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Peds, surg Peds, surg Presentation Transcript

  • Pediatrics Highyield – conjunctivitis, jaundice, breast milk, cows milk, child abuse, sexual abuse, orthopedic disorders, Congenital heart disorders, GI disorders, Cystic fibrosis, bronchiolitis, ADHD, Immunizations, Child UTIs – Vesicoureteric reflux
  • Neonatology Ophthalmology
  • Neonatal Conjunctivitis Chemical Conjunctivitis (most common) - due to silver nitrate     Mild palpebral edema and clear, sterile Eye Discharge Onset <24 hours within eye prophylaxis at birth Resolves within 48 hours of birth HSV Conjunctivitis     Onset within 14 days of birth Up to 20% of HSV infected infants are affected Risk of disseminated Herpes Simplex Virus Findings    Keratitis or Cataracts Chorioretinitis Optic Neuritis
  • Neonatal conjunctivitis  Gonorrheal Conjunctivitis     Onset within 2-5 days of life Severe lid edema, and purulent exudates  next step , obtain gram stain  may reveal intracellular gram –ve diplococci Rx  Ceftriaxone x 1 dose, saline irrigation of eyes Chlamydia Conjunctivitis     Onset within 7-14 days of birth Initial mild watery discharge  Progresses to copious and purulent discharge Diagnosis  Giemsa staining of epithelial cell scrapings from tarsal conjunctivae will reveal intracytoplasmic inclusions Rx  Oral erythromycin x 2 weeks
  • Normal Vitals in children
  • Normal Vital Signs in Childhood Age Heart Rate (beats/min) Blood Pressure (mm Hg) Respiratory Rate (breaths/min) Premature 120-170 * 55-75/35-45† 40-70‡ 0-3 mo 100-150 * 65-85/45-55 35-55 3-6 mo 90-120 70-90/50-65 30-45 6-12 mo 80-120 80-100/55-65 25-40 1-3 yr 70-110 90-105/55-70 20-30 3-6 yr 65-110 95-110/60-75 20-25 6-12 yr 60-95 100-120/60/75 14/22 12 * yr 55-85 110-135/65/85 12-18
  • Neonatology SKIN COMPLETELY EDITED
  • Erythema Toxicum     Sterile papules and yellow vesicles on a erythematous base Distributed on face and body Wright’s stain reveals eosinophils Do not rx with antibiotics
  • Q A 2 –day old child was brought for general examining and while examining you notice several yellow vesicles and papules on an erythematous base. They are distributed on the neonate’s face and the chest. The vesicular fluid obtained for analysis and a wrights stain reveals numerous eosinophils. Most likely diagnosis:  A. Milia  B. Staphylococcal folliculitis  C. Candida dermatitis  D. Miliaria rubra  E. Erythema toxicum ANS. E Next step  reassure mother and observe 
  • Diaper Dermatitis   Diaper rashes are common between 9 to 12 months of age Etiology Diaper Irritant Dermatitis  Candida diaper dermatitis  Bacterial diaper dermatitis  Seborrheic Dermatitis  Acrodermatitis Enteropathica 
  • Irritant Diaper dermatitis        Most common cause of diaper rash Etiology : Iirritation by urine, feces, moisture and friction Rash is seen mainly in the areas in contact with the diaperbuttocks, medial thighs, labia and scrotum. The skin fold areas are not involved because there is no contact with the diaper Erythema, papules, and areas of scaling are present. Secondary infections with bacteria and yeast are common. How to prevent Irritant diaper dermatitis? a. Keep the diaper area dry :     Use disposable diapers or frequently change the wet diapers Apply petroleum jelly after each diaper change to decrease skin contact with moisture. Apply powder in the area to keep it dry and decrease friction If above measures fail, use low-potency steroids
  • Candida Dermatitis     One of the etiologies of diaper dermatitis Involves deep skin folds ( Skin folds spared in irritant dermatitis) Characterized by bright red rash with peripheral scaling and satellite papular lesions Rx  ketoconazole, nystatin local creams
  • Bacterial Diaper dermatitis     Bacterial infection complicationg the irritant dermatitis Etilogy : S.aureus Charecterized by pustules and crusted lesions Rx : Topical Mupirocin or Neosporin.
  • Seborrheic Dermatitis    Can occur in the diaper area. Red and scaly waxy patches. Usually, there is concomitant involvement of axillary & neck folds and skin behind the ears  referred to as “Cradle cap”  appears at 2-3 weeks of life and disappears by 3-4 month. Rx : In severe cases, use Ketoconazole or hydrocortisone cream
  • Acrodermatitis Enteropathica       Etiology : zinc deficiency Scales and crusty papules in the peri-oral and the diaper area. Infant may be withdrawn and may have loss of appetite Paronychia and loss of scalp hair, eyebrows, and eyelashes may occur. There might be associated diarrhea indicating an underlying malabsorption syndromes. Rx :  Completely response to zinc supplements.
  • Neonatology ENT Completely edited
  • Choanal Atresia Complete obstruction of one or both nares Pathophysiology  remember that Infants are obligate nose breathers until 4 months old Signs  Bilateral Choanal atresia    Cyanosis that is relieved with crying Unilateral Choanal atresia    Diagnosis usually delayed by years Foul mucus discharge from affected nares Upper Respiratory Infection may result in distress Diagnosis  Check patency with stethoscope (listen over nares)  Try passing Small feeding tube  unable to pass via nares  Lubricate 5 french tube and insert  Normally should meet no resistance Management: Bilateral Choanal Atresia  Bilateral Choanal Atresia in newborn is an emergency  Stabilization  Oral Airway  Surgical repair  Laser burrowing of bony palate
  • CLEFT LIP Occurs in 1 in 700 births. Occurs due to failure of closure of medial nasal and maxillary processes leads to cleft lip. Often, associated with cleft palate. Failure of fusion of palatal processes leads to cleft palate. Etiology :      Family History Asian ethnicity Maternal ETOH consumption Maternal anti-convulsant use ( eg: Phenytoin) Maternal Diabetes Associations:  Pierre Robin Syndrome  Micrognathia , Cleft Palate and Glossoptosis  Trisomy 13 Syndrome  Holoprosencephaly  Cleft palate may be associated with Pituitary abnormalities (Panhypopituitarism) & Hypothalamus anomalies (Kallmann's Syndrome)  Problems with Cleft Lip/ palate     Recurrent otitis media often requiring ear tubes Hearing loss with cleft palate Speech problems with cleft palate Dental issues like tooth dislocation
  • Management – cleft lip/palate  Feeding of Newborn     Isolated cleft lip usually does not cause feeding problem Encourage breast feeding  breast feeding strengthens facial muscles of the kid and eases repair Cleft lip associated with cleft palate or isolated cleft palate may require special nipples or a palatal obturator plate (Plastic dental appliance that covers cleft in palate and improves sucking) Surgical Treatment  Cleft lip:    Cleft lip alone  Usually repaired at 10 to 12 weeks ( 3 months) Remember "Rule of Tens "  a rule of thumb used by surgeons to determine a child’s readiness for surgery  ten weeks of age, ten pounds in weight and ten grams of hemoglobin. If the child meets all the three criteria, child reaches all three criteria, surgical risks are greatly minimized Cleft palate :  Surgical repair before age 2 years ( best age is usually between 9 to 18 months) i.e; before speech develops ( to ensure normal speech)  Its is a complicated surgery and is done when the baby is bigger and better able to tolerate it (between 9 and 18 months)  Surgical revision may be needed at 4 to 5 years
  • Q.1 During your rotation in the birth rooms, you come across a full term baby that is delivered and noted to have cleft lip and palate. The baby is otherwise healthy. The mother is very concerned and anxious. She asks you if there is any treatment available immediately. What is the most appropriate response? A. Surgery needs to be done urgently to prevent permanent defect B. Your baby is healthy. Does not need any therapy C. Your baby will benefit from surgery between 9 to 12 months. D. Your baby should get cleft palate repair by 3 months to prevent speech defects E. Your baby has a permanent defect for which no treatment options are available. 
  • Ans. C    Baby has cleft palate. Surgery for cleft palate is more complicated than the cleft lip and requires the baby to be big enough to tolerate it. The goal is to do the surgery between 9 & 18 months in order to facilitate normal speech development. Surgery for cleft lip can be done at 10 weeks ( 3 months) not cleft palate. Choice D is incorrect Baby will not be able to tolerate these surgeries now  choice A is incorrect
  • Neonatology Hematology
  • Rh Sensitization Pathophysiology (Rh- mom , Rh+ father, Rh+baby)  Maternal antibody Formation to fetal Rh ( first baby not affected usually  mother gets access to fetal RBCs suring delivery. Second baby if Rh+ve will get affected)    Results in Hemolytic Disease of the Newborn    IgM forms in 7 days  Does not cross placenta IgG forms in 21 days  Crosses placenta easily Neonatal Hemolytic Anemia Fetal Hydrops If mother Rh- , always check father’s Rh type
  • Rh Sensitization Indications for giving RhoGAM (xD) to Rh Negative Mother  Standard Timing    Additional Indications        Week 28 gestation Postpartum (under 3 days postpartum if baby Rh+) Placenta Separation Labor Third Stage Termination or Spontaneous Abortion after 6 weeks Antepartum bleed Abruptio Placenta Abdominal Trauma Procedures (Give RhoGAM within 72 hours of procedure)    Amniocentesis or Cordocentesis Chorionic Villus Sampling External version
  • RHOGAM Dosing   Dosing Standard RhoGAM Dosing  Before 12 weeks gestation: RhoGAM 50 mcg IM RhoGAM 50 mcg IM has limited availability  Now RhoGAM 300 mcg IM is given at this time    After 12 weeks gestation: RhoGAM 300 mcg IM First Trimester Bleeding or Late Pregnancy Bleeding  RhoGAM dose based on Kleihauer-Betke Test
  • Kleihauer-Betke Indications  Measures fetal cells in maternal circulation  Used in assessing for Rh Sensitization  If Maternal blood Rh negative and if there is Large antepartum bleed Mechanism  Blood Film stained with acid elution  Fetal Hgb more acid resistant  Fetal RBC darkly stained, Maternal RBC "ghosts" Technique  Count Fetal cells per 50 low power fields  Five cells per 50 (lpf) = 0.5 ml bleed Interpretation  Calculate Maternal Blood Volume (ml) =   Calculate Fetal Whole Blood (ml) =   (Pre-pregnant weight in kg) x 70 ml/kg x (1.0 + (0.5 x weeks gestation/36)) - Estimated Blood loss (ml) at time of test (Fetal Cell Count/Maternal Cell Count) x Maternal Blood Volume Rh Immune Globulin (RhoGAM) Dose  Give 300 ug per 30 ml fetal whole blood or 15 ml pRBC
  • Neonatology Gastroenterology
  • Duodenal Atresia       Presents soon after birth Persistent vomiting Associated with Downs Do AXR – Double bubble appearance Confirm with ultrasound Surgery as soon as possible  duodenoduodenostomy
  • Congenital Pyloric Stenosis      Presents at 6 to 8 weeks with vomiting Hypochloremic metabolic alkalosis, hypokalemia Physical – olive shaped epigastric mass Ultrasound confirmatory Rx – Surgery/ Pyloromyotomy
  • Failure to pass Meconium  By 48 hours. Consider following differential Cystic fibrosis  Imperforate Anus  Hirschprung disease 
  • Hirschprung disease   Congenital megacolon Lack of intramural ganglionic cells    C/F :         Submucosa level (Meissner's Plexus) Myenteric level (Auerbach's Plexus Presentations: Age dependant Newborn  No meconium in 24-48 hours of birth First month of life  Progressive abdominal distention, Small caliber stools (pencil-thin) & failure to thrive Two to three months of life  Enterocolitis (fever, explosive bloody Diarrhea)  Initial presentation in 33% of patients Older Childhood  progressive Constipation, Fecal Impaction & Abdominal distention Rectal exam  Reveals no stool in the ampulla Diagnosis can be made with barium enema, revealing a transition zone between the constricted aganglionic segment and the proximal, normally dilated segment. Anal manometry useful in daignosis. Rectal biopsy shows lack of ganglion cells and confirms the daignosis Rx : ilio-anal anastomosis, in severe cases  colostomy
  • Neonatal Jaundice Physiological vs. Pathological
  • Physiological Jaundice     Never Never occurs less than 24hrs after birth ( NOT ON DAY 1  consider from 2 to 14 days. Usually does not persist more than 1 week in duration ) Breast Feeding Jaundice Physiologic Jaundice  Transient limitation of Bilirubin conjugation ( due to immature glucuronyl transferase) , Increased Hemolysis  Hemoglobin drops from 20 to 12 in first week Exaggerated Physiologic Jaundice : occurs with   Low glucuronyl transferase (Hepatic immaturity) Risk factors      Breast Feeding Jaundice Prematurity Asian ethnicity Weight loss Complications : Kernicterus most seen with pathological jaundice, however can be seen with breastfeeding jaundice or exaggerated physiological jaundice
  • Breast Feeding Jaundice Pathophysiology  Early Breast Feeding Jaundice   Same as mechanism as exaggerated physiologic Jaundice Late Breast Feeding Jaundice  Nonesterified long-chain fatty acids in breast milk  Competitively inhibit glucuronyl transferase Labs  Early-Onset Breast Milk Jaundice – within 3-4 days of birth    Same course as exaggerated physiologic Jaundice Total Bilirubin peaks < 17 mg/dl by day 4 of life Late-Onset Breast Milk Jaundice    Bilirubin peaks between day of life 6 to 14 Total Bilirubin often 12 to 20 mg/dl Hyperbilirubinemia may persist 2-3 months
  • Breast Feeding Jaundice - Management Early onset Breast Feeding Jaundice ( bili < 17)  Encourage mothers to nurse frequently (8-10x per day)  Avoid supplementation if possible     Monitor Serum Bilirubin daily as outpatient   Do not supplement with glucose or sterile water Continue Breast Feeding even if supplementing Formula indicated only for inadequate milk production Phototherapy when Indicated Mothers may express milk after feedings  Increases milk volume Management: Late onset Jaundice (Bilirubin 17-20 mg/dl )  Diagnosis     Interrupt Breast Feeding for 24-48 hours Monitor Serum Bilirubin levels every 12-24 hours  Bilirubin should decrease by 3 mg/dl per day and this confirms diagnosis of brest milk jaundice. Resume Breast Feeding after decreased Serum Bilirubin This management if improves jaundice, confirms Breast Feeding Jaundice
  • Pathological Jaundice Criteria  Jaundice in first 24 hours of life or after day 14  Serum Bilirubin rises > 5 mg/dl in the first 24 hours  Direct Bilirubin (conjugated) >2mg/dl ( even during the period of physiological jaundice, when u see high direct bilirubin suspect biliary obstruction)  Term Infant   Serum Bilirubin >17 mg/dl Any Jaundice that persists longer than 1 week   Preterm Infant   Serum Bilirubin >15 mg/dl Any Jaundice that persists longer than 2 weeks    Except in Breast Feeding Jaundice Except in Breast Feeding Jaundice Complications : Kernicterus, Anemia, Failure to thrive Rx : Phototherapy ( contraindicated in conjugated hyperbilirubinemia) , Exchange transfusion if phototherapy is not effective or if bili is very high ( > 30mg%)
  • Phototherapy Mechanism  Bilirubin absorbs light – very ensitive to blue light and undergoes photoisomerization  Photoisomerization  Converts toxic bilurubin to non toxic which is then excreted in bile Contraindications  Conjugated Hyperbilirubinemia  Risk of bronze baby syndrome Adverse Effects  Loose stools , Skin Rashes , Overheating , Dehydration ( due to Insensible water loss , Diarrhea) Electrolyte disturbance ( Hyponatremia, Hypokalemia)  Bronze baby syndrome    Dark, grayish brown discoloration of skin May persist for months Associated with Conjugated Hyperbilirubinemia
  • Neonatalogy Birth Trauma
  • Clavicle # from Birth Trauma Most common newborn orthopedic injury Signs  Pain with movement and Moro reflex  Pseudoparalysis of extremity on fracture side  Sternocleidomastoid muscle spasm on affected side  Crepitus at fracture site  Palpable bony irregularity at fracture site Precautions  Assess concurrent injury to adjacent structures  Cervical spine , Brachial plexus & Humerus Radiology  Chest XRay Management  Immobilize arm and shoulder 7-10 days  Safety pin infants sleeve to shirt Prognosis  Excellent, even for displaced fractures Course  Palpable callus formation in 7 to 10 days  Fracture heals in 4 to 6 weeks 
  • Torticollis from Birth Trauma Etiologies  Sternocleidomastoid muscle injury from Birth Trauma  Hematoma and fibrosis results in muscle shortening  Muscle adaptation from abnormal intrauterine position  Cervical vertebral abnormalities  Suggested by limited neck ROM at birth Pathophysiology  Unilateral shortening of sternocleidomastoid muscle Associated Conditions  Congenital asymmetric contractures of hip abductors  Unilateral Congenital Hip dysplasia Signs  Head Tilt toward the affected side  Limited neck range of motion    May suggest cervical vertebral abnormality Face and skull asymmetry from lack of position change Palpable mass within sternocleidomastoid muscle  Gradually disappears and is replaced by fibrous knot
  • Torticollis - Management Radiology  Neck XRay  Indicated for significantly limited neck ROM  Ultrasound Hips   Remember to Assess for concurrent Congenital Hip dysplasia Indicated for significant hip abductor tightness Management  Positioning head opposite affected side  Padded bricks , Sandbags  Passive Stretching    Rotate infants head to affected side Tilt head backwards (extend) away from affected side Surgical release of sternocleiodomastoid muscle  Indicated for limited range of motion at 1 year Course  Minimal signs at birth  Torticollis will be evident by 2 to 3 weeks  Recovery over 3 to 4 months with therapy  Complete resolution by 1 year with therapy
  • Brachial Plexus Injury from Birth Trauma  Injuries may occur intrapartum prior to delivery: 50%   Unrelated to Shoulder Dystocia or excessive traction Possibly from fetal shoulder against symphysis pubis General  Follows difficult or prolonged delivery Mechanism of injury  Upper plexus Injury  Lateral flexion of neck against fixed head, shoulder  Lower plexus Injury  Arm forced upward Types  Duchenne-Erb Paralysis (Waiter's Tip Deformity)  Klumpke's Paralysis (Clawhand Deformity)  Whole Arm Paralysis (uncommon)  Limb completely flaccid , Hands dry and atrophic & All reflexes absent Signs: General  Arm motionless at side with elbow extended  Moro Reflex absent on affected side  Swelling above clavicle due to hemorrhage  Traumatic neuritis   Thoracic root injury   Tenderness to palpation Horner's Syndrome Differential Diagnosis: Pseudoparalysis  Clavicle Fracture & upper humerus#
  • Brachial Plexus Injury from Birth Trauma Associated Conditions  Phrenic Nerve palsy from Birth Trauma  Horner's Syndrome Radiology: XRay Shoulder and XRay arm  Assess for concurrent fracture ( r/o pseudoparalysis ) Management  Prevent fixed soft tissue contractures   Gentle repetitive range of motion shoulder and elbow Supportive splints for wrist and fingers Reconstructive surgery for late deformities Prognosis ( what to tell the mother ???)  Improvement in first week suggests full recovery  No improvement by 6 months suggests permanent deficit  No improvement expected after 2 years  Older patients     Underdevelopment of Upper extremity Humerus shortened Contractures and disuse atrophy
  • Erb-Duchenne Palsy Most common type associated with Brachial Birth Trauma Pathophysiology  Upper Roots (C5 to C6) Injury Signs: Waiter's Tip  Arm adducted and internally rotated  Forearm pronated  Wrist flexed  Finger function and grasp reflex are normal  Moro Reflex and biceps reflex absent on affected side  Waiter's Tip position if C7 involvement Prognosis  Fair to good recovery of arm function: 50-80% 
  • Klumpke’s Palsy Least common form of Brachial Birth Trauma Pathophysiology  Injury to C7, C8, and T1 spinal nerves Signs: Clawhand deformity  Hand Intrinsic Muscle Weakness  Grasp reflex absent on affected side  Biceps reflex and radial reflex present  Horner's Syndrome may be associated    Occurs if T1 sympathetic fibers are affected Upper part of arm unaffected
  • Phrenic Nerve Injury – Birth Trauma Pathophysiology  Associated with Brachial Birth Trauma  leads to Unilateral diaphragm paralysis Signs  Respiratory distress  Diminished breath sounds on affected side Radiology: Ultrasound or Fluoroscopy of diaphragm  Diaphragm elevated on affected side  Affected diaphragm moves upward with inspiration Management  Pulmonary toilet while resolving  Refractory cases  Diaphragmatic plication Course  Resolves over 1 to 3 months
  • Moro Reflex     A normal reflex present in newborn infants. Absence of the Moro reflex in an infant is abnormal. Presence of a Moro reflex in an older infant, child, or adult is also abnormal. Two-sided absence of the Moro reflex suggests damage to the central nervous system (brain or spinal cord). One-sided absence of the Moro reflex  the possibility of a fractured clavicle or injury to the brachial plexus, which can occur because of birth trauma. Conditions associated with brachial plexus injury include Erb's palsy and ErbDuchenne paralysis. Paralysis on one side of the body may also produce an asymmetrical Moro reflex .
  • Neonatology Surgery
  • Gastroschisis - Omphalocele
  • Omphalocele      Covered abdominal wall defect at Umbilicus in newborn  Defect at base of Umbilical Cord (2 to 10 cm)  Normal abdominal viscera and contained within sac , Abdominal contents herniate via defect ( Intestine , Liver, Gall Bladder Stomach, Bladder , Pancreas , Spleen ) Associated conditions (67% of cases)  Trisomy 13 , Trisomy 18 , Congenital Heart Disease (VSD up to 25% of cases), Gastrointestinal disorders ( Midgut volvulus , Malrotation , Meckel's Diverticulum & Imperforate anus), Renal anomalies Diagnosis : Usually diagnosed by prenatal Obstetric Ultrasound RX  Apply warm dressing over the defect  Rx is surgery on first day of life Prognosis : chromosomal abnormalities associated with poor prognosis
  •       Gastroschisis Open peri-umbilical abdominal wall defect in newborns Risk factors : Intrauterine Growth Retardation , Prematurity & Young mother (< 20 yrs age) Pathophysiology  Abdominal wall defect lateral to Umbilicus with evisceration of small intestine and ascending colon , Bowel may be abnormal - matted and thickened Diagnosis : Usually diagnosed by prenatal Obstetric Ultrasound Complications  Necrotizing enterocolitis, Bowel perforation Management  Initial step  Apply warm fluid-impermeable dressing over defect   Orogastric Tube for decompression Fluid Resuscitation (high evaporative losses)     Blood Culture & Broad spectrum antibiotic coverage    Maintenance IV fluids: D10W or 1/4NS Start with 20 cc/kg bolus over 30 minutes Fluid requirements in gastroschisis 2.5x normal Ampicillin + Gentamicin Surgical repair on first day of life Parenteral Feeding
  • Breast Feeding A Very High Yield Know each and everything!
  • Advantages of breast feeding         Lower Incidence of Infantile Colic Most Important method of maternal-infant bonding Easier to digest than formula (related to protein)  Human milk is digested in 1.5 hours where asFormula is digested in 4 hours Does not induce allergic response (contrast to formula)  no Diarrhea, Gastrointestinal tract bleeding or Atopic Dermatitis Lower Incidence of feeding problems like Gastroesophageal Reflux (Regurgitation) & Constipation Colostrum contains multiple immune factors  Macrophages ( Complement, Lysozyme & Lactoferrin ) Secretory IgA antibodies  Infant receives 0.5 to 1g Secretory IgA per day thru breast milk  provides Bacterial, Viral, and protozoal protection Lower Incidence of infection  Bacteremia , Meningitis , Botulism Gastrointestinal infection , Lower respiratory infection , Otitis Media & Urinary Tract Infection
  • Advantages of breast feeding Advantages to mother  Faster return to pre-pregnancy weight  Decreased postpartum bleeding  Increased Bone Mineral Density  Lower Incidence of Ovarian Cancer  Lower Incidence of premenopausal Breast Cancer  Remember breast feeding is not guaranteed contraception
  • Contraindications - breastfeeding Contraindications: Absolute  Maternal HIV Infection  Chemical Dependency ( drug abuse )  Important medication use that contraindicates lactation ( chemo rx, ergot alkaloids)  Cardiovascular medications to avoid in Lactation are Acebutolol & Amiodarone  Untreated syphilis  Active/ untreated TB  Herpes  only if there are active lesions on breast Contraindications: Relative  Tobacco Smoking in lactation  Significant nicotine exposure via breast milk , 10x greater exposure than in bottle fed infants
  • Herbs and Teas considered safe in Lactation!   Avoid Caffeine more than 2 beverages per day Herbs      Chamomile Garlic Ginger Ginseng Teas       Chicory Orange Spice Peppermint Raspberry Red bush tea Rose hips
  • Amblyopia - Children
  • Amblyopia ( Lazy Eye ) Poor vision that cannot be corrected by eye glasses which has no organic cause Etiologies  Strabismus (most common cause of amblyopia)    Anisometropia (Refractive Amblyopia)   Misalignment of eyes Large difference in Refractive Error between eyes Deprivation Amblyopia        Congenital Cataract Retinoblastoma Corneal scarring Vitreous opacity Severe Ptosis Optic atrophy Iatrogenic patching
  • Amblyopia ( Lazy Eye ) Pathophysiology Occurs in developmentally immature eye Occurs in developmentally immature eye during first 6 months of life      Normally visual acuity improves rapidly after birth 20/400 => 20/80 and Eye fully matures by age 9 years However, normal maturity requires clear, equal, aligned image for each eye  if at all there is conflicting data with Strabismus (2 competing images) or Anisometropia (1 clear, 1 blurred image)  the brain suppresses information from the "bad" eye Continued suppression leads to permanent vision loss in the bad eye. Children should be screened for visual acuity/ strabismus  to take measures to prevent Amblyopia
  • Amblyopia Management: Relies on forcing the child to use amblyopic eye  Patch "good", dominant eye  May use Atropine to blur dominant eye Prognosis  Remember that Amblyopia irreversible after age 9 years
  • Breath Holding Spells Recognize and Reassure!
  • Differential Diagnosis – Pediatric Spells          Complex Partial Seizure (Most common Seizure) Absence Seizure Infantile Spasms (Tuberous sclerosis , Phenylketonuria (PKU) , Maple syrup urine disease , nonketotic hyperglycemia) Migraine Headache Benign Positional Vertigo Narcolepsy or Cataplexy Night Terrors Infant apnea Breath Holding Spell       Cyanotic Syncope Pallid Syncope Prolonged QT interval or other cardiac arrhythmias Benign Syncope Psychogenic Seizures Rage Outbursts
  • Breath Holding Spells Characteristics  Transient episodes of breath holding  Associated with child becoming limp and unresponsive  Seizure-type activity may occur  Spells can occur as often as several times a day or as rarely as once a year. Types  Cyanotic Breath Holding Spell (most common)  Pallid Breath Holding Spell Diagnostics  Electroencephalogram (EEG) normal Evaluation  Do a Thorough history and examination  Consider the differential and Rule-out other pediatric spell  because life-threatening conditions may present similarly to BHS, diagnosis of the benign condition can be difficult  Therefore, evaluation of breath-holding episodes requires the consideration and elimination of other, more worrisome explanations.
  • Cyanotic BHS More common Breath Holding Spell than Pallid Spell  Episode onset after age 6 months, resolve by 5 years Triggers  Occurs following a stressor such as scolding Course  Initial: Brief, shrill cry  Next: Forced expiration and apnea ensues  Next: Cyanosis and loss of consciousness  Variable: Clonic movements may occur 
  • Pallid BHS Less common than Cyanotic Breath Holding Spell  Age of onset 12-24 months Trigger: Pain  Strike body part on falling  Startled Course  Initial: Stops breathing  Next: Immediate loss of consciousness  Next: Infant becomes limp and pale  Variable: Tonic Seizure, Bradycardia, Asystole >2 sec 
  • Table 1. Differentiation of severe BHS from generalized seizures and cardiac disturbances Feature Severe BHS Generalized seizures Cardiac disturbances Age at onset Often infancy Rarely infancy Variable Family history of BHS Often positive None None Precipitating event Usually present Usually absent Usually absent Sleep state Always awake Asleep or awake Awake, often with stressor Pallor or cyanosis Always; before syncope Variable; after syncope Variable Myoclonic jerks Variable; few beats Usually Absent
  •         BHS - Management Reassure parents that although BHS are frightening to observe  children will outgrow them  By the time patients are 4 years old, 50% of BHS resolve; by age 6 - 90% have done so; and by age 7 or 8, virtually all of them resolve. Are there any long term effects ?  parents should be told that evidence suggests no serious long-term effects of benign BHS in otherwise healthy children  these patients do not have increased risk of epilepsy or other neurologic problems  The only significant finding on subsequent follow-up of children with BHS was a mildly increased incidence of syncope later in life, especially in childhood or adolescence. When a child with hx of BHS becomes upset and cries  reasonable efforts to calm the child should be made  If an episode occurs despite these measures, observation of the child and prevention of injury are generally all that is required If child loses consciousness  place the child in a lateral supine position to help avoid injury and possible aspiration Once an episode has resolved, the child should be reassured. Avoid drawing excessive attention to the event or expressing extreme worry to the child  as this may encourage the behavior Medications are not usually indicated In severe BHS associated with Bradycardia or Asystole or in patients with multiple daily episodes  0.1 mg Atropine tid is effecive in preventing BHS  Referral to a pediatrician should be made in all cases in which pharmacologic therapy is being considered.
  • Respiratory Diseases Completely edited including Qs
  • Acute Epiglottitis          Caused by H.influenzae. Incidence has gone down dramatically since the introduction of HiB vaccine. Common age 2 months to 7 years Onset  Acute Classic presentation is open mouth, protruding tongue and drooling ( dysphagia/ difficulty swallowing occurs due to swollen epiglottis  manifests as drooling) Stridor may be present. Voice sounds “Muffled” The child is often agitated and appears toxic, fever often present. Spontaneous cough is absent( in contrast to Croup where there is “Barky” cough  Remember Epiglottitis patients actually “Look” worse than they “Sound” where as croup patients “sound” worse than they look) Look for signs of upper airway obstruction : flaring of the nasal alae, suprasternal/ supraclavicular retraction, use of accessory muscles and intercostal retractions (these signs may be absent at initial presentation) Direct exam of Epiglottis by tongue depression  shows cherry red, swollen epiglottis. ( BUT AVOID TONGUE DEPRESSION AS ANY IRRITATION OF EPIGLOTTIS CAN PRECIPITATE COMPLETE AIRWAY OBSTRUCTION )
  • Thumb sign on lateral neck x-ray Black arrow  the tip of the epiglottis. White arrow  pre-epiglottic space (vallecula). The normal epiglottis is thin or triangular in appearance. Here, it appears enlarged and rounded  looks like a thumb-print ( path gnomonic x-ray appearance of epiglottitis)
  • Acute Epiglottitis  Diagnosis :      Clinical ( differentiate from Croup). Supportive diagnosis can be obtained by lateral neck radiographs if the child is stable to be transported to x-ray department  shows enlarged epiglottis protruding from the anterior wall of the hypopharynx (thumb sign). Negative lateral radiographs do not rule out the diagnosis. CBC reveals marked leucocytosis with left shift ( croup can have leucocytosis but bandemia is usually absent) Diagnosis can be confirmed by direct visualization but do not use tongue depressors. Visualization should only be done by laryngoscopy with anesthetist at the bedside and child prepared for intubation. Direct laryngoscopy is pathognomonic  demonstrates a large, almost spherical, edematous, cherry-red epiglottis. Rx :    Once Epiglottitis confirmed (laryngoscopy)  First step INTUBATE!  ( Remember ABCs) Antibiotics  DOC is Ceftriaxone. Ampicillin is alternative. Cultures should be obtained from the epiglottis and from blood. Racemic epinephrine and Corticosteroids can be potentially harmful here ( unlike in “Croup”)
  • Croup           Laryngotracheobronchitis leading to subglottic edema ( in epiglottitis, supraglottic area is involved) Etiology : MCC parainfluenza viruses, other causes – influenza, RSV, Adenoviruses Onset – insidious ( preceded by URI symptoms) Common age 3 months to 3 years Spontaneous “BARKY” Cough is present. Inspiratory stridor that is increased by crying is seen. Child usually does not appear toxic ( Sounds worse than he looks) No droolong or dysphagia On examination, Epiglottis is red but not swollen. Lateral neck x-ray negative for thumb sign. A posterior-anterior view of the neck may demonstrate a classic “Steeple” sign in only 50% cases (a narrowed column of subglottic air)
  • “Steeple” Sign   The arrow points to the narrowed column of subglottic air ( due to subglottic edema). A lateral neck x-ray in croup may show overdistended hypopharynx
  •  Treatment      Mild cases  Humidified air at home, use humidifiers ( humidity can reduce subglottic edema). If child is hypoxic or cyanotic  hospitalize use humidified oxygen Moderate to severe cases  Racemic epinephrine by nebulizer & Systemic Corticosteroids ( dexamethasone). With nebulized epinephrine and dexamethasone, improvement can be seen in 2 to 3 hours. Observe for improvement and if improves, discharge home. DO NOT GIVE ANTIBIOTICS Indications for admission in Croup:         Croup Child less than 1 year Cyanosis No improvement/ worsening despite above therapy Worsening stridor/ accessory muscle use ( intercostals, neck muscles) Decreased alertness Follow-up cannot be guaranteed Use of racemic epinephrine and corticosteroids has almost eliminated the need for intubation. However, if no improvement seen and if there is evidence of worsening respiratory compromise despite above therapies  intubation In severe croup that failed to respond to racemic epinephrine  use Heliox ( mixture of helium and oxygen)
  • Q        A 2 year old boy is brought to the emergency department with complaints of throat pain, inability to swallow and drooling. The throat pain, difficulty swallowing, and drooling started in the afternoon and have worsened over the night. There is mild cough and nasal congestion for 2 days now. His past history is significant for frequent ear infections. Mother is not very sure if he received all his immunizations. On examination, he looks tired, his temperature was 102F, blood pressure 100/60, respiratory rate was 32 with some accessory muscle use, saturating 100% on room air. He coughs occasionally. Rest of the physical exam is benign. A lateral neck x-ray was negative. CBC reveals leucocytosis with left shift. The most appropriate next step in management: A. Ceftriaxone B. Examination of epiglottis by tongue depression C. Racemic epinephrine D. Corticosteroids E. Laryngoscopy followed by Urgent intubation F. Humidified air
  • Ans. E      Presence of dysphagia, drooling, absence of typical “barky” cough and CBC with left shift favors Epiglottitis more than Croup. A negative lateral neck x-ray does not rule out epiglottitis. First step is always intubation ( patient is already in distress with respiratory rate 32) Next step after securing airway is Ceftriaxone. Racemic epinephrine and corticosteroids are contraindicated in epiglottitis.
  • Q2       A 2 year old girl presents to the emergency room with fever, cough, runny nose, stridor and difficulty breathing. The child has been having nasal congestion and rhinorrhea for past 3 days. Temperature is 101, RR 30. No cyanosis. Child looks restless and anxious. She has an audible continuous stridor even at reat and a barky cough. On examination, she has bilaterally significantly decreased breath sounds and moderate intercostal retractions. The most appropriate next step in management: A. Humidified air B. Humidified oxygen C. Laryngoscopy followed by Urgent Intubation D. Racemic Epinephrine and Dexamethasone E. Ceftriaxone
  • Croup Score      Calculate Croup score to determine whether croup is mild, moderate or severe  then take a decision on treatment. Scoring  Level of Consciousness  Alert: 0  Restless, anxious: 2  Disoriented : 3  Cyanosis  None: 0  When crying : 2  At Rest: 3  Stridor  None: 0  With Agitation: 1  Intermittent at Rest: 2  Continuous at rest : 3  Air Entry  Normal: 0  Decreased: 1  Moderately decreased: 2  Severely decreased : 3  Retractions  None: 0  Mild: 1  Moderate: 2  Severe: 3 Interpretation of score  Very mild < 2  Mild to moderately severe – 2 to 9  Severe croup > 9 PRESENCE OF PULSUS PARADOXUS INDICATES SEVERE CROUP NO NEED TO REMEMBER EVERYTHING, REALIZE THE COMPONENTS OF SCORE AND QUICKLY ASSESS SEVERITY IN THE QUESTION !!
  • Ans.D     This is a severe croup. For moderate to severe croup, use Racemic epinephrine + steroids For Mild croup  use Humidified air. If child hypoxic – use supplemental oxygen, humidified. Intubation used only if racemic epinephrine+ steroid combination fails to improve symptoms.
  • CVS - PEDS
  • CVS Anomalies – Congenital Associations  Trisomy 21 (50% Incidence of Congenital heart disease)    Trisomy 18 (95% Incidence of congenital heart disease)     Aortic Coarctation Hypertension Biscuspid aortic Valve Marfan's Syndrome    Ventricular Septal Defect Turner Syndrome (45, XO)   Ventricular Septal Defect Trisomy 13 (80-90% Incidence congenital heart disease)   Ventricular Septal Defect Patent Ductus Arteriosus Aortic aneurysm Mitral Valve Prolapse Noonan Syndrome   Pulmonic stenosis Aortic Coarctation
  • Congenital Heart Disease Common Etiologies  Cyanotic Congenital Heart Disease (5 T's)       Transposition of the Great Vessels Tetralogy of Fallot ( decreased pulmonary circulation on cxr) Tricuspid valve atresia Total anomalous pulmonary venous return Truncus arteriosus Acyanotic Congenital Heart Disease: Left to right shunt    Ventricular Septal Defect – pan systolic murmur Atrial Septal Defect – fixed split of s2 Patent Ductus Arteriosus – machinary murmur
  • Causes of Pediatric CHF– Remember age of presentation!  Presentation: Week 1  Arteriovenous fistula   Aortic Coarctation (Interrupted aortic arch)    Decreased pulses Left Ventricular Hypertrophy Hypoplastic left heart Syndrome      Asymmetric pulses Aortic Stenosis   Increased Pulses Most common CHF cause in first week Decreased pulses Right Ventricular Hypertrophy Hyperactive precordium Myocarditis    Decreased pulses Right Ventricular Hypertrophy Decreased precordium
  • Causes of Pediatric CHF  Presentation: Weeks 2 to 4   Acyanotic (PaO2 >150 on 100% O2)        Onset occurs with drop in pulmonary vascular resistance  Pressure drops allowing left to right shunt Coarctation of Aorta  Most common CHF cause in first 2-4 weeks Aortic Stenosis Myocarditis Patent Ductus Arteriosus Arteriovenous fistula Ventricular Septal DefecT Cyanotic (PaO2 <150 on 100% O2)       Hypoplastic left heart Syndrome (Uniformly fatal) Total Anomalous pulmonary venous return Truncus arteriosus Transposition and VSD Tricuspid atresia and VSD Single Ventricle
  • ORTHO- PEDS LIMPING CHILD
  • Causes of Limp in Kids  Age under 2 years      Ages 3-5 years   Toxic or Transient Synovitis (most common) Ages 5-9 years    Congenital Hip dysplasia (most common) Toddler's Fracture Tibial Stress Fracture Cerebral Palsy Legg-Calve-Perthes Disease (most common) Muscular Dystrophy Ages 11-16 years     Slipped Capital Femoral Epiphysis (most common) Legg-Calve-Perthes Disease Juvenile Rheumatoid Arthritis Osteochondritis Dissecans of the Knee
  • SCFE         Occurs during maximal pubertal growth spurt - age 13 to 15 years in males and age 11 to 13 years in females Most common hip disorder in adolescents Blacks are more affected Child is usually overweight/ obese Mechanism – Femoral epiphysis can slip before the closure of epiphyseal plate Signs  Hip is held in abduction and external rotation and internal rotation is extremely limited Dx: clinical and then,obtaion Hip XRay  may show Widened epiphyseal plate and displacement of femoral head Management – SCFE is an Orthopedic Emergency!    Immediately hospitalize and schedule internal fixation Use spica hip casting for 6 to 8 weeks  Decreases risk of Femoral Neck Fracture and protects epiphyses In case of severe chronic Slipped Capital Femoral Epiphyses , osteotomy needed to realign and stabilize
  • Leg-Calve Perthes Disease      Osteonecrosis of the femoral head Age group affected : 4 to 9 yrs Exam reveals trendelenberg gait and internal rotation is affected Diagnosis : x-ray hip Orthopedic consult
  • Transient Tenosynovitis of the Hip      Most common cause of limp and hip pain in children under 10 yrs of age Afebrile, non toxic child ROM of hip – abduction, internal/external rotation are affected ESR only slightly elevated, Arthrocentesis fluid clear. ( unlike septic cases Make sure to rule out septic arthritis
  • Congenital Dislocation of Hip      Common in girls > boys Common with breech deliveries Screen all kids with ortolani & Barlow maneuvers Ultrasound is confirmatory Management – Very Important
  • CHILD PSYCHIATRY ADHD, CONDUCT DISORDER, OPPOSITIONAL DEFIANT SYNDROME, TOURTTES SYNDROME, AUTISM, SELECTIVE MUTISM
  • Genito-urinary system Nocturnal enuresis Encopresis Vesico-ureteric reflux Frequent UTIs
  • Surgery Highyield
  • Diverticultis     Left lower quadrant pain, tenderness, leucocytosis, fever +/Complications  LGI bleed, perforation –”walled off”, diverticular abscess, sepsis, shock ( ? Imaging, ?when ) ( when someone has pneumaturia  it’s a complicated diverticulitis) Medical management – NPO, ivf, antibiotics Surgery : only for complicated diverticulitis ( abscess, perforation) or recurrent diverticultis > 1 episode ( i.e; surgery should be considedered following 1st episode)
  • Emergency Surgery in Diverticulitis  Stage patients with acute diverticulitis and perforation with the following classifications:      Stage I: confined pericolic abscess Stage II: distant abscess (retroperitoneal or pelvic) Stage III: generalized peritonitis (noncommunicating) Stage IV: fecal peritonitis (communicating) Treat patients according to their respective stage:    In patients with Stage I abscess, begin with conservative therapy but individualize treatment as needed, noting that abscesses <2 cm and confined to the mesocolon are most likely to respond to conservative therapy In patients with Stage II abscess or nonresolving Stage I abscess, carry out surgical or percutaneous drainage under radiological guidance ( consider percutaneous drainage if pt is too unstable to undergo surgery) Send patients with peritonitis (Stage III or IV) to surgery as soon as possible
  • Elective Surgery - diverticulitis Consider elective colon resection in patients who:  Have had two resolved episodes of acute diverticulitis  Are under age 40 ( its believed that complication rate is high in the young)  Are immunocompromised
  • Prognosis counselling - diverticulitis Counsel patients that:  Only 10% to 25% of patients with diverticula will ever develop acute diverticulitis  Only one third of patients will ever develop a recurrence following a single episode of acute diverticulitis  Patients are less likely to respond to medical therapy with each recurrent episode of acute diverticulitis  Surgery should be considered following the second episode of acute diverticulitis
  • Follow Up - Diverticulitis Follow-up  Colonoscopy 6 weeks after diverticulitis episode    Define extent of Diverticulosis Evaluate for Colon Cancer Barium Enema may be used as alternative option
  • Cholelithiasis    Remember indications for emergency surgery vs. Elective surgery When do you do percutaneous drainage of gall bladder When do you ERCP with Stenting – elective vs. emergent
  • OTHER ISSUES        PERICARDIOCENTESIS THORACENTESIS TUBE THORACOSTOMY NEPHROSTOMY NEPHRECTOMY DPL EXPLORATORY LAPOROTOMY