronic dis.
Treatment :—
1- treatment of ppt. factors of IDA.
2-oral iron therapy ( 4-6mg\kg of elemental iron for 8wk) Response to iron therapy
24-48 hr: mood change( decrease irritability) 36-48 hr:- bone marrow response, erythroid hyperplasia 48-72 hr : reticulocytosis(peaking at 5-7days ) 4-30 :-days increase Hb level 1-3 :-months repletion of stores 3- blood transfusion :– is indicated :-
a- Hb of less than 4 gm/ dl b-superimposed infection which interfere with response .
Prevention of IDA :-
1- bottle fed infant should receive iron containing formula untill12 month of age and
exclusive breast infant should receive iron after 6 month of age 2- should introduce iron enrich food at 6 month of age followed by
transition to limited amount of cow milk and increased solid food at 1 year
3- adolescent female menstruating need heavy diet enrich with iron .
Nutritional vitamin d deficiency
Ttt
Prevention
stoss therapy, vitamin D (300,000-600,000 IU) is administered orally (preferred) or intramuscularly as 2-4 doses over 1 day. Since the doses are observed, stoss therapy is ideal in patients in whom adherence to therapy is questionable.
The alternative strategy is daily vitamin D with a minimum dose of 2,000 IU/day for a minimum of 3 mo. Either strategy should be followed by daily vitamin D intake of 400 IU/day if <1 yr old or 600 IU/day if >1 yr old.
Children who have symptomatic hypocalcemia might need intravenous (IV) calcium acutely, followed by oral calcium supplements, which typically can be tapered over 2-6 wks. in children who receive adequate dietary calcium. Transient use of IV or oral 1,25-D (calcitriol) is often helpful in reversing
hypocalcemia in the acute phase by providing active vitamin D during the delay as supplemental vitamin D is converted to active vitamin D.
Prevention:
Most cases of nutritional rickets can be prevented by universal administration of 400 IU of vitamin D to infants <1 year old. Older children with risk Fe factors for inadequate intake should receive 600 IU/day. Vitamin D may be administered as a component of a multivitamin or as a vitamin D supplement
Vitamin D dependent rickets
Type 1 Children with vitamin D–dependent rickets type 1A, an autosomal recessive disorder, have mutations in the gene encoding renal 1α-hydroxylase, preventing conversion of 25-D into 1,25-D. These patients normally present during the 1st 2 yr of life and can have any of the classic features of rickets, including symptomatic hypocalcemia. They have normal levels of 25-D but low levels of 1,25-D.
Vitamin D–dependent rickets type 1B is secondary to a mutation in the gene for a 25-hydroxylase. Patients have low levels of 25-D but normal levels of 1,25-D.
Treatment Vitamin D–dependent rickets type 1A responds to long-term treatment with 1,25-D (calcitriol), it is important to ensure adequate intake of calcium.
Vitamin D–dependent rickets type 1B may respond to pharmacologic doses of vitamin D2 (3,000 U/day) as a result of alternative enzymes with 25hydroxylase activity or residual activity of the mutant protein.
Vitamin D–Dependent Rickets, Type 2
Patients with vitamin D–dependent rickets type 2A have mutations in the gene encoding the vitamin D receptor, preventing a normal physiologic response to 1,25-D. Levels of 1,25-D are extremely elevated in this autosomal recessive disorder.
Most patients present during infancy, although rickets in less severely affected patients might not be diagnosed until adulthood. Less severe disease is associated with a partially functional vitamin D receptor. Approximately 50–70% of children have alopecia, which tends to be associated with a more severe form of the disease and can range from alopecia areata to alopecia totalis. Epidermal cysts are a less common manifestation.
Vitamin D–dependent rickets type 2B appears to result from overexpression of a hormone response element–binding protein that interferes with the actions of 1,25-D. Alopecia may be present.
Treatment Some patients respond to extremely high doses of vitamin D2 (25-D or 1,25-D), especially patients without alopecia, All patients should be given a 3-6 mo trial of high-dose vitamin D and oral calcium. Patients who
do not respond to high-dose vitamin D may be treated with long-term IV
calcium, with possible transition to very high dose oral calcium supplements. Treatment of patients who do not respond to vitamin D is difficult.
XLH
IX
TTT
Investigations: S ca normal , S pho decrease , PTH normal or increase , ALP increase , 25 vit D normal , 1,25 vit D relatively decreased.
Treatment Patients respond well to a combination of oral phosphorus and 1,25-D (calcitriol). The daily need for phosphorus supplementation is 1-3 g of elemental phosphorus divided into 4 or 5 doses.
Established & maintaining bf
Criteria of adequacy of breast feeding
Criteria of inadequate breast feeding
1- initiate breast-feeding within 1 hr of birth and four hrs. after s.c. and if there is no contraindication for oral feeding we should start breast feeding, to go into rhythmic sucking.
2- Rooming in: that is to put the baby beside his mother Place the newborn and mother skin-to-skin to satisfied her and decrease the worry of the mother.
3- No need extra water unless the weather is hot. Do not give sterile water, glucose, or formula
unless indicated
4- The baby must be exclusively breast fed in the first 4 and 6 months of life
5- 85% of the milk will be finish in the first 5 min. of feeding and in the 2 nd five min. the baby finish all milk, slow feeder infant take about 15-20 min.
6- Feeding at night will lead to prolactin secretion and milk supply.
7- Psychological factor: no factor important than happy and relax state of the mother, and the mother should be fully alert when breast feed her baby.
8- The infant should be fed on demand, but infant who cannot be fed on demand he/she should be fed every 3 hrs. on day and every 4 hrs. at night.
9- Bottle feeding will stop breast feeding because it lead to confusion of the baby between the nipple and the teat of the bottle.
10- Mother’s diet should be balanced.
Criteria of adequacy of breast feeding
1- The baby is calm, happy and sleep well after feeding.
2- Normal bowel motion, no constipation.
3- Normal urine output.
4- Normal weight gain: 20-25 gm/day. Criteria of inadequate breast feeding
1- the baby is crying most of the time.
2- Long meal time (grasp the breast for a long period).
3- Very short sleep.
4- Loss of weight or failure to gain weight.
5- Constipation.
6- oliguria.
Mastitis
Nipple pain
Nipple fissure and sore
Mastitis
Mastitis may follow breast engorgement or a condition called a blocked duct. it occurs in 23% of lactating women and is usually unilateral, manifesting with localized warmth, tenderness, edema, and erythema after the 2nd postdelivery week. Sudden onset of breast pain, myalgia, and fever with fatigue, nausea, vomiting, and headache can also occur. Organisms implicated in mastitis include Staphylococcus aureus, Escherichia coli, group A streptococcus, Haemophilus influenzae, Klebsiella pneumoniae, and Bacteroides spp. Diagnosis is confirmed by physical examination. Oral antibiotics and analgesics, while promoting breast-feeding or emptying of the affected breast, usually resolve the infection. A breast abscess is a less-common complication of mastitis, but it is a more serious infection that requires intravenous antibiotics as well as incision and drainage, along with temporary cessation of feeding from that breast.
Causes of blocked duct and mastitis:
1- infrequent or short breast feeding
2- poor draining of part or all the breast due to pressure from clothes, pressure from finger during feeds
3- damaged breast tissue (due to trauma)
4- bacteria allowed entry (due to nipple fissure) 4- hare lip.
Treatment:
Improve draining of breast by treat the cause like remove the narrow clothes, advise frequent feeding, start feeding on an affected side then on affected side, gentle massage toward nipple, warm compress, if no improve use antibiotics like fluxacillin, erythromycin, complete rest.
-Nipple Pain
Nipple pain is one of the most common complaints of breast-feeding mothers in the immediate postpartum period. Poor infant positioning and improper latch are the most common reasons for nipple pain beyond the mild discomfort felt early in breast-feeding. If the problem persists and the infant refuses to feed, consideration needs to be given to nipple candidiasis, and both mother and baby should be treated if candidiasis is found. In some cases, especially if accompanied by engorgement, it may be necessary to express milk manually until healing has occurred
-Nipple fissure and sore nipple:
Causes: improper position or attachment (latch on), or due to Candida infection. Treatment: treat the cause like correct position and attachment, treat Candidiasis for baby and mother, wash breast once and avoid use soap, avoid medicated lotion or ointment, rub hind milk on areola after feed.
Ci of bf
A-on mother side:
1- mental and neurological disease of the mother.
2- infections like malaria, septicemia, typhoid fever, T.B., viral hepatitis and CMV infection.
3-secretion of toxic drug: like anticoagulant, antithyroid drugs, cytotoxic drugs. 4-chronic debilitatory disease, like H.F., renal failure, un controlled D.M.
B-on baby side:
1- inborn error of metabolism, like galactosemia, phanylketonurea.
2- cleft lip and palate.
Colostrum
It is the 1 st milk produced after delivery continue for 3 days. At 3rd -10 th day of infant life it transform into the transitional milk and finally to mature milk, the amount of colostrum is 15-50 ml/day it is bright lemon in color, more alkaline than mature milk and has more specific gravity, also have anti-infective and laxative effect which is benefit to get rid from
mecanium.
Content of colostrums: more protein, more mineral, less CHO and fat.
Protein 2.7 gm/100ml, fat: 2.9 gm/100ml, lactose 5.3gm/100ml, mineral 0.5 gm/100ml Comparison between human milk and cow’s milk
Material
Protein gm/100ml
Fat
Carbohydrate (lactose)
Calorie
Mineral
Water
Human milk
1 (30% casein, 70 % whey)
4 (6o % unsaturated, 40% saturated)
7
67 Kcl/100ml
0.2%
Cow’s milk
3.3 (80% casein, 20% whey)
4 (40% unsaturated, 60% saturated)
4.5
67 Kcl/100ml
0.8%
The same
Vitamins: cow’s milk is low in vit. C and D, breast milk contain adequate vit. C and D provided that the mother in good diet and exposed to some light, cow’s milk contain more vit. K than human milk, both types contain adequate vit. A and B complex. Contraindicated:
Probably save but give with caution:
Bacterial content: although human milk is essentially uncontaminated by bacteria, pathogenic organisms in significant number may enter the milk from mastitis. Tubercle, typhoid bacilli, herpes, hepatitis B, rubella, mumps, HIV and CMV may be found at times in the milk of women infected by these organisms.
Cow’s milk however is good culture for pathogenic bacteria, and many infections are milk borne including streptococcal disease, diphtheria, typhoid fever, salmonellosis and brucellosis, in addition to bacteria that cause G.E and diarrhea.
Digestibility:
The stomach empties more rapidly after human milk than after whole cow’s milk. The curd of cow’s milk is reduced in size by boiling and makes less tough and much smaller by evaporation or by add acid and alkali.
Drugs and bf
Contraindicated:
Probably save but give with caution:
Bacterial content: although human milk is essentially uncontaminated by bacteria, pathogenic organisms in significant number may enter the milk from mastitis. Tubercle, typhoid bacilli, herpes, hepatitis B, rubella, mumps, HIV and CMV may be found at times in the milk of women infected by these organisms.
Cow’s milk however is good culture for pathogenic bacteria, and many infections are milk borne including streptococcal disease, diphtheria, typhoid fever, salmonellosis and brucellosis, in addition to bacteria that cause G.E and diarrhea.
Digestibility:
The stomach empties more rapidly after human milk than after whole cow’s milk. The curd of cow’s milk is reduced in size by boiling and makes less tough and much smaller by evaporation or by add acid and alkali.
drugs and breast feeding
Antineoplastic, amphetamine, bromocriptine, cimetidine, chloramphenicol, ergots, heroin, immunosuppressant, iodide, meprobamate, nicotin, Tetracycline, methimazol (antithyriod). Avoid or give with great caution:
Aspirin (salicylats), atropine, birth contracaptive pill, cascare, calcifirol, metoclopramide, metronidazole, Phenobarbital, primidine.
Anesthetic, Acetaminophen, Aldomet, Chloropromazine, Cadine, Digoxin, Hydralazin, Prednisollon, Theophyllin.
Dried milk
dried milk: prepared by evaporating water from milk to dry for each 100cc of liquid milk is transformed into 12.5gm powder (1:8).
a- dried whole milk: fat content is 3.5%.
b- dried skim milk: non fat skim milk, fat content o.5%, in half skim milk fat content is 1.5% are available for infant with fat intolerance, should not be used in 1 st 2 y. of life, it’s high protein and mineral content may cause sever dehydration.
Advantages of dried milk:
1- sterile and highly saluted.
2- composition is constant.
3- can be stored for along period.
5- can be modified to different children.
6- less expensive.
Modified formula;
1- low lactose milk
2- lactose free milk e.g. isomil for galactosemia
3- hypo allergic milk (isomil) contain no milk protein, replaced by Soya protein completely
4- phenylalanine free milk (lofenalac) for phenylketonuria
5-Low Na milk for congested heart failure
