Transcript 九十一年六月分CPC 助猜三軍總醫院小兒科

九十一年六月分CPC
助猜三軍總醫院小兒科
林偉仁大夫/李春銘主治
2002,JUN 18th
Present illness
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A female had been born to a 22-year-old women with birth history
of G3P3A0, GA: 39+ wks, NSD, BBW: 3346 gm (75 percentile ),
Apgar score: 79 at 15 min. BBL: 49.5CM (75 percentile) and
HC: 33.4 CM (75 percentile ).
Because of congenital heart disease(CHD) suspected by fetal
echocardiogram and uneventful pregnancy delivery with fetal
distress, bradycardia and cyanosis, this newborn admitted to our
NICU initially and the echocardiogram revealed large ASD(1.22
cm), muscular VSD(0.34 cm), R’t peripheral pulmonary artery
stenosis (RPPS), pulmonary hypertension and r/o abnormal
pulmonary venous return.
Present illness
During the first year of life, she had 3 episodes of
bronchiolitis or bronchopneumonia and one
gastroenteroritis. Due to failure to thrive BW: 5.8 kg(<3
percentile), BL: 67 cm(<3 percentile) when she was oneyear-old), she was admitted for ASD repair on March 8,
2002.
 Before the surgical procedure on March 11, 2002, her CV
condition showed progressively severe pulmonary
hypertension and cardiomegaly followed.
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Hospital course
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However, a series of stressful, complicated episodes
occurred after operation. First of all, surgical wound
infection with MRSA cultured was noted on March 23
after successful extubation. But the following respiratory
distress then impending respiratory failure of her was
present. Bronchoscope had found tracheal stenosis with
bronchomalacia later. CXR showed bilateral exaggerative
infiltration of lung, especially R’t upper lung and
cardiomegaly was also revealed. The result of sputum
culture was MRSA.
Hospital course
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Unfortunately, pulmonary hemorrhage and acute
fulminent hepatic failure (AST/ALT revealed 8140/2840
U/L) occurred on April 7, and April 10 respectively.
Meanwhile, DIC test had been shown positive finding.
Repeated echocardiogram showed severe MR(4+), TR(4+);
mild to moderate AR(2+), PR(2+); enlarged L’t atrium and
R’t atrium RV-RA pressure gradient about 36 mmHg with
normal LV ejection fraction. Due to unstable viral sign and
occasional oliguria ( CCR: 57 ml/kg/1.73m2 pm March
24), dopamine and dobutamine were administered.
Hospital course
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Brain-echo showed generalized brain
atrophy and benign subarachinoid fluid collection,
coarse face and mild hypotonia were also present.
Massive ascites and engorged hepatic vein, IVC
and hepatosplenomegaly were scanned by
abdominal sonogram.
Hospital course
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her general condition became worse day
by day, and sinus bradycardia then frequent VPCs
presented, urinary retention, imbalance electrolyte
with hypokalemia, hypocalcaemia, and
hypoglycemia were also noted but unresponsive to
any correction. Due to ineffective resustation, P’t
was expired on May 5, 2002.
CBC
Date
WBC
HGB
PLT
DCB/S/L/M
CRP(mg/
dl)
3/8
8560
11.9
310K
0/31/60/4
0.1
3/11
15600
10.2
156K
2/75/20/3
3/21
23000
9.5
436K
1/85/9/3
2070
DIC
4/9
4/15
17000
11600
10.6
11.9
121K
208K
17/30/10/
32
0.95
11/40/11/
34
3.0
1700
1276
5/1
12400
11.4
255K
12/30/11/
33
1.10
5/4
14700
10.2
105K
0/82/16/1
0.32
1364
Blood
GAS
Date
PH
PO2
PCO2
HCO3-
BE
Sat
3/11
7.32
161
44
22.6
-2.3
99
3/12
7.40
127
37
22.9
-1.1
99
3/24
7.49
126
72
54.8
30.0
99
3/24
7.51
117
57
45.4
21.7
99
4/3
7.47
90
53
38.5
14.6
97
4/12
7.50
29
54
42.0
16.9
63
4/20
7.43
32
50
33.1
7.7
64
4/25
7.57
29
49
44.8
20.7
67
5/3
7.35
30
58
32.0
5.7
54
5/5
7.00
21
99
Others
 Ascite
culture, EBV, CMV, HBV, HCV, HAV study:
Negative
 Urine culture (May 4): Yeast like pathogen and
Fungus culture: candida
 Antibiotics treatment:
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Cefazolin + Netromycin (March 11 – March 24)
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Vancomycin + Fortum ( March 24 – April 11)
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Vancomycin + Metropenem (April 11 – May 5)
Abnormal finding
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CV condition:
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Congenital heart disease-- large ASD(1.22 cm), muscular VSD (0.34 cm), r’t
peripheral pulmonary artery stenosis (RPPS), pulmonary hypertension and r/o
abnormal pulmonary venous return.
Progressively severe pulmonary hypertension and cardiomegaly
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MR(4+), TR(4+); Mild to moderate AR(2+), PR(2+); Enlarged l’t atrium and r’t atrium RV-RA
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pressure gradient about 36 mmhg.
Massive ascites and engorged hepatic vein, IVC and hepatosplenomegaly.
Infection:
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Frequent infection: 3 episodes of bronchiolitis or bronchopneumonia and one
gastroenteroritis during her first year.
MRSA infection in surgical wound, sputum culture
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Urine culture: Yeast like pathogen and Fungus culture: candida
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DIC
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Abnormal finding
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Immunodeficiency:
 Absolute lymphocyte count< normal range (2180-8270 12mo-23mo)
 Frequent infection
Multiple organ failure:
 Oliguria--CCR: 57 ml/kg/1.73m
 Pulmonary hemorrhage and acute fulminent hepatic failure.
 Respiratory failure
 Flumient hepatic failure
 Generalized brain atrophy
Coarse face and mild hypotonia.
Tracheal stenosis with bronchomalacia.
Metabolic alkalosis
Failure to thrive
Hypokalemia, hypocalcaemia, and hypoglycemia unresponsive to any correction.
請教出題老師
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What is the coarse face feature?(cleft palate)
Is there any abnormal physical finding of this baby?(absence
tonsile )
Does any parathyroid hormone and thyroid function test been
checked?
Dose blood culture showed any abnormal finding?
Dose other abnormal finding of chest x ray?
Doses any immunoglobulin or T-cell function test been checked?
Is there any complication during perioperation or postoperation?
Pulmonary hypertension
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Secondary:
 Increase pulmonary blood flow from CHD
 VSD
 AVSD
 PDA
 Isolated ASD, after many decades.
 Irreversible pulmonary hypertension(with cyanosis)
 Pulmonary venous obstruction
 Obstructed anomalous pulmonary venous return
 Pulmonary vneoocclusive disease
 Left sided heart failure
 Dilated cardiomyopathy
 Mitral valve stenosis or severe incometence
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Lung disease, airway obstruction, hypoventilation– cor pulmonale
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RV hypertrophy, right side heat failure secondary lung or airway disease
Atrial Septal Defect
 Ostium
secundum defect: The most common yet least
serious type of ASD
 Ostium
primum defect: failure of the endocardial cushions to
close the ostium primum. Because endocardial cushions also form the
mitral and tricuspid valves, ostium primum defects virtually always are
associated with a cleft in the anterior mitral valve leaflet.
 Sinus
venosus defect: This ASD is found in the posterior
aspect of the septum near the superior vena cava
 Coronary
sinus septal defect: The least common type of
ASD. A portion of the roof of the coronary sinus is missing.
Mortality/Morbidity
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In developed countries, the rate of mortality from ASD is very
low (ie, <1%). Morbidity secondary to ASD is unusual and is
limited typically to the following 3 groups of patients:
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Perhaps 1% of infants diagnosed with moderate or large (ie, nonrestrictive)
ASDs but no ductus arteriosus have tachypnea and fail to thrive. Pulmonary
artery pressure, is at or near systemic level in these individuals.
A second group of patients, in whom ASDs go unrecognized until later
childhood, may develop arrhythmias (eg, atrial fibrillation) or pulmonary
hypertension.
A third group of patients with ASDs has an embolic stroke as the initial
presentation.
Surgical Care
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Not all children with an ASD are candidates for surgery, which is indicated only for
those children with clinically significant left-to-right shunting.
Generally, a pulmonary-to-systemic flow ratio of 1.5:1 or more is considered the
principal indication for surgical repair.
Because cardiac catheterization is rarely necessary, echocardiographic evidence
of right atrial and right ventricular enlargement usually is considered evidence of a
significant left-to-right shunt and an indication for surgical closure of the ASD.
Ideally, surgery is performed in children aged 2-4 years; however, surgery may be
performed earlier if a child has evidence of CHF.
Operative mortality rate is low in patients with uncomplicated ASDs.
Postoperative morbidity in individuals with ASDs almost exclusively is due to
accumulation of pericardial fluid, which occurs in approximately one third of cases.
Occasionally, tamponade occurs and requires pericardiocentesis.
Trabecular (muscular) VSD
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This form is the second most common type of VSD, occurring
in 5-20% of most series.
Muscular VSD is also known as Swiss cheese VSD.
Frequently, spontaneous closure of muscular VSD occurs in
the first 2 years of life, the majority by 6 months.
AVSDs
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Atrioventricular septal defects, characterized by a deficiency of the atrioventricular
septum, are a broad spectrum of malformations presumed to result from abnormal
or inadequate fusion of the superior and inferior endocardial cushions with the midportion of the atrial septum and the muscular (trabecular) portion of the ventricular
septum.
Pulmonary hypertension and an early tendency to increase pulmonary vascular
resistance are common. AV valvular insufficiency increases the volume load on
one or both vesicles. With time, progressive pulmonary vascular disease increases
the right-left shunt so that clinical cyanosis develops.
With complete AVSD, CHF and intercurrent pulmonary infection usually appear in
infancy. The liver is enlarged and the infant shows sings of failure to thrive.
Mortality/Morbidity:
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Prognosis depends on the magnitude of the left to right shunt, the degree
of elevation of pulmonary vascular resistance, and the severity of AV valve
insufficiency.
Surgical for complete AVSD is more difficult, especially in infants with
cardiac failure and pulmonary hypertension. The risk of developing
pulmonary hypertension as early as 6-12 mo of age, surgical intervention
must be performed during infancy.
Morbidity in infancy and early childhood is generally caused by mitral
regurgitation (MR). Severe MR causes CHF, failure to thrive in infants and
may result in death if left untreated.
Immunodeficiency
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Most immunodeficiency diseases lead to repeated or chronic infections.
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Two or more systemic bacterial infection(sepsis, osteomyelitis or meningitis)
Three or more serious respiratory or documented bacterial infecions(cellulitis, draining
OM, lymphadenitis within 1 yr)
Infctions occureing at unusual sited
Unusual pathogens
Patients with defects in immunoglobulins (B cells), complement proteins or
phagocytes are very susceptible to recurrent pyogenic infections;
 Screening
 Absolute
tests for T-cell defects
lymphocyte count(normal result indicates Tcell defect unlikely)
Immunodeficiency
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T cell deficiencies are usually marked by repeated opportunistic
infections caused by viruses, fungi, and protozoans. Since B cell
function is largely T cell-dependent, T cell deficiency also results in
humoral deficiency. Thus, T cell deficiency leads to a combined
deficiency of both humoral and cell-mediated immunity.
 Infections
can be treated by administration of the
appropriate anti-microbial agents. Some T cell
deficiencies can be corrected by bone marrow
transplantation or fetal thymus graft.
Infective endocarditis
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Native valve endocarditis
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Congenital heart disease (15% of NVE) - Underlying etiologies include a patent
ductus arteriosus, ventricular septal defect, tetralogy of Fallot, or any native or
surgical high-flow lesion.
Approximately 70% of cases are caused by Streptococcus species including
Streptococcus viridans, Streptococcus bovis, and enterococci. Staphylococcus
species cause 25% of cases and generally demonstrate a more aggressive acute
course.
Mortality/Morbidity:
Increased mortality rates are associated with increased age, infection involving the
aortic valve, development of congestive heart failure, central nervous system (CNS)
complications, and underlying disease. Mortality rates also vary with the infecting
organism.
Mortality rates in native valve disease range from 16-27%. Mortality rates in
patients with prosthetic valve infections are higher. More than 50% of these
infections occur within 2 months after surgery.
Fungal endocarditis
Fungal endocarditis is found in intravenous drug users and intensive care unit
patients who receive broad-spectrum antibiotics.
 Blood cultures are often negative, and diagnosis frequently is made after
microscopic examination of large emboli.
 Mortality/Morbidity: The mortality rate remains 75-90% because of difficulty
making the diagnosis, lack of effective antifungal antibiotics, need for surgical
intervention in most cases, presence of underlying or predisposing conditions,
and frequent comorbid conditions in these typically critically ill neonates and
children.
Although a small number of patients have survived with medical therapy alone, the
majority of survivors have required both medical and surgical treatment. Operative
intervention is almost always required.
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Fungal endocarditis
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fewer than half of candidal endocarditis cases yield positive blood cultures and
other causative organisms are even less frequently identified in blood
Culture of urine, sputum, cerebrospinal fluid, synovial fluid, lymph node, and/or
bone marrow may offer the only evidence of systemic fungal infection.
Chest radiography
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A chest radiograph may reveal cardiomegaly.
Echocardiography
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Transthoracic echocardiography is less sensitive than transesophageal
echocardiography but is also less invasive.
Vegetations and intracardiac thrombi are the most common types seen but are rare
nonetheless.
Echocardiography may demonstrate pericardial effusion.
Normal valves are rarely involved.
Echocardiography may suggest myocardial abscesses.
Echocardiography may demonstrate associated myocarditis or pericarditis.
Metabolic alkalosis
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Causes:
 Chloride-responsive type
 Gastric fluid loss (vomiting, NG drainage)
 Volume contraction -- stimulates release of renin-angiotensin
 Chronic furosemide therapy
 Congenital chloride diarrhea
 Posthypercapnia syndrome -- Chronic CO2 retention causes a compensatory
increase in HCO3 levels.
 Hypoparathyroidism
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Chloride-resistant type
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Primary aldosteronism
Bartter syndrome –urine Cl loss, plasma renin and aldosterone increase.
Liddle syndrome
Excessive ingestion of licorice
Chronic potassium depletion
Primary reninism
Hyperglucocorticoidism
Milk-alkali syndrome
Severe metabolic alkalosis
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Is associated with increased morbidity and mortality, probably due to its
profound influences on multiple organ systems and, more importantly, to
tissue anoxia caused by hypoventilation and shift of the oxygendissociation curve to the left.
Cardiovascular system: Life-threatening arrhythmias are the most
significant adverse effect of metabolic alkalosis. Because of heightened
electrical excitability, ventricular arrhythmias can occur, which often are
unresponsive to antiarrhythmic agents.
Neuromuscular system: Patients with severe metabolic alkalosis can
develop obtundation and marked muscle weakness that resolve only with
correction of the pH.
Ionized calcium concentration: Metabolic alkalosis may cause a decrease
in ionized calcium because of increased binding of calcium to plasma
proteins; consequences include tetany and seizures.
Fulminant Hepatic Failure
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Infectious agents: In approximately 50% of patients, FHF is
caused by acute viral hepatitis, commonly caused by hepatitis
viruses A; B; non-A, non-B; D; or E. Many viruses other than
hepatitis also are recognized causes of FHF in childhood,
including Epstein- Barr virus; cytomegalovirus (CMV);
paramyxovirus; varicella-zoster virus; herpesvirus types 1, 2,
and 6; parvovirus; and adenovirus.
Circulatory causes: Circulatory causes are uncommon in FHF.
They include congestive heart failure, cardiomyopathy, sepsis,
shock, cyanotic heart disease, obstructive lesions of the aorta,
vascular occlusions, myocarditis, and severe asphyxia.
Fulminant Hepatic Failure
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In the US:In the pediatric age group, exact incidence of FHF remains
unknown, but it is estimated to be approximately 50 cases per year.
Mortality/Morbidity:
The mortality rate may reach 80-90% in the absence of liver
transplantation. In some pediatric series, survival rates of 50-75% have
been reported.
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Complications:
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Infections: Bacterial and fungal infections commonly occur, leading to the
development of peritonitis, pneumonia, urinary tract infections, or
septicemia.
Ascites, splenomegaly, hepatomegaly
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The ascites frequently is a component or a complication of hepatic sirrhosis,
congestive heart failure, nephrosis, or carcinoma. (transudate)
Obstructed venous blood flow from intrahepatic or extrahepatic etiologies
can cause splenomegaly. The most common causes include portal vein
thrombosis, hepatic cirrhosis, and congestive heart failure.
Excessive antigenic stimulation from infection causes most splenomegaly
in children. Viral infections are the most frequent culprits, and the
associated splenomegaly usually is transient and only mild to moderate in
severity.
Other common infectious etiologies include bacterial, protozoal, and
fungal infections. Concomitant generalized lymphadenopathy is common
in many of these infectious etiologies.
Hepatomegaly with underlying systemic disorder present--- cardiovascular
disease( right heart failure)
Hypokalemia
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be due to a total body deficit of potassium,
which may occur due to chronic inadequate
intake, long-term diuretic or laxative use, and
chronic diarrhea, hypomagnesemia, or
hyperhidrosis.
 Acute causes of potassium depletion include
diabetic ketoacidosis, severe gastrointestinal
losses from vomiting and diarrhea, dialysis,
and diuretic therapy.
Hypokalemia
 Mortality/Morbidity:
 Mortality
is rare, except when hypokalemia is
severe or occurs in a patient with underlying
heart disease requiring digoxin therapy,
following cardiac surgery, or when
accompanied by arrhythmia.
Hypocalcemia
The concentration of calcium in the serum is critical
to many important biological functions, including the
following:
 Calcium messenger system by which extracellular
messengers regulate cell function
 Activation of several cellular enzyme cascades
 Smooth muscle and myocardial contraction
 Nerve impulse conduction
 Secretory activity of exocrine glands
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Hypoparathyroidism
Aplasia or hypoplasia - DiGeorge syndrome, velocardiofacial syndrome, maternal
diabetes mellitus or treatment with retinoic acid, VATER complex (vertebral defects,
anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal
abnormalities), CHARGE association (coloboma, heart defects, choanal atresia,
renal abnormalities, growth retardation, male genital anomalies, ear abnormalities)
Symptoms:
weakness , muscle cramps, abnormal sensations such as tingling, burning and
numbness (paresthesias) of the hands excessive nervousness, loss of
memory, headaches and uncontrollable cramping muscle movements of the
wrists and feet.
Other symptoms may be spasms of the facial muscles (Chvostek Sign), the
contraction of muscles produced by mild compression of nerves (Trousseaus
Sign), malformations of the teeth, including enamel and roots of the teeth; and
malformed finger nails.
Complications of
hypoparathyroidism
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Are largely due to hypocalcemia.
Neurologic: Hypocalcemia leads to neuromuscular irritability. Affected
patients may experience paresthesias, muscle cramping, tetany, or
seizures. However, patients can be asymptomatic. Neck muscle cramping
can cause dystoniclike neck movements.
Cardiac: Hypocalcemia causes prolongation of the QTc interval. Affected
individuals may be asymptomatic or suffer syncope, seizure, or death due
to arrhythmias, such as polymorphic ventricular tachycardia.
Respiratory: Laryngospasm, a form of tetany, can lead to stridor and
significant airway obstruction.
Bronchoscopy
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Tracheo/broncho malacia is the most common cause of expiratory stridor.
It is caused by a defect on the cartilage resulting in the loss of rigidity
necessary to maintain the tracheal lumen patent or by an extrinsic
compression of the trachea.
Tracheal stenosis can be congenital or secondary to extrinsic
compression. Congenital stenosis is usually in the for on complete
tracheal rings, characterized by a persistent stridor, and requires surgery
based on severity of symptoms. The most common extrinsic causes of
stenosis include vascular rings, slings, and a double aortic arch that
encircles the trachea and esophagus. External compression could result in
tracheomalacia as well. Patients usually present during the first year of life
with noisy breathing, intercostal retractions, and a prolonged expiratory
phase.
DiGeorge Syndrome Hx.
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DiGeorge syndrome (DGS), which was described by Angelo DiGeorge, MD, in 1965, ---congenital cardiac anomalies, craniofacial dysmorphology, and learning dysfunction, all of
which were traced to a defect in the third and fourth pharyngeal pouches during
embryogenesis.
10 years later, in Japan, Kinouchi et al described the conotruncal anomalies face (CTAF)
syndrome, composed of congenital conotruncal cardiac anomalies, characteristic facies,
learning dysfunction, and developmental delay
Shprintzen et al described their experiences in a craniofacial clinic with a syndrome of
congenital conotruncal cardiac anomalies, characteristic facies, velopharyngeal dysfunction
with or without cleft palate, and learning dysfunction, which they termed the velocardiofacial
syndrome (VCFS).
Genetic support for this came in 1981
A common area of deletion, known as the DiGeorge syndrome critical region (DGCR), was
found on band 22q11.2. As a result, these 3 syndromes have been combined into one
genetic entity with variable phenotypic presentations.
CATCH 22 be used for this group, since it describes the findings of cardiac anomalies,
abnormal facies, thymic hypoplasia, cleft palate, and hypocalcemia on chromosome 22
DiGeorge Syndrome
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A variable degree of hypoplasia of the thymus and parathyroid
glands is more frequent than total aplasia. (partial DiGeorge
syndrome– they may have little trouble with infections and grow
normally. )
Complete DiGeorge syndrome resemble patients with severe
combined immunodeficiency (SCID) in their susceptibility to
infections with low grade or opportunistic pathogens, including
fungi, viruses and Pneumocystis carinii, and to graft versus host
disease(GVHD)
Severe combined immunodeficiency disease
(SCID)
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Failure of stem cells to differentiate into T and/or B cells.
Infants with SCID have very few lymphocytes in their blood (<3000/ml), and
there are no or few lymphocytes in their lymphoid tissue (including the thymus,
which has a fetal appearance).
SCID patients are susceptible to all microbial infections, most notably rotavirus,
cytomegalovirus, Candida albicans and Pneumocystis carinii.
Symptoms occur in early infancy and prove fatal within the first year of life if left
untreated. They have prolonged diarrhea, develop pneumonia, and may die of
progressive infection if immunized with live organisms.
Bone marrow transplants are the treatment of choice.
Chromosome 22q11 deletion syndrome
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The estimates are now closer to 1:4,000.
The characteristic facies of this syndrome are often subtle in
infancy and not fully manifested until the child is older;
therefore, they are not common causes of genetic
investigation. The same is true of developmental delays,
which often are not noticed until the child is of school age. A
recent review of a large series reported involvement as
follows: cardiac system (49%), developmental delay (16%),
behavioral disturbance (7%), otolaryngologic system (6%),
psychiatric symptoms (3%), and mental retardation (2%).
Chromosome 22q11 deletion syndrome
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Mortality/Morbidity: The aspects of the deletion syndrome that lead to the
greatest morbidity and mortality are cardiac. Only a small fraction of patients
experience recurrent infection secondary to immunodeficiency, which involves
primarily the T-cell lineage. Failure to thrive may be observed during early infancy
in those with cleft palates and swallowing difficulties.
Age of presentation depends largely on the severity and nature of the defect, thus
those with more serious cardiac defects and/or hypocalcemia observed in classic
DGA are diagnosed in the neonatal period.
Recurrent infections usually present in patients older than 3-6 months. Some
individuals without hypocalcemia who have normal immune function, mild cardiac
defects, and minimal facial anomalies may not be diagnosed until late childhood.
(partial Digeorge syndrome)
Chromosome 22q11 deletion syndrome
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interrupted aortic arch, followed by a right aortic arch.
bicuspid aortic valve, membranous ventricular septal defects, aberrant right
subclavian artery, and atrial septal defects.
Patients usually have characteristic facies, which become more pronounced as the
children grow into the second decade. Many affected children present when aged
1-2 months with poor suck as a result of the velopharyngeal insufficiency alone
and/or in combination with the generalized hypotonia that sometimes is observed
in these infants.
IMAGE:
 Thymus: Chest radiographs can demonstrate a decreased thymic silhouette
but are unreliable. MRI is slightly better; however, thymic size is a poor
predictor of immune function.
Chromosome 22q11 deletion syndrome
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Alcohol consumption during the early stages of fetal
development may be one of many environmental explanations
for the microdeletion.
Prenatal testing for DiGeorge syndrome is widely available and is
recommended for fetuses that have been detected as having
cleft palate or heart malformation through ultrasound, and have
at least one parent testing positive for the 22q11 microdeletion.
Infants with the 22q11 microdeletion should be monitored for
hypocalcemia, renal function and low lymphocyte count. Babies
with low lymphocyte counts should be seen by an immunologist
and should not be given live vaccine immunizations.
Diagnosis of mortality:
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Sepsis with DIC (MRSA), R/O Fungal endocarditis
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Congestive heart failure with pulmonary hypertension.
Congenital heart disease with AVSD S/P repair with Postoperative mediastinitis
Arrythemia
R/o hypoparathyrodism
R/O Chromosome 22q11 deletion syndrome
Fulminant Hepatic Failure
Acute renal failure
Acute respiratory failure
Metabolic alkalosis
Hypocalcemia
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