END EXAM Flashcards
Etiology of Metabolic acidosis
- Loss of base (GIT e.g. diarrhea, or renal e.g. renal tubular acidosis)
- Abnormal acid accumulation, e.g.:
a. Lactate in shock, hypoxia or RD
b. Ketones in DKA
c. Uremic toxins in renal failure
d. Some in-born errors of metabolism
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Treatment of Metabolic acidosis
- Treatment of the cause; eg
correction of shock: 20 ml/kg
Oxygen for hypoxia and RD,
Fluids and insulin for DKA - Alkali therapy with sodium bicarbonate
a. Indicated mainly for cases due to bicarbonate loss rather than those with acid
accumulation, especially those with treatable causes
b. Ensure adequate ventilation and perfusion
c. Give 2 mEq/Kg or correct according to base deficit in blood gases, over 30 minConsider the Na content given
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Investigations of Small VSD
-CXR, ECG: Normal
-ECHO: diagnostic
Treatment of small VSD
- Reassurance (Spontaneous closure is common)
- Prophylaxis against infective endocarditis
Examination of small VSD
a. General: Normal
b. Cardiac: Pansystolic murmur
history of large VSD
- Onset: second week of life
- Feeding difficulties, failure to thrive (FTT) and excessive sweating in infants
- Dyspnea, exercise intolerance in older children
- Recurrent chest infections (Cough)
on examination of large VSD
a. General
= FTT (Heart failure)
= Recurrent chest infections
b. Cardiac
= Inspection and Palpation
o Biventricular enlargement mainly the left ventricle (active precordium)
o Systolic thrill over the Lt parasternal area
= Auscultation
o Accentuated S2 (pulmonary hypertension)
o Murmur
- Timing: Pansystolic
- Character: Harsh
- Maximum intensity: Lt parasternal area (3° and 4” spaces) |
- Selective a propagation: ‘ All over the precordium
INV of VSD
- Chest X ray
= Heart: biventricular enlargement
= Chest: Lung plethora - ECG: biventricular hypertrophy (mainly the left ventricle)
- ECHO will assess
- Position and size of the defect and blood flow across
- Pulmonary pressure
- Cardiac dilation and efficacy of contractility
Treatment of VSD
Treatment
A) Medical
= Infective endocarditis (Prophylaxis and treatment)
= Proper nutrition
=» Management of HF: discuss
= Treatment of chest infections
B) Surgical closure (Surgery or catheter)
= Indications:
a. Large defect with failure of medical treatment
b. Infant 6-12 months old with large VSD and pulmonary hypertension
= Surgery should be delayed in stable child with moderate VSD. “Spontaneous closure”
= Surgery is contraindicated in patients with Eisenmenger syndrome
= Heart-lung transplantation is the only surgical option for Eisenmenger syndrome
= Pulmonary artery banding : to limit increased pulmonary blood flow may be
useful in multiple muscular VSD
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what is Tetralogy of fallot
- Large conoventricular VSD
- Pulmonary stenosis (usually infundibular, may be valvular)
- Overriding aorta
- RVH.
clinical picture of tetralogy of fallot
1.Cyanosis:
- Onset: Usually delayed (3-4 months) due to gradual narrowing of the
infundibulum and closure of the PDA
- May appear in the neonatal period (Severe cases)
- May be absent (Pink Fallot): symptoms appear with exercise only
2.Dyspnea
3.Hypercyanotic spell
4.Squatting.
Examination of TOF
B) Examination
a. General
Failure to thrive
Central cyanosis, appear on the under surface of tongue
Clubbing (1-2 years)
b. Cardiac
= Inspection and Palpation
o Left parasternal pulsation (RVH)
o Systolic thrill over the Lt 2” intercostal space.
= Auscultation
o Single S2 (S2 is slightly louder than normal due to anterior displacement of the aorta)
o Harsh ejection systolic murmur at 2™ left intercostal space due to pulmonary stenosis
Inv of TOF
CBC: increased Hb and increased hematocrit (microcytosis if there is iron deficiency)
2. Chest X ray : Coeur en Sabot (= Boot-shape)
3. ECG: Hypertrophy of the right atrium and right ventricle
4. ECHO
5. Cardiac catheterization: to visualize the coronary and pulmonary arteries
Treatment of TOF
PIPI
A) Medical
#Hypercyanotic spells
#Propranolol
= Iron
* Prostaglandin (PG1): in duct dependent pulmonary circulation( done in severe
cases presenting in neonates)
“ Infective endocarditis (Prophylaxis and Rx)
“ Partial exchange transfusion (using FFP or albumin), When? If hematocrit is > 65-
70%
* Prostaglandin (PG1): in duct dependent pulmonary circulation( done in severe
cases presenting in neonates)
B) Surgical
a. Palliative: Blalock-Taussig (anastomosis between Subclavian artery and the
ipsilateral pulmonary artery). Can be considered as “artificial PDA”
b. Total correction (at 6-9 months): Closure of VSD, infundibular resection and
pulmonary valvotomy
treatment of Hypercyanotic spells
- Positioning (knee-chest position/squatting)
- O» therapy
- IV fluid
NaHCOs: to correct acidosis
Sedation (SC Morphine)
IV B-Adrenergic blockers (Propranolol): to relax the infundibulum
Clinical picture of TGA
1.Deep central cyanosis (Early)
- Onset: Within the 1* few hours or days of life and Not relieved by 100% O2
2.Dyspnea
3.Manifestations of HF
4.Recurrent chest infections (Cough…)
Examination of TGA
B) Examination
a. General
= Failure to thrive (Heart failure) ;
= Central cyanosis Central cyanosis
= Clubbing (>1 year) in survivors
b. Cardiac
Inspection and Palpation: Left parasternal pulsation (RVH)
Auscultation
Accentuated S2
Murmurs: No murmur (if intact interventricular septum).
investiagation of TGA
- CBC: increased Hb and increased hematocrit
- CXR
= Heart: Egg-on-side, narrow pedicle (narrow upper mediastinum)
= Chest: Lung plethora - ECG: Hypertrophy of the RV and right atrium
- ECHO is diagnostic and prognostic
Treatment of TGA
- Prostaglandin: maintains the patency of ductus arteriosus
- Catheter: balloon atrial septostomy : Rashkind procedure ( urgent shunt)
- Surgical repair: Within the first 2-3 weeks of life: Arterial switch
most common oragnism causing infective endocarditis
Streptococcus viridans
Staphylococcus aureus
high risk causes of infective endocarditis
= RHD: Lt sided valves > Rt sided valves > Regurgitation > Stenosis
= CHD: Fallot tetralogy, TGA, VSD, PDA, Coarctation (Not ASD secundum)
“ Prosthetic valve, previous infective endocarditis, surgical shunts, residual defect
Intravenous drug use
history of previous endocarditis and cardiac transplantation
investigations of infective endocarditis
A) Laboratory
Blood culture (Repeated 3 times after proper skin decontamination)
= CBC, ESR, CRP
B) Imaging
= CXR, ECG
= ECHO (Vegetations)
= Transesophageal echocardiography for prosthetic valves
Treatment of infective endocarditis
A. Empirical therapy till culture results
1.Anti-staphylococcal penicillin (methicillin) + Aminoglycoside (gentamycin)
2. Suspected methicillin resistant S.aureus: Vancomycin + gentamycin
B. According to culture
Streptococcus viridans: Penicillin G or ampicillin or ceftriaxone for 4 weeks
and gentamycin for 2 weeks
Staph.aureus: vancomycin for 6 weeks AND gentamycin for 5 days.
Enterococci: penicillin or ampicillin for 4-6 weeks AND gentamicin for 2
weeks.
HACEK: ceftriaxone alone or ampicillin + gentamycin for 4 weeks
Vancomycin if penicillin or ceftriaxone are not tolerated
Amphotericin B for fungal infection.
Patients with prosthetic valves should be treated for 6 weeks according to culture
surgical care
in worsening valve obstruction or regurege or large vegetations or periventricular abscess or heart failure
Obstruction
Regurgitation
Large vegetations
Abscess
Heart failure