Aquifer - GI/GU Flashcards
In general, a pattern of insidious onset of abdominal pain suggests what?
Inflammation of the visceral peritoneum alone or a well-contained process like an abscess
In general, crampy or colicky abdominal pain suggests what?
Obstruction in a peristaltic organ (like a bowel or ureter)
Progression of abdominal pain from a dull, diffuse pain to a sharp, well-defined pain suggests what?
Disease progression and possible need for surgery
DDx - Abdominal Pain and Vomiting (adolescent female)
- Appendicitis
- Cholecystitis
- Pregnancy
- Hepatitis
- Pancreatitis
- PID
- UTI
- Acute gastroenteritis
- Mesenteric adenitis
- Ovarian torsion
Presentation of appendicitis?
Classic pattern (60%): periumbilical pain followed by migration of pain to the RLQ; diffuse abdominal pain is possible (as in the case of peritonitis due to rupture)
Note - tenderness over McBurney’s point is commonly seen in adults, but less frequently found in children
Common: anorexia, N/V, fever (non-specific finding)
Uncommon: diarrhea
Presentation of cholecystitis?
Steady, usually constant pain, most often in the RUQ, that may radiate to the shoulder
Murphy’s sign (specific for cholecystitis) - increased pain upon palpation of the area when the patient takes a deep breath
Pain worsens after eating, especially fatty foods
Episodes may be intermittent (colicky) and accompanied by decreased appetite, N/V
Less common in children than adults, but does occur
Presentation of pregnancy?
Delayed or missed periods
Non-specific complaints - lower abdominal pain, urinary frequency, fatigue, N/V
Must be considered even when sexual activity is denied
Chadwick’s sign (bluish color of vaginal wall and cervix), changes to the uterus
Ectopic pregnancy must be considered, especially with history of STI alone or with PID
Presentation of unruptured ectopic pregnancy?
Lower abdominal pain, vaginal bleeding, abnormal menstrual history
Physical exam may be completely normal, though classic signs include diffuse abdominal tenderness and unilateral adnexal or cervical motion tenderness
Fever and uterine changes are rare
Presentation of ruptured ectopic pregnancy?
Surgical emergency
Abominal guarding suggesting intraperitoneal bleeding, hypotension correlates with degree of blood loss
Presentation of hepatitis?
Fever, malaise, diffuse or RUQ abdominal pain, N/V, NO diarrhea
Jaundice, change in color of urine
Onset of symptoms depends on etiology
Alcohol use may directly cause hepatitis or predipose to increased risk-taking behaviors and acquisition of infectious hepatitis
Hepatitis A is transmitted fecal-oral, recent travel would make this a possibility
Hepatomegaly on exam
Presentation of pancreatitis?
Diffuse abdominal pain, but other patterns (epigastric or RUQ) are more common; band-like pain radiating to the back
Pain is constant and usually severe
N/V almost always present
Low-grade fevers are common
Causes include gallbladder disease, infection, alcohol use, injury, certain medications, and inherited conditions
Presentation of PID?
Abdominal pain, more typically in the lower abdomen; RUQ pain occur with Fitz-Hugh-Curtis syndrome, an occasional (5%) complication of PID caused by N. gonorrhea or C. trachomatis - this pain is sudden and may refer to the R shoulder
Fever, if severe
Vomiting (sometimes)
Cervical motion tenderness, uterine tenderness, and adnexel tenderness
Purulent cervical discharge
Presentation of UTI?
Dysuria, frequency, and urgency
Poorly localized abdominal pain
Fever or CVA tenderness suggests pyelonephritis
Previous history of UTIs may suggest underlying structural abnormalities
More common in sexually active women
Presentation of acute gastroenteritis?
Vomiting
Diarrhea typically becomes the most pronounced symptom after a few days
History of sick contacts
Presentation of mesenteric adenitis?
Acute or chronic abdominal pain
May mimic appendicitis
Dx - U/S
Viral (most common) or bacterial infection, IBD, and lymphoma
Presentation of ovarian torsion?
Most common in post-menarchal women, can happen in any age
Abdominal pain (stabbing) in the lower abdomen or pelvic region
N/V
Mot common condition requiring emergency surgery in the pediatric population?
Acute appendicitis (60,000-80,000 cases/year in the US)
What age group is appendicitis more common in?
School age children (vs. children <5 y/o)
What percent of children presenting with abdominal pain have acute appendicitis?
1-8%
True or false - up to 1/3 of pediatric patients have atypical presentations, leading to missed diagnoses and a high incidence of perforation
True
Diagnosis of appendicitis?
Difficult, requires an accurate history and thorough physical
CBC with differential or CRP
What is McBurney’s point? Sensitivity and specificity for appendicitis?
1.5-2” from the anterior superior spinous process of the ilium on a straight line drawn from that process to the umbilicus
Sensitivity - 50-94%
Specificity - 75-86%
Presentation of testicular torsion?
Usually occurs in early adolescence
Acute onset of severe hemi-scrotal pain, N/V, may cause referred adominal pain
Physical exam - enlarged tender testis, scrotal edema, absence of cremasteric muscle reflex
Management of testicular torsion?
Emergent urology consult
Dx mainly by clinical suspicion, color doppler or nuclear testicular scan may be useful but should not delay Rx if Dx is evidence
Surgical exploration and detorsion must occur promptly (irreversible changes can occur within 4 hours)
Indications for a pelvic examination in adolescents?
- Abdominal vaginal discharge
- Unexplained dysuria or urinary tract symptoms in a sexually active female
- Dysmenorrhea unresponsive to NSAIDs
- Amenorrhea
- Abnormal vaginal bleeding
- Lower abdominal pain
- Contraceptive counseling for an IUD or diaphragm
- Pap test (21+ years only)
- Suspected/reported rape or sexual abuse
- Pregnancy
- Suspected PID
Diagnostic criteria for PID?
CDC recommends empiric treatment for PID in sexually active females with pelvic/lower abdominal pain if no other cause is identified and at least one of the following minimum criteria is met: cervical motion tenderness, uterine tenderness, adnexal tenderness.
Supportive criteria (enhance specificity of minimum criteria): oral temperature >101 F, abnormal cervical mucopurulent discharge or cervical friability, presence of abundant WBCs on saline microscopy of vaginal fluid, elevated ESR or CRP, documentation of cervical infection with N. gonorrhea or C. trachoamtis
Who is at highest risk for PID and why?
Sexually active females 15-19 years:
Fewer protective antibodies in the vagina compared to older women
Cervical ectropion which represents the transitional zone between columnar and squamous epithelium is not fully matured. Cells in this zone are easily susceptible to STDs, and the cervix is therefore easier to infect
Behavioral factors including intercourse during menses, infrequent or no condom use, and multiple sexual partners
Microorganisms involved in PID?
C. trachomatis and N. gonorrheae have been implicated in 1/3-1/2 of cases. However, it is often polymicrobial and may include GP and GN anaerobes and aerobic facultative bacteria found in women with BV
Lower-tract infection with these pathogens leads to an alteration of the normal vaginal flora and allows bacteria such as E. coli, Bacteroides species, other anaerobes, Mycoplasma hominis, or Ureaplasma urealyticum access to the uterus and fallopian tubes
Complications of PID?
Short-term: sepsis, perihepatitis, periappendicitis, tubo-ovarian abscess, other intra-abdominal abscess
Long-term: ectopic pregnancy, infertility, chronic abdominal pain, increased risk of recurrent PID
Rx for PID?
Ceftriaxone (gonorrhea) + Doxycycline or Azithromycin (chlamydia) + consider metronidazole (anaerobe)
Never use a single agent
When should a patient with PID be hospitalized?
Pregnancy
Previous noncompliance
High fever
Intractable vomiting
Inability to exclude a surgical emergency
Inadequate response on oral therapy within 72 hours
Tubo-ovarian abscess
Most common cause of abdominal pain in school-age children?
Functional abdominal pain
What is functional abdominal pain?
Pain without demonstrable evidence of a pathologic condition such as an anatomic, metabolic, infectious, inflammatory, or neoplastic disorder
Diagnosis of functional abdominal pain without additional diagnostic evaluation?
Children 4-18 years with chronic abdominal pain when there are no alarming symptoms or signs, the physical exam is normal, and stool sample tests are negative for occult blood.
Treatment of functional abdominal pain?
Reassurance that no serious illness is present, follow closely, refer for psychological evaluation and treatment if appropriate
List some of the red flag symptoms/signs of abdominal pain requiring further evaluation.
- Involuntary weight loss
- Deceleration of linear growth
- GI blood loss
- Significant vomiting
- Chronic severe diarrhea
- Persistent RUQ or RLQ pain
- Unexplained fever
- Family hx of IBD
- Abnormal or unexplained physical findings
Rectal exam in pediatric patients can aid in the diagnosis of what illnesses?
GI bleeding
Intussusception
Rectal abscess
Impaction
DDx - Abdominal Pain and Bloody Stools (school-aged)
- IBD
- Celiac disease
- Bacterial gastroenteritis
- Giardiasis
- Peptic Ulcer Disease
- HSP
Presentation of IBD?
Severe and acute or mild and subacute abdominal pain
Bloody stools
Presentation of celiac disease?
6-24 months of age Chronic abdominal pain Abdominal distention Diarrhea (common) Anorexia Vomiting Poor weight gain Can present with occult blood loss leading to anemia (gross blood would be unusual)
Variable presentation
Bacterial GI infections (give examples) frequently cause bloody diarrhea and are relatively common. ___ is another bacterial cause of colonic infection following exposure to antibiotics.
Salmonella, Shigella, Yersinia, Campylobacter
C. difficile
What is the most common intestinal parasite in the US?
Giadia lamblia
Presentation of Giardiasis?
Acute or chronic abdominal pain with few other symptoms
Travel history
Most do not have weight loss, though some may
Less likely than other parasites or bacterial organisms to cause grossly bloody stool
Presentation of PUD?
Relatively uncommon in children
Recurrent abdominal pain
Occult blood - frankly bloody stools are not consistent with this diagnosis
Lab Evaluation of Abdominal Pain and Bloody Stools
- CBC with differential (anemia, elevated platelet count (acute phase reactant))
- ESR (acute phase reactant - would support IBD)
- LFTs (low protein and albumin - malnutrition, hepatic disease with poor synthetic function, or losses from a protein-losing enteropathy)
- IgA tissue transglutaminase antibodies (TTG) - sensitive and specific for celiac (small bowel biopsy showing villous atrophy is the gold standard, IgA antiendomysial antibodies are useful, antigliadin antibodies are less reliable)
- Stool ova and parasites (can also do Giardia-specific antigen tests)
- Stool culture/C. diff toxin if suspected
Red flags for possible Crohn’s disease in a child with abdominal pain?
Pain that awakens the child at night
Pain that can be localized
Involuntary weight loss or growth deceleration
Extraintestinal symptoms (fever, rash, joint pain, aphthous ulcers, dysuria)
Sleepiness after attacks of pain
Positive family history of IBD (only positive in ~30% of patients)
Abnormal labs such as guaiac-positive stool, anemia, high platelet count, high ESR, hypoalbuminemia
Abnormalities in bowel function (e.g., diarrhea, constipation, incontinence)
Vomiting
Dysuria
Pathology of ulcerative colitis?
Generalized inflammation confined to the mucosa, starting the rectum and involving a variable extent of colon proximally
Crypt abscess common
Rarely, patients may have discontinuous inflammation at diagnosis or event relative rectal sparing - becomes more confluent over the course of the illness
Pathology of Crohn’s?
Inflammation in any portion of the alimentary tract, from mouth to anus
Mucosal inflammation may become more generalized or remain patchy and may extend into the submuocsa, muscularis, and serosa
Transmural inflammation can result in fistual formation
Definitive diagnosis of CD or UC?
Upper endoscopy and colonoscopy +/- small bowel series, MRI, or video capsule endoscopy
Small bowel imaging -> CT enterograph and MR enterography (replaced fluoroscopic small bowel follow-through as modality of choice)
-UC limited to colon, but can show evidence of ileal inflammation (backwash ileitis)
True or false - the phenotype of pediatric vs. adult IBD differs.
True
What elements of the clinical history can help determine disease severity in CD?
# of diarrheal stools/day Daily abdominal pain ratings Ratings of well-being Presence of other related symptoms/findings Abdominal fullness/palpable mass Hematocrit Height growth velocity Weight
The onset of IBD typically occurs in which decades?
Second and third (25-30% develop symptoms before age 20, 5% before age 10)
Goals in treatment of pediatric IBD?
Eliminate symptoms and improve quality of life
Restore normal growth
Eliminate complications
Treatment of CD?
Induction therapy (remission of disease) - often corticosteroids +/- enteral nutrition therapy Maintenance therapy - immunomodulators (thiopurines, MTX), anti-TNF (moderate to severe CD)
How do corticosteroids blunt the inflammatory response?
Downregulate production of inflammatory cytokines, interfere with NFKB cell production
What is the single greatest risk factor for the development of IBD?
Having a first-degree relative who has the disease
DDx - RUQ Mass + Pallor
9-month-old infant
- Hepatic neoplasm
- Hydronephrosis
- Neuroblastoma
- Teratoma
- Wilms’ tumor (nephroblastoma)
- Constipation
Presentation of hepatic neoplasm (infant)?
Rare in infants
Must be considered with an asymptomatic RUQ abdominal mass in young infants
Jaundice may be a feature
Pathophysiology and presentation of hydronephrosis (infant) as a RUQ mass?
Obstruction at the UPJ can lead to hydronephrosis and a palpable kidney sometimes manifesting as a flank mass
Hydronephrosis causing a palpable mass would usually present with a UTI
A multicystic kidney may also cause such an obstruction
What is the most frequently diagnosed neoplasm in infants (>50% present before age 2)?
Neuroblastoma
Presentation of neuroblastoma (infant)?
Likely diagnosis in an infant <1 year with an asymptomatic RUQ abdominal mass and pallor, and no jaundice.
May cross the midline
May also present with fever and weight loss
Children with abdominal neuroblastoma may be asymptomatic or may appear chronically ill or have bone pain from metastases to the bone marrow or skeleton
May also present as a painless mass in the neck or chest
Presentation of teratoma (infant)?
Rare malignant tumor
May present as a painless abdominal mass +/- symptoms; may cause pressure effects on neighboring structure resulting in abdominal or back pain, N/V, constipation, and/or urinary tract symptoms
Presentation of Wilms’ tumor (nephroblastoma)?
Median age at diagnosis: 3 years
Likely diagnosis in a child with an asymptomatic RUQ abdominal mass with no lymphadenopathy or jaundice and who is growing and developing normally
Generally smooth and rarely cross the midline
Associated symptoms occur in half of patients and include abdominal pain and/or vomiting; may also be hypertensive
Initial workup for abdominal mass + why?
- CBC w/differential - extent of anemia, cytopenia (concern for bone marrow infiltration), not specific
- Catecholamine metabolites (VMA and HVA) - neuroblastoma
- CXR - metastases to the bone (chest CT or MRI only if mets are seen)
- Skeletal survey - metastases to the bone
- Abdominal U/S - identify a mass, show organ of origin, solid/cystic/combined (CT not needed if purely cystic)
- Abdominal XR - presence of a mass +/- calcifications
- Abdominal CT - calcifications, better picture of anatomy, consistency of tumor, evaluation of lungs
Best choice for first imaging for an abdominal mass?
U/S
Imaging findings of neuroblastoma?
CT: calcifications + heterogenous mass with cystic areas representing either hemorrhage or necrotic tumor
CXR: lymph node involvement in the chest or other tumors in the posterior mediastinum
Metastases to regional lymph nodes, liver, bone marrow, skeleton
Lab findings of neuroblastoma? (Histopathology, urinary, CBC)
Small round blue cells or small uniform cells containing dense, hyperchromatic nuclei and scant cytoplasm forming small cell rosettes
Elevated urinary HVA/VMA
CBC: may show anemia or other cytopenias secondary to BM infiltration
Imaging findings of Wilms’ tumor?
U/S: intrarenal mass
CT: heterogenous mass with areas of low density (necrosis); pseudocapsule may be observed (demarcation between tumor and normal renal parenchyma)
CXR: pulmonary metastases
Lab findings of Wilms’ tumor?
Possible hematuria
Imaging finding of a hepatic tumor?
Abdominal XR: hepatic enlargement with tumor
CT: tumor
Chest CT: pulmonary mets
Lab findings of a hepatic tumor?
Dx depends on histologic examination
LFTs usually normal, but liver enzymes and bilirubin may be elevated in 20% of cases
AFP levels increased in most patients
Imaging finding of teratoma? (No labs)
CT (best option): well-defined masses with both solid and cystic components
XR: identifiable only if calcified components such as teeth or bony fragments are present
Lab findings of constipation? (No labs)
Abdominal XR: readily identified, no other evaluation needed
What is Stage 4S Neuroblastoma?
Localized primary tumor as in stage I or II with dissemination limited to liver, skin, or bone marrow
Prognosis of stage 4S neuroblastoma?
In infants less than 1 year of age, these tumors may spontaneously regress due to the unique nature of this tumor derived from embryonal cell lines
Genetics of neuroblastoma?
1% due to inherited (AD w/low penetrance) form
Vast majority due to somatic mutations
DDx - Vomiting and Diarrhea
toddler
- Viral gastroenteritis
- Bacterial gastroenteritis
- Small bowel obstruction
- Appendicitis
- IBD
Presentation of viral gastroenteritis?
Common in children
Vomiting and diarrhea
Sick contacts (viral easily transmitted)
Presentation of bacterial gastroenteritis?
Classically bloody or profuse diarrhea
Presentation of a small bowel obstruction?
Vomiting, not diarrhea
Bilious if obstruction is below the Ampulla of Vater
Presentation of appendicitis?
Abdominal pain is the primary feature
Vomiting and diarrhea, and fever, may be present
Presentation of IBD?
Chronic bloody diarrhea, not usually with vomiting
What must always be assessed in a child with vomiting and/or diarrhea?
Dehydration
Most reliable assessment of fluid status by phone?
Child’s level of activity, ability/desire to take fluids by mouth, urine output (frequency/amount)
Discuss the determination of degree of dehydration.
- Subtract current weight from his/her weight immediately prior to the illness -> assume water weight
- Weight loss (grams) = water loss (mL)
- Concert to “percent dehydration” = percent of total euvolemic body weight lost as water
Clinical estimation of degree of dehydration based on mental status?
Minimal (<3%) - well/alert
Mild/moderate (3-9%) - normal or fatigued or irritable
Severe (>9) - apathetic or lethargic or unconscious
Clinical estimation of degree of dehydration based on thirst?
Minimal (<3%) - normal
Mild/moderate (3-9%) - thirsty, eager to drink
Severe (>9) - drinks poorly, unable to drink
Clinical estimation of degree of dehydration based on pulse?
Minimal (<3%) - normal
Mild/moderate (3-9%) - normal or increased
Severe (>9) - tachycardia (bradycardia in most severe cases)
Clinical estimation of degree of dehydration based on quality of pulse?
Minimal (<3%) - normal
Mild/moderate (3-9%) - normal or decreased
Severe (>9) - weak, thready, or impalpable
Clinical estimation of degree of dehydration based on breathing
Minimal (<3%) - normal
Mild/moderate (3-9%) - normal or fast
Severe (>9) - deep
Clinical estimation of degree of dehydration based on eyes
Minimal (<3%) - normal
Mild/moderate (3-9%) - slightly sunken
Severe (>9) - deeply sunken
Clinical estimation of degree of dehydration based on tears
Minimal (<3%) - present
Mild/moderate (3-9%) - decreased
Severe (>9) - absent
Clinical estimation of degree of dehydration based on mouth/tongue
Minimal (<3%) - moist
Mild/moderate (3-9%) - dry
Severe (>9) - parched
Clinical estimation of degree of dehydration based on skin fold
Minimal (<3%) - instant recoil
Mild/moderate (3-9%) - recoil in <2 seconds
Severe (>9) - recoil in >2 seconds
Clinical estimation of degree of dehydration based on capillary refill
Minimal (<3%) - normal
Mild/moderate (3-9%) - prolonged
Severe (>9) - prolonged/minimal
Clinical estimation of degree of dehydration based on extremities
Minimal (<3%) - warm
Mild/moderate (3-9%) - cool
Severe (>9) - cold, mottle, cyanotic
Clinical estimation of degree of dehydration based on urine output
Minimal (<3%) - normal
Mild/moderate (3-9%) - decreased
Severe (>9) - minimal
When is oral rehydration therapy used?
Mild-moderate dehydration
Why should sports drinks, apple juices, colas, etc. not be used for rehydration in the setting of gastroenteritis?
Their relatively low sodium concentration can lead to hyponatremia
Basic steps of fluid management for any pediatric patient who is dehydrated?
- Replace the fluid deficit (2-bag approach: IV insulin + 2 bags of fluid (dextrose-free IV fluid containing a balanced electrolyte solution with appropriate amounts of potassium and phosphorus + second fluid as above with 10% dextrose)
- Provide maintenance fluids
- Replace any ongoing fluid losses (vomiting, diarrhea, NG tube output, insensible losses due to fever or tachypnea)
How are maintenance fluids calculated?
First 10 kg: 4 mL/kg/hr
Second 10 kg: 2 mL/kg/hr
Any additional kg: 1 mL/kg/hr
Recommended fluid replacement volume for mild-moderate dehydration?
50-100 mL/kg over 2-4 hours
Fluid therapy for severe dehydration?
Volume restoration via IV bolus therapy with an isotonic saline solution (normal saline, lactated Ringer’s, balanced electrolyte solution)
Repeated 10-20 mL/kg boluses given up to 3x until the patient has improved to only mild dehydration or normal fluid status
Why is normal saline the preferred replacement fluid in pyloric stenosis?
High chloride content
Does not contain lactate (could worsen alkalosis)
Solid foods in the setting of vomiting and diarrhea?
If not dehydrated, continue to eat age-appropriate diets
If dehydrated, eat as soon as they have been rehydrated
Breastfeeding and formula feeding can continue through the period of rehydration
DDx - Recurrent Emesis
infant
- GER
- Milk protein allergy
- Viral gastroenteritis
- Malrotation +/- volvulus
- Inborn error of metabolism
- Pyloric stenosis
- Intussusception
- CNS disease
- UTI
Presentation of an infant with recurrent emesis due to a milk protein allergy?
May present with vomiting immediately after eating, but more typically will present with a rash or loose stools
Does not typically cause dehydration
Presentation of viral gastroenteritis (infant)?
Isolated vomiting early in the course (possibly)
Large watery stools (hallmark)
Dehydration due to fluid losses
Not typically bilious (above ligament of Treitz)
Presentation of malrotation +/- volvulus?
Bilious emesis
Significant abdominal pain (if bowel ischemia from volvulus)
Blood in stool, but not in vomitus
May present in shock
Presentation of pyloric stenosis?
Escalating pattern of forceful (projectile) non-bilious vomiting
Can have rapid dehydration due to inadequate fluid absorption, but typically have a vigorous appetite until late in the clinical course
HYPOCHLOREMIC HYPOKALEMIC METABOLIC ALKALOSIS
Signs: visible peristaltic wave after eating, palpable olive in the epigastric region
Most common form of bowel obstruction in children between 6 months and 6 years?
Intusussception
Presentation of intusussception?
Paroxysms of severe, colicky, crampy abdominal pain with inconsolable crying
Passage of currant jelly stool containing blood and mucus
Palpation of a sausage-shaped mass in the right abdomen
Vomiting (bilious or non-bilious), lethargy, toxic appearance, +/- signs of pain
Dx and Rx intusussception?
Air or barium enema to reduce the telescoped segment
Initial evaluation of intusussception?
U/S
Typical site of intusussception? In HSP?
Normally - ileo-cecal
HSP - ileo-ileal
Why is intusussception in HSP not reduced by air/barium enema?
Because it is usually ileo-ileal, not ileo-cecal
(Dx - U/S, Rx - surgery
Diagnostic work-up for possible pyloric stenosis?
Ultrasound - confirms pyloric hypertrophy
Upper GI - narrow pyloric channel (string sign), indentation of the hypertrophied pylorus on the antrum of the stomach, and delayed gastric emptying; if concern for malro/volvulus, include imaging of the contrast passing through the SI as well
Electrolytes
What must be done prior to pyloromyotomy?
Correct electrolyte abnormalities and dehydration
DDx - Vomiting
school-age
- Gastroenteritis
- GI obstruction
- Pyelonephritis
- DKA
- Increased ICP
- Appendicitis
Presentation of DKA?
Vomiting (usually precipitated by acidosis), increased RR, vague diffuse abdominal pain
Significant dehydration (due to vomiting and osmotic diuresis); can lead to altered mental status (always concerning for cerebral edema)
Preceding history of eneuresis and polydipsia (suggests newly presenting diabetes)
Can be precipitated by an infection; otherwise, fever is not seen
Common signs/symptoms of cerebral edema?
Headache, recurrence of vomiting, inappropriate bradycardia, hypertension, hypoxia, restlessness/irritability, lethargy, CN palses (6), abnormal pupillary responses (unequal, fixed dilated, absent response, etc.)
Cushing’s triad?
Inappropriate bradycardia, hypertension, and irregular respirations
Risk factors for cerebral edema in DKA?
Young age High BUN concentration at presentation Profound acidosis with hypocapnia Attenuated rise in the measured serum sodium with treatment Administration of bicarbonate
What are Kussmaul resspirations?
Pattern of rapid and deep breathing when a patient is attempting to blow off the excess CO2 caused by metabolic acidosis
Distinctive because other causes of tachypnea lead to rapid, SHALLOW respirations
Initial management steps for DKA?
- Manage hyperglycemia and acidosis
- fluid resuscitation will help lower blood glucose, but only insulin will correct the metabolic derangements of DKA by suppressing lipolysis and ketogenesis
- insulin drip (0.1 units/kg/hr) after initial volume expansion
- Monitor glucose every 30 minutes to 1 hour
- Bicarbonate should not be routinely given because of the well-described paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis + associated with increased risk of cerebral edema - Hospital admission
- Consultation with an endocrinologist
What causes the lab abnormalities in DKA?
Insufficient insulin -> catabolic state characterized by hyperglycemia and ketogenesis
Elevated glucose, elevated serum/urine ketones, metabolic acidosis (low pH and decreased bicarbonate level)
Sodium may be low due to dilutional effects, renal losses, and lab effects related to high glucose
Potassium may be low, normal, or high depending on the level of acidosis and intracellular shifts
Creatinine is often elevated related to hypovolemia
Acidosis seen in DKA?
Metabolic acidosis with an elevated AG related to ketone body production and lactic acidosis from poor perfusion
Calculate AG?
Na - HCO3 - Cl
DDx - elevated AG metabolic acidosis
MUDPILES
Methanol Uremia DKA Paraldehyde INH/iron Lactic acidosis Ethanol/ethylene glycol Salicylates
What happens to potassium in DKA?
Acidosis and lack of insulin drive K out of the cells and into the serum. As this is corrected with treatment, serum potassium will drop, reflecting true total body levels.
Cause of hyponatremia in DKA?
Osmotic movement of water into the extracellular space in response to the hyeprglycemia and hyperosmolarity (diulational) as well as from increased renal losses
Corrected sodium in the presence of hyperglycemia?
= {[(measured glucose – 100)/100] x 1.6} + measured sodium
Admitting orders for a patient in DKA?
NPO until blood sugars, neurologic status, and vomiting resolve
Continuous monitoring of vitals during rehydration/electrolyte correction
Hourly neuro checks to monitor for signs of cerebral edema
Monitor I/O to assess hydration status
Insulin orders (insulin drip until acidosis resolves = bicarbonate >15 or normal AG -> transition to subcutaneous insulin)
Serum glucose every 60 minutes
Serum electrolytes hourly (including Ca, Mg, Ph)
Serum pH every 60 minutes (done with VBG)
Urine dipstick for ketones
Presentation of biliary atresia?
Healthy-appearing infant who develops jaundice, dark urine, and acholic (pale) stools between 3-6 weeks of age
Umbilical hernias are a common condition in newborns - they are more common in what two patients?
Premature infants
Congenital hypothyroidism
Prognosis of umbilical hernias?
Vast majority close spontaneously by 5 years of age
Dx DKA?
Random blood glucose >200 mg/dL AND
Venous pH <7.3 or serum bicarbonate <15 AND
Moderate/large ketonuria or ketonemia
