General Surgery Pediatrics Flashcards
Calculation of IV fluid requirements
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
Minimal acceptable systolic BP in children
(i.e. 5th percentile of normal blood pressure) = 70mmHg + (2 x age in years)
What can contribute to fluid losses
fever, vomiting, respiratory distress, diarrhea, urine output
Anti-emetic contraindication
anti-emetics not recommended for vomiting of unknown aetiology, vomiting due to anatomic abnormality, surgical abdomen or infants
Anti-emetic types and their different indications
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
Vomiting red flags on history or physical exam
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
Type of fluid for bolus
bolus fluid should be isotonic to body serum osmolality to stay in extracellular compartment, so should be normal saline (NS)
Type of fluid for maintenance
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
PO fluid rehydration is always preferred vs IV except which situations
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
Unacceptable oral rehydration therapies
boiled skim milk, homemade electrolyte solution and chicken broth is not recommended due to risk of containing high sodium content
Acceptable oral rehydration therapies
acceptable ORT includes Pedialyte, Lytren, Rehydralyte and WHO formula
substitute ORT includes Gatorade and water
Pyloric stenosis clinical presentation
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
Pyloric stenosis complications
dehydration, jaundice
Pyloric stenosis pathophysiology
unknown
Pyloric stenosis physical exam
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
Pyloric stenosis investigations
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
Pyloric stenosis treatment
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
Pyloric stenosis electrolyte and acid base abnormalities
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
Best indicator for volume status
urine output
Intussusception pathophysiology
collapse of intestine unto itself like a telescope, which can occlude blood flow causing ischemia and necrosis
Intussusception epidemiology
commonly occur in age 3-9 months
rare to occur in patients <3 months and >3 years, where alternative diagnosis need to be considered
Intussusception clinical presentation
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
Intussusception investigation
X-ray shows lack of bowel gas
intussusception usually diagnosed by ultrasound: pseudo-kidney sign or target / doughnut sign (bowel wall on bowel wall)
Intussusception treatment
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
Differential for emesis in peds
pyloric stenosis
feeding intolerance
GERD
infection: urinary tract infection, central nervous system infection, gastro-intestinal infection
Anatomy of the appendix
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
Appendicitis epidemiology
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)
Appendicitis pathophysiology
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
Appendicitis clinical presentation
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
Appendicitis complications
bowel perforation, peritonitis, phlegmon, abscess formation
Appendicitis mortality
0.6% in uncomplicated appendicitis
5% in complicated appendicitis (perforated)
20% mortality in elderly
Appendicitis imaging
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
Appendicitis diagnosis
diagnosis usually based on clinical history / exam confirmed by imaging (ultrasound or CT with IV contrast)
Appendicitis management
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)
Appendectomy indications
Appendicitis that is uncomplicated (no perforation, no phlegmon / abscess)
Appendicitis with peritonitis
Appendectomy complications
Spillage of bowel content
Pelvic abscess
Enterocutaneous fistula
Management of appendix phlegmon/abscess
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
Management of appendix perforation
No surgery unless peritonitis
Long term IV antibiotics
What investigation should be ordered in elderly patients who present with appendicitis
in elderly patients with appendicitis, colonoscopy to rule out colorectal cancer
Meckel’s Diverticulum epidemiology
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
Meckel’s Diverticulum pathophysiology
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
Meckel’s Diverticulum location
usually within 2 feet of ileo-cecal junction
Meckel’s Diverticulum increases the risk of …
by being tethered to body wall, Meckel’s diverticulum predispose to cyst, inflammation and volvulus
Meckel’s Diverticulum clinical presentation
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
Meckel’s Diverticulum investigation
Technetium 99m to show gastric mucosa (parietal cells) in imaging
Meckel’s Diverticulum treatment
surgical resection of diverticulum when patient is stabilized
Malrotation and volvulus pathophysiology
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
Malrotation and volvulus clinical presentation
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
Malrotation and volvulus mortality
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
Malrotation and volvulus investigation
upper GI series can detect malrotation
Malrotation and volvulus treatment
fluid resuscitation
prophylactic antibiotics
surgical derotation of volvulus with correction of malrotation by dividing Ladd’s bands, correct base of mesentery and appendectomy
Malrotation and volvulus rate of recurrent volvulus
recurrent volvulus is rare (<1%)
