peds wk3 GI surgeries Flashcards

1
Q

gastroschisis and omphalocele incidence

A

rare 0.3-2:10,000 live births,

etiology unclear

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2
Q

what is gastroschisis

A

defect of anterior abdominal wall to the right of the umbilical cord.
no sac-bowel is exposed to the intrauterine environment,
bowel is matted, thickened, covered with an inflammatory coating,
usually involves only large and small intestines

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3
Q

what does gastroschisis result in?

A

malabsorption issues,
results in peritonitis, extracellular fluid loss,, significant heat loss,
fascial defect is 2-5cm

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4
Q

what artery or vein cause vascular event resulting abnormality for gastroschisis

A

right omphalomesenteric artery or right umbilical artery

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5
Q

In gastroschisis, abnormality of _____ ________ artery or _____ ______ vein, results in ischemia to ______ _______ area and _______ abdominal wall growth and weakened area ruptures as abdominal organs grow

A

right omphalomesenteric artery,
right umbilical vein,
right paraumbilical area,
dysplastic

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6
Q

OmphaloCele

A

“central”

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7
Q

what is omphalocele?

A

Central defect of umbilical ring/base of umbilical cord.
Abdominal contents are within a sac.
Umbilical cord embedded in sac.
Fascial defect >4cm.

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8
Q

in Omphalocele what does the sac contain at what percentage of time?

A

stomach, large and small intestine, liver (30-50%)

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9
Q

If sac in omphalocele is less than 4cm?

A

Considered umbilical hernia, (can be as big as 10-12cm)

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10
Q

risk factors for gastroschisis?

A

young maternal age, tobacco and alcohol exposure during development

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11
Q

Embryology of omphalocele?

A

week 7-12 midgut herniates into umbilical cord,

week 12 abdominal cavity is large enough, gut re-enters abdomen. (in omphalocele, gut fails to return)

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12
Q

Associated anomalies with gastroschisis?

A

usually isolated lesion

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13
Q

Associated anomalies with omphalocele?

A

50-70% incidence of other anomalies,
20-30% incidence of chromosomal abnormalities,
Beckwith-wiedemann syndrome, reiger syndrome, prune belly syndrome,
Trisomy 13, 15, 18, 21,
cardiac 20%

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14
Q

associated anomalies with beckwith-wiedemann syndrome

A
(macrosomia)
omphalocele,
visceromegaly,
macroglossia,
mild microcephaly
hypoglycemia
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15
Q

Omphalocele survival rates

A

isolated defect 95-97%,
without congenital heart defect 70%,
with congenital heart defect 20%,
prematurity also contributes to increased mortality

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16
Q

comparison of gastroschisis

A
1:10,000
isolated lesion,
lateral defect(usually right),
umbical cord normal,
bowel exposed, thickened, edematous
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17
Q

comparison omphalocele

A

1:4,000-7,000
assoc. anomalies common,
central defect,
umbilical cord within defect,
sac covers organs, bowel normal

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18
Q

surgical management of omphalocele and gastroschisis

A

replacing the viscera and repairing the defect,
primary vs staged repair with soli/mesh chimney,
staged-organs gradually returned to the abdominal cavity over 3-14 days

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19
Q

negative effects of tight abdominal closure

A

impairs diaphragmatic excursion-inadequate vent, increased airway pressure,
impedes venous return-profound hypotension,
aortacaval compression- bowel ischemia, decreased CO, renal and hepatic dysfunction,
Abdominal compartment syndrome

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20
Q

Unsafe for primary closure

A
intragastric pressure >20mmHg,
Change in CVP >4mmHg above baseline,
ETCO2 >50mmHg,
Peak inspiratory pressure >35cmH2O,
CVP change >4 above baseline can indicate reductions in venous return and CI
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21
Q

Fluid resuscitation

A

massive fluid losses from peritonitis, edema. Ischemia, protein loss, third space loss results in dehydration metabolic acidosis, hypovolemic shock.
maintenance fluid- D5 or D10 in 0.2 NS,
Replacment fluid-isotonic solution at 2-4 times main rate,
Urine output 1-2mL/kg/hr
Monitor glucose electrolytes, acid/base.
NS or LR as replacement (8-15mL/kg/min

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22
Q

how to prevent heat loss from exposed viscera

A

cover abd. contents with warm, saline soaked gauze,

or plastic bowel bag

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23
Q

preoperative management

A

treat sepsis with broad spectrum antibiotics,
avoid trauma to organs,
prevent aspiration-decompression of stomach with orogastric tube
chest xray, echo, ABG, CBC

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24
Q

anesthetic management

A

ASA standard,
2 pulse ox-pre ductal (right arm) and post ductal (left foot),
2 large bore IVs above diaphragm(d/t aortacaval compression, 24g large)
a-line,
foley,
airway pressure,
CVP-changes in blood volume, magnitude of visceral compression

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25
Q

Induction

A

preoxygenate, atropine, decompress stomach,
IV RSI w/ cricoid pressure,
IH induction and ETI,
Awake intubation

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26
Q

Maintenance

A
Avoid N2O,
Oxygen/air/IH agent,
muscle relaxation,
opioids-fentynal boluses, remi infusion,
FIO2 to maintain SPO2 95-97%, PaO2 50-70 mmHg (full-term)
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27
Q

Fluids

A

D5 .2 NS,
Third space isotonic 8-15mL/kg/hr,
replace blood loss with washed PRBCs (decreased K in Washed)

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28
Q

How to prevent hypothermia

A

Room temp 80,
full access bair hugger blanket,
fluid warmer,
plastic wrap for extremities, head, leave the babies hat on

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29
Q

extubation multiple factors

A
size of patient/prematurity,
associated anomalies,
size of defect(small defect-easier to extubate),
type of repair, 
intraop events,
hemodynamic status
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30
Q

postop management

A

mechanical vent 24-48hrs-great improvement in resp compliance,
fluid requirements closely monitored,
circulatory compromise-cyanotic lower limbs, owel sichemia,
prolonged postop ileus-TPN required for days to week,
prevent infection,
bowel distention

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31
Q

postop complications

A
pneumonia,
necrotizing enterocolitis,
renal insufficiency,
abdominal wall breakdown,
gastroesophageal reflux,
need for further surgeries related to bowel obstruction or adhesions causing issues
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32
Q

what is congenital diaphragmatic hernia and incidence

A

defect in that diaphragm allows herniation of abdominal organs into the thoracic cavity through a diaphragm that fails to full develop early in gestation.
1:2,500-3,000 live births

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33
Q

CDH associated anomalies

A

malrotation of the gut-40%,
CV 20%
CNS, GI, GU 15-30%

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34
Q

CDH classification

A

Posterolateral 80-90% left 75%,
Anteromedial 2%,
Para esophageal 15-20%

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35
Q

CDH complication factors

A

bilateral lung hypoplasia,
pulmonary htn and arteriolar reactivity (abnormal vasculature),
left ventricular dysfunction.
These facots result in significant short and long term morbidity and a 30-50% mortality rate

36
Q

CDH patho

A

Abdominal viscera occupies the left thoracic cavity and interferes with the development of the lung resulting in pulmonary hypoplasia. Viscera-midgut, stomach, parts of descending colon, L kidney, L lobe of liver

37
Q

CDH which way do abdominal contents shift mediastinum?

A

Right.

38
Q

CDH chronic lung disease d/t

A

small number of airways,
simple arterial branching pattern,
increased smooth muscle mass in resistance vessels,
left ventricular abnormalities

39
Q

what is usally the problem in CDH ventilation or oxygenation?

A

vent-rising CO2

40
Q

CDH classic triad progression

A

appear within minutes to hours,
Dyspnea,
Cyanosis,
Apparent dextrocardia(heart points to the right instead of the left)

41
Q

CDH physical exam

A
bulging chest and scaphoid abdomen,
decreased breath sounds,
distant or right displaced heart sounds,
bowel sounds in the chest,
ches xray bowel loops in the chest and mediastinal shift
42
Q

what is the key to survival of CDH

A

prenatal diagnosis for birth in high level nicu w/ experienced pediatric surgeons.
On US, bowel in the thoracic cavity can be seen.

43
Q

T/F: Previously CDH was considered neonatal surgical emergency wotj GOAL to hyperventilation with 100% O2 to produce pulmonary vasoconstriction with hyperoxia and respiratory acidosis

A

FALSE,
Pulmonary vasoDILATION,
respiratory ALKALOSIS
(ended up causing a secondary lung injury)

44
Q

Previous intervention of CDH of hyperventilation caused over distention of lung tissue and damage to the alveolar and capillary membranes. Net effect-

A

inflammatory response that caused release of vasoactive mediators, worsening pulmonary vasoconstriction and pulmonary HTN

45
Q

New Goals of medical management of CDH

A
Stabilize prior to surgery for 24-48hrs,
Maximize arterial oxygenation
-intubate, mech vent w/ low inflating pressures ,20-30cmh2o, maintain muscle relaxation, improve pulmonary perfusion, 
Correct acidosis,
Prevent hypothermia,
Prevent pain
46
Q

When can surgery occur for CDH?

A

BP normal for age and stable for 24 hrs,
preductal sat >85 (preferably 90-95) with FIO2 less than 0.5,
No acidosis (lactate <3),
urine output 1 to 2mL/kg/hr

47
Q

Continued medical management goals

A

Bag mask vent has potential to create distention of stomach and intestines resulting in decreased chest compliance,
improve pulmonary perfusion by hypervent (PaCO2 25-30mmHg) but unless right to left shunting occured, permissive hypercapnea (55-60) should occur helping to provide less aggressive vent support resulting in 2nd lung injury, fent infusion, minimal handling,
Nitric oxide-causes vascular smooth muscle relax, decreased PVR,
ECMO

48
Q

CDH after intubation tidal volumes should be

A

5-10mL/kg

49
Q

ECMO most common cannulation sites

A

IJ and common carotid

50
Q

Complications of ECMO

A
Bleeding at cannulation sites,
ICH,
Sepsis,
HTN,
brain death,
clots to brain,
microemboli to fingers/toes(lose them)
51
Q

ECMO criteria

A

weight more than 2.0kg,

gestation >35wks

52
Q

ECMO long term survival

A

without ecmo >80%

after ecmo 50-60%

53
Q

CDH Preoperative prep

A

Eval for other anomalies,
labs-cbc, lytes, glucose, abg, T+C,
IV access-upper extremities, internal jugular (vena cava sometimes compressed after reduction of hernia),
PREVENTION OF HYPOTHERMIA

54
Q

CDH Preop management

A

vent support
meticulous management of fluids and nutrition,
hemodynamic monitoring,
often a honeymoon period followed by deterioration
-increased intrabdom pressure
-decreased perfusion of the viscera and the periphery
-decreased diaphragmatic excursion
-worsening pulmonary compliance
(unexplained reasons, usually require NO and ECMO)

55
Q

CDH Anesthetic management monitors

A
ASA standard,
aline,
foley,
precordial stethoscope at right axilla,
ng to decompress the stomach,
IV access,
core temp management-PREVENT HYPOTHERMIA
56
Q

CDH anesthetic management Induction

A

Awake intubation,
RSI,
Avoid mask ventilation or positive pressure vent before intubation

57
Q

CDH anesthetic management Maintenance

A

AVOID N2O,
TIVA-remifentanil infusion and muscle relax,
IH agent, opioids, muschle relax,
Avoid hypoxia, acidosis which increase PVR and cause R>L shunting,
Replace blood loss

58
Q

Hypothermia does what to PVR and cause what type of shunting through PDA or patent foramen ovale

A

INCREASE PVR,
increase right to left shunting,
Also increases oxygen consumption

59
Q

why avoid N2O in CDH?

A

higher o2 concentration required, n2o could expand viscera and cause compression of lungs

60
Q

CDH Surgical Repair

A

Open vs thoracoscopic,
subcostal abdominal approach most common,
transthoracic(can cause CO2 increase with insufflate) or throracoabdominal also possible,
primary closure vs staged repair with silo - abdomen must be able to accommodate return of viscera

61
Q

Surgical complications CDH

A

Hypoxemia from pulmonary htn, pulmonary hypoplasia, respiratory compromise from distention of stomach, increase intrabdominal pressure,
contralateral pneumothorax,
IVC compression, hypotension (must differentiate between pulm htn crisis or pneumo quickly)

62
Q

how to treat pulm htn crisis vs pneumo

A

add NO and hypervent or perform needle decompression and chest tube placement

63
Q

CDH outcomes-pulmonary, musculoskeletal deformities, GI, Neuro

A

resp-first year post op multiple resp infections, later near normal,
MSK mild chest deform
GERD, bowel obstruction,
d/t pulm htn lack of perfusion lead to cognitive issues.

64
Q

Pyloric stenosis incidence

A

1 in 500 live births,
4 times more in males,
acquired not congenital,
more often if a parent had same condition

65
Q

pyloric stenosis patho

A

gross thickening of the circular smooth muscle of the pylorus,
results in gradual obstruction of the gastric outlet,
causes forceful projectile nonbilious vomiting “across the room and hitting wall”,
present between 2-8wks of life (most commonly 4 wks and 4 kg)

66
Q

pyloric stenosis diagnosis

A

palpate olive-sized mass in the upper aspect of abdomen,

verified by upper GI series with barium, xray or abdominal US

67
Q

pyloric stenosis clinical presentation

A

persistent vomiting results in the loss of acidic gastric juices rich in hydrogen, chloride, and to a lesser degree Na ions,
vomitus does not contain the alkaline secreations of the duodenum,
kidneys begin secreting K ions in exchange for hydrogen in an attempt to maintain normal arterial pH,
patient develops a metabolic alkalosis- decreased Na and Cl
after vomiting, pt is hungry again-differentiates from other etiologies of chronic vomiting

68
Q

pyloric stenosis clinical presenttion

A

a dehydrated infant with a hyponatremic, hypokalemic, hypochloremic metabolic alkalosis (very important)
severe cases can manifest as metabolic acidosis secondary to severe dehydration and hypoperfusion

69
Q

pyloric stenosis treatment

A

Medical emergency NOT surgical emergency,
Correct fluid and electrolyte imbalance by administering IV fluids containing Na, KCl, and glucose-D5 0.45% NSS with KCl 40meq/L for 12-48hrs.
After correction, surgical correction performed.

70
Q

what is the primary anesthetic concern in in pyloric stenosis?

A

Aspiration of gastric fluid,
suction stomach with large bore (14 fr) catheter at least 3 timesbefore intubation, RSI (do not ventilate),
Atropine for vagal response

71
Q

how is tracheoesophageal fistula characterized?

A

by esophageal atresia with or without a communication (fistula) between the esophagus and trachea.

72
Q

Most common TEF type

A

C

73
Q

Incidence of TEF

A

most common esophageal anomaly 1:3,000-4,500,
Survival >90%,
prenatal hx - prematurity (20-40%), polyhydramnios(infant cannot swallow amniotic fluid)(60%)
Type E often escapes dx until later in life w/ recurrent pneumonias

74
Q

TEF clinical presentation

A
inability to manage oral secretions,
excessive salivation,
choking on first feed,
coughing,
cyanosis,
aspiration,
gastric distention,
pneumonia
75
Q

TEF diagnosis

A

inability to pass suction cath or orogastric tube into the stomach,
chest xray confirming position of catheter in esophageal pouch, air in the stomach and intestines

76
Q

TEF Associated anomalies VATER or VACTERL

A
vetebral anomalies,
anorectal,
cardiac 20-25%,
TEF,
Esophageal atresia,
Renal,
Limb,
35-65% overall
77
Q

TEF surgical repair

A

identification and ligation of the fistula,
Primary or staged using stomach and intestine,
placement of feeding gastrostomy,
chest tube

78
Q

TEF Preop Prep

A
Minimize pulmonary complications
NPO,
HOB 30 or consider prone or later,
esophageal sump to LCWS,
12lead, echo mandatory,
central for TPN,
Labs,
medical stable- treat pneumonia, optimize volume and acid/base
79
Q

TEF anesthetic management

A
Priorities
oxygenation,
ventialtion,
securing airway,
prevent aspiration
Monitors
ASA STandard,
Precordial stethoscope over LEFT chest,
Aline
80
Q

TEF Induction

A

Induction-concerns are aspiration, gastric distention, resp compromis,
unstable infant-consider gastrostomy insertion and awake intubation;this allows ETT positioning without PPV
Stable infant- IH induction with spont vent vs IV induction,(avoid or min PPV-small TV, low PIP)

81
Q

TEF ETT position

A

Goal-above carina, below the fistula

Technique-right mainstem intubation, withdraw ETT until breath sounds are confirmed at the L axilla

82
Q

TEF Maintenance

A

L lateral decubitus position for R thoracotomy,
after ligation of fistula, muscle relax and controlled vent,
Tech- IH agent, opioids,
AVOID N2O

83
Q

TEF Intraoperative Complications

A

R mainstem intubation,
Intubation of fistula,
Obstruction of ETT from secretions, blood, infectious material,
obstruction/compromise of trachea or bronchus by surgeon,
atelectasis, lung retraction,
Hypothermia,
Hypoglycemia,
Resumption of fetal circulation- R to L shunting

84
Q

TEF Emergence

A

Goal-extubate at end of surgery to prevent manipulation of anastomosis from ETT,
Pt must be able to maintain airway patency-reintubate could damage repair,
consider that pt may have tracheomalacia or tracheal collapse

85
Q

TEF postop

A

No extension of the head-puts tension on the anastomosis,
No esophageal suctioning beyond the level of esophageal anastomosis,
Long term- esophageal stricture, tracheomalacia, GERD