General Surgery Pediatrics Flashcards

1
Q

Calculation of IV fluid requirements

A

total fluid intake = deficit + maintenance + ongoing losses

Deficit:

deficit can be calculated directly or indirectly

1) direct calculation
based on measured fluid ins & outs and exact weights
usually only in ICU setting

2) indirect calculation
estimate of deficit based on clinical assessment
estimated deficit categorized according to % weight loss

<1 year: mild = 5% = 50mL/kg; moderate = 10% = 100mg/kg; severe = 15% = 150mL/kg

> 1 year: mild = 3% = 30mL/kg; moderate = 6% = 60mL/kg; severe = 9% = 90mL/kg

a) mild dehydration usually only has findings on history only
tachycardia usually 1st physical sign of dehydration, because pediatric patients have limited space for stroke volume increase and thus rely on increased heart rate to compensate and increase cardiac output

b) moderate dehydration usually has physical exam findings
physical exam: irritability, sunken fontanelle, sunken eyes, dry mucus membrane, delayed capillary refill, decreased urine output

c) severe dehydration usually present as shock
physical exam: decreased level of consciousness, hypotension

pediatric patients usually only have hypotension after severe volume loss (>25% or >200mL volume deficit) as sudden sign of cardiovascular decompensation, but will
quickly decrease after that point

replacement of deficit volume in setting of normal sodium usually consist of the following
fluid bolus 10-20mL/kg over 15-30 minutes
left over deficit (after subtracting fluid bolus) divided into halves, where the first half is replaced over next 8 hours and the second half is replaced over next 16 hours

replacement of deficit volume in setting of hyponatremia or hypernatremia should be done slowly to ensure slow correction of sodium level

Maintenance Rate:
maintenance replace insensible and sensible losses as function of energy expenditure

maintenance rate based on “4:2:1” rule: 4mL/kg/hr for first 1-10kg; 2mL/kg/hr for 11-20kg; 1mL/kg/hr for >20kg

Ongoing Loss:
ongoing loss estimated based on measurement of fluid loss from drains, NG tubes, chest tubes, urine output, stool output

on-going based on gestalt usually replaced over 8, 16 or 24 hours

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2
Q

Minimal acceptable systolic BP in children

A

(i.e. 5th percentile of normal blood pressure) = 70mmHg + (2 x age in years)

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3
Q

What can contribute to fluid losses

A

fever, vomiting, respiratory distress, diarrhea, urine output

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4
Q

Anti-emetic contraindication

A

anti-emetics not recommended for vomiting of unknown aetiology, vomiting due to anatomic abnormality, surgical abdomen or infants

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5
Q

Anti-emetic types and their different indications

A

anti-histamine (Diphenhydramine, DImenhydrinate) for motion sickness

pro kinetics dopamine antagonist (Chlorpromazine, Metoclopramide, Domperidone, Droperidol) for chemotherapy induced vomiting

serotonin antagonist (Ondansetron) for chemotherapy and post-operative vomiting, cyclic vomiting

anticholinergic (Scopolamine) for motion sickness

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6
Q

Vomiting red flags on history or physical exam

A

prolonged vomiting (>12 hours in neonate, >24 hours in children <2 years; >48 hours in older children)

profound lethargy

significant weight loss

obstruction: bilious vomiting, projectile vomiting in infants, hematemesis, hematochezia, marked abdominal distension or pain

increased ICP: bulging fontanelle, headache, positional trigger for vomiting, vomiting on awakening, altered level of consciousness, seizure, focal neurologic abnormalities, history of head trauma

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7
Q

Type of fluid for bolus

A

bolus fluid should be isotonic to body serum osmolality to stay in extracellular compartment, so should be normal saline (NS)

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8
Q

Type of fluid for maintenance

A

pediatric patient have following electrolyte requirements

100mL/100kcal H2O
2-3mEq/100kcal Na+; 2-3mEq/100kcal K+; 5mEq/100kcal Cl-
5g/100kcal glucose

Na deficit (in setting of normal serum Na): 
mild dehydration = 4-6mEq/kg/d
moderate dehydration = 6-8mEq/kg/d
severe dehydration = 8-10mEq/kg/d

D5WNS is always used for maintenance fluid, because it replaced daily glucose requirement
D5WNS usually run with 20mEq/L KCl to replace K and Cl

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9
Q

PO fluid rehydration is always preferred vs IV except which situations

A

patient cannot tolerate PO fluids

patient is severely dehydrated

patient requires close measurement of ins and outs

PO fluid hydration should always be tried before IV fluids, especially for mild and moderate dehydration

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10
Q

Unacceptable oral rehydration therapies

A

boiled skim milk, homemade electrolyte solution and chicken broth is not recommended due to risk of containing high sodium content

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11
Q

Acceptable oral rehydration therapies

A

acceptable ORT includes Pedialyte, Lytren, Rehydralyte and WHO formula

substitute ORT includes Gatorade and water

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12
Q

Pyloric stenosis clinical presentation

A

onset at age 2-8 years

progressive projectile non-bilious emesis (vomiting) “hungry vomiter”

may have coffee ground (from gastritis) emesis

otherwise healthy and well

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13
Q

Pyloric stenosis complications

A

dehydration, jaundice

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14
Q

Pyloric stenosis pathophysiology

A

unknown

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15
Q

Pyloric stenosis physical exam

A

palpable olive mass in right upper quadrant or epigastrium, which is specific for pyloric stenosis

visible gastric peristaltic waves

gastric distention

need to examine fontanelle, eyes, mucous membrane, skin turgor and urinary output for volume status

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16
Q

Pyloric stenosis investigations

A

diagnosis of pyloric stenosis confirmed by ultrasound
ultrasound is the gold standard for diagnosing pyloric stenosis

enlarged pyloric sphincter on ultrasound

pyloric stenosis can be shown by upper GI series

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17
Q

Pyloric stenosis treatment

A

pre-operative care to stabilize patient, because patient at risk for electrolyte abnormalities and dehydration from vomiting

electrolyte abnormalities need to be corrected so that anesthesia will be safe

fluid resuscitation if dehydrated

surgical treatment
Ramstedt’s pyloromyotomy
slice open pyloric muscle fibre without perforating mucosa
surgery is NOT an emergency surgery

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18
Q

Pyloric stenosis electrolyte and acid base abnormalities

A

vomiting of HCl deplete Cl, causing hypochloremia

vomiting of HCl cause metabolic alkalosis, which is compensated by peeing bicarbonate, which takes K along with it, causing hypokalemia and aciduria

correct metabolic alkalosis, hypochloremia, hypokalemia and paradoxical aciduria if present

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19
Q

Best indicator for volume status

A

urine output

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20
Q

Intussusception pathophysiology

A

collapse of intestine unto itself like a telescope, which can occlude blood flow causing ischemia and necrosis

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21
Q

Intussusception epidemiology

A

commonly occur in age 3-9 months

rare to occur in patients <3 months and >3 years, where alternative diagnosis need to be considered

22
Q

Intussusception clinical presentation

A

85% present with intermittent colicky abdominal pain
80% present with non-bilious vomiting
65% present with (sausage shaped) abdominal mass
60% present with rectal bleeding (red currant jelly) in late stages

symptoms can be non-specific early in its course

23
Q

Intussusception investigation

A

X-ray shows lack of bowel gas

intussusception usually diagnosed by ultrasound: pseudo-kidney sign or target / doughnut sign (bowel wall on bowel wall)

24
Q

Intussusception treatment

A

air or contrast enema is both diagnostic and therapeutic, where air enema forces open intussusception region

surgery:
surgical reduction of intussusception only if refractory to air or contrast enema

bowel resection if bowel necrosis as result of intussusception

25
Q

Differential for emesis in peds

A

pyloric stenosis

feeding intolerance

GERD

infection: urinary tract infection, central nervous system infection, gastro-intestinal infection

26
Q

Anatomy of the appendix

A

appendix usually 5-7mm in diameter

appendix located at base of cecum where the teniae coli meet

relative location of appendix varies between individuals
majority (65%) of appendix are retrocecal

minority (30%) of appendix are pelvic

some appendix are retroperitoneal or within inguinal or femoral canal

27
Q

Appendicitis epidemiology

A

appendicitis can occur at any age

commonly appendicitis in late teens and early 20s
presentation is atypical in the very young (<14) and old (>30)

28
Q

Appendicitis pathophysiology

A
1) appendix lumen obstructed secondary to
lymphoid hyperplasia
stone (fecalith or appendicolith)
malignancy (colon cancer)
fibrosis or stricture

2) luminal obstruction leads to bacterial overgrowth appendix, resulting in inflammation, swelling and distended appendix
3) distension of appendix lead to venous obstruction, resulting in edema and ischemia of appendix
4) progressive ischemia lead to necrosis (gangrene) and eventually perforation
5) perforation can be complicated by pus formation (phlegmon -> abscess) and peritonitis

29
Q

Appendicitis clinical presentation

A

GI symptoms: nausea & vomiting, anorexia, abdominal pain (poorly localized -> umbilical region -> right lower quadrant (McBurney’s point) as well localized and sharp pain), diarrhea

systemic symptoms: fever, chills

abdomen exam: tenderness at McBurney’s point, positive Rovsing’s sign, positive psoas sign (retrocecal appendix), positive obturator’s sign (pelvic appendix), peritoneal signs (rigidity, guarding, rebound tenderness) if perforation
McBurney’s point (inferior appendix) = along line from umbilicus to anterior superior iliac spine (ASIS), 1/3 from umbilicus and 2/3 from ASIS
Rovsing’s sign = pain at McBurney’s point on release after deep palpation at left lower quadrant
psoas sign (in retrocecal appendix)= pain at McBurney’s point on passive hyperextension of hip
obturator sign (pelvic appendix) = pain at McBurney’s point on external or internal rotation of right hip with hip and knee flexed at 90 degrees
30
Q

Appendicitis complications

A

bowel perforation, peritonitis, phlegmon, abscess formation

31
Q

Appendicitis mortality

A

0.6% in uncomplicated appendicitis

5% in complicated appendicitis (perforated)

20% mortality in elderly

32
Q

Appendicitis imaging

A

abdominal / pelvic ultrasound or CT with IV contrast are gold standard for diagnosis of appendicitis

1) Pelvic ultrasound in thin patient:
enlarged (in diameter >6mm)
inflamed (non-compressible) appendicitis
specific (can rule in appendicitis) but not sensitive (cannot rule out appendicitis)

2) CT with IV Contrast in patients where appendix is not visualized on ultrasound:
inflammation of appendix (enlarged oedematous appendix, fat stranding)
specific and sensitive

3) Pelvic MRI in pregnant female where appendix cannot be visualized on ultrasound: inflamed appendix
4) abdominal X-ray: usually normal, free air under diaphragm if perforation, calcified fecolith at RLQ

33
Q

Appendicitis diagnosis

A

diagnosis usually based on clinical history / exam confirmed by imaging (ultrasound or CT with IV contrast)

34
Q

Appendicitis management

A

1) General management
Fluids, electrolyte correction
pre-operative IV antibiotics (e.g. Ceftriaxone +
Metronidazole IV)

2) Surgery
preparation: laboratory investigation for labs, preoperative IV antibiotics x 24 hours only

procedure: laparoscopic appendectomy (open surgery if peritonitis)

35
Q

Appendectomy indications

A

Appendicitis that is uncomplicated (no perforation, no phlegmon / abscess)

Appendicitis with peritonitis

36
Q

Appendectomy complications

A

Spillage of bowel content

Pelvic abscess

Enterocutaneous fistula

37
Q

Management of appendix phlegmon/abscess

A

No surgery

Long term antibiotics IV then step down to PO (2 weeks)

Drainage by interventional radiology

May consider appendectomy in 6 weeks after resolution of symptoms

38
Q

Management of appendix perforation

A

No surgery unless peritonitis

Long term IV antibiotics

39
Q

What investigation should be ordered in elderly patients who present with appendicitis

A

in elderly patients with appendicitis, colonoscopy to rule out colorectal cancer

40
Q

Meckel’s Diverticulum epidemiology

A

common, occurs in 2% of population

more common in males than females

majority of Meckel’s diverticulum is asymptomatic
only 2% of Meckel’s diverticulum develop symptoms

majority (85%) of symptomatic Meckel’s diverticulum present before age of 4

41
Q

Meckel’s Diverticulum pathophysiology

A

in fetal development, small intestine attached to omphalomesenteric canal (to umbilicus), which is closed later in development

omphalomesenteric canal / duct aka vitellin duct

in Meckel’s diverticulum, proximal portion of omphalomesenteric canal remains open, where the remnants form a diverticulum on the anti-mesenteric side of distal small intestine

42
Q

Meckel’s Diverticulum location

A

usually within 2 feet of ileo-cecal junction

43
Q

Meckel’s Diverticulum increases the risk of …

A

by being tethered to body wall, Meckel’s diverticulum predispose to cyst, inflammation and volvulus

44
Q

Meckel’s Diverticulum clinical presentation

A

1) bleeding in 60% of cases
ectopic gastric mucosa in diverticulum can cause ulcer, which then bleed
painless rectal bleeding
no associated abdominal pain
blood loss can be massive with severe anemia necessitating blood transfusion

2) bowel obstruction in 25% of cases
obstruction either intussusception or volvulus

3) inflammation in 15% of cases
present like acute appendicitis

45
Q

Meckel’s Diverticulum investigation

A

Technetium 99m to show gastric mucosa (parietal cells) in imaging

46
Q

Meckel’s Diverticulum treatment

A

surgical resection of diverticulum when patient is stabilized

47
Q

Malrotation and volvulus pathophysiology

A

the intestines did not properly rotate during embryology and thus are not properly placed in abdominal cavity

in malrotation, the angle of Treitz and cecum lie side by side, where the narrow base of mesentery allows gut to twist around the superior mesenteric artery (volvulus)

clamping of superior mesenteric artery cause bowel ischemia and possibly necrosis

48
Q

Malrotation and volvulus clinical presentation

A

malrotation by itself is asymptomatic

malrotation increases risk of volvulus which then cause symptoms

can present in acute or chronic form

acute form present in 1st month of life: usually healthy full term baby who is well, but then develops feeding difficulties with bilious vomiting -> abdominal distension with tenderness or erythema and rectal bleeding

chronic form at any age: frequent vomiting, hematemesis, intermittent cramp abdominal pain, diarrhea or constipation, malabsorption and failure to thrive

49
Q

Malrotation and volvulus mortality

A

if presentation or diagnosis is delayed, volvolus can progress to massive necrosis of intestine with high mortality (>65%), therefore bilious vomiting is an emergency in children

50
Q

Malrotation and volvulus investigation

A

upper GI series can detect malrotation

51
Q

Malrotation and volvulus treatment

A

fluid resuscitation

prophylactic antibiotics

surgical derotation of volvulus with correction of malrotation by dividing Ladd’s bands, correct base of mesentery and appendectomy

52
Q

Malrotation and volvulus rate of recurrent volvulus

A

recurrent volvulus is rare (<1%)