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Where and who of intussusception

Mostly ileocecal junction, but older kids can have ileoileo
Infancy to 3 years. Rare before 3 months of age.
Male female ratio 4:1

Clinical presentation of intussusception

Colicky abdominal pain that grows morefrequent as disease progresses
Vomiting rare in first few hours, but develops usually after 6-12 hours
"Current jelly stool" is a late finding, rare, ominous.
Stool is usually guiaic positive even in the absence of gross blood

(Apathy or lethargy may be the only presenting sign in up to 10% of cases. Some infants may be mistakenly evaled for AMS, may receive an LP, etc).

Physical exam of intussusception

May be normal between attacks.
Sausage-shaped mass in the right sid e of the abdomen, or horizontal in the epigastrium.
1/3 of patients will not have a palpable mass.

Diagnosis and work up of intussusception

Presumptive diagnosis is usually made by history alone.

Plain films of abdomen --> mass or filling defect in the RLQ, but it can be normal.

U/S --> sen/spec>90%. Donut or target sign. Reasonable first study in patients with atypicaly presentation, in whom the diagnosis is ambiguous.

Air contrast enema - diagnosis and therapy. First evaluation tool in children with a convincing history.

Air contrast vs straight up barium enema for intussusception diagnosis and treatment..

Air insufflation is preferred over barium because it enables better control over colonic pressure, and in the case of perforation, avoids spillage of barium into the peritoneum

Air contrast for intussusception

Should be done alongside surgical consultation..

Recurrence rate of intussusception

5-10%, usually within first 24-48 hours after reduction... second attempt at air reduction is usually successful.

Triad of Acute Cholangitis

Charcot triad: Pain, fever, and jaundice

50-70% of presenting patients

Pentad of acute cholangitis

Reynolds pentad: Pain, fever, jaundice, plus AMS and hypotension.

<5% of presenting patients

Most common organisms for acute cholangitis

E. coli
Entrooccus and anaerobes are less frequent.

Initial labs for evaluation of acute cholangitis

Blood cultures
Chem profile

Possible imaging studies to evaluate acute cholangitis

Ultrasound - Sensitive for intrahepatic biliary dilation, but poor at identifying choledocholithaisis, with a sens of <30%

(Up to 1/3 of patients with choledocholithiasis do not have evidence of biliary dilation, and cholangitis can occur before the bile duct becomes dilated.)

Nuclear hepatobiliary imaging, aka HIDA - can detect biliary obstruction earliier than US, with higher sensitivity.

Magnetic resonance cholangiopancreatography - Most accurate, with sens of 97%.

ERCP for diagnosis of acute cholangitis

No longer viewed as an initial diagnostic option, and is reserved for therapy.

Management of acute cholangitis

Supportive with resotration of fluid and electrolytes
Antibiotics: broad spectrum including GN coverage (Ciprofloxacin 500mg BID). Anaerobic coverage should be included if there is a history of prior instrumentation.

85% of patients will respond allowing for semi-elective biliary drainage within 48h.

Emergent drainage is indicated in patients who do not respond to conservative measures or when clinical deterioration occurs --> hypotension or AMS.

Alcoholic pancreatitis, epidemiology

2nd most common cause of pancreatitis

Clinical features of acute pancreatitis

Acute epigastric pain, around waist, RUQ, occasionally LUQ. Pain may radiate to the back, vary from mild and tolerable discomfort to severe, constant, and incapactiating distress. Maximum may be reached 30 minutes from onset, and may last for days.

Pain worse when supine, and can be relieved by sitting up with the trunk flexed and knees drawn up.

N/V in most.

Abdominal distention due to GI hypermobility and chemical peritonitis is a frequent complaint.

Physical exam findings in acute pancreatitis

Fever, tachy, hypotension in severe disease (shock 2/2 hypovolemia 2/2 exudation into retroperitoneal space, pancreatic hemorrhage, vomiting, and increased vasodilation and vascular permeability).

Abd exam --> diminished or absent bowel sounds. Upper abdominal tenderness and guarding in variable degree.

Cullen sign --> ecchymoses in the periumbilical region; and Turner sign --> ecchymoses in the flanks. Late findings.

Jaundice is not common, and its presence suggests common bile ductobstruction from edema tha tcompresses the intrapancreatic portion, or obstruction from a gallstone.

Pulmonary findings in acute pancreatitis?

Seen in 10-20% of cases. Indicates severe acute pancreatitis. Ranges from hypoxemia to ARDS. Shallow respiration and tachypnea are from diaphragmatic inflammation, pleural effusions, and respiratory compromise.

Small <1cm max height and medium <2cm max height pleural effusions are common with acute pancreatitis, and typically resolve spontaneousy.

Large effusions --> pancreatico-pleural fistula, and can be assoc with a pancreatic pseudocyst.

How to make a diagnosis of acute pancreatitis

1. Characteristic abdominal pain
2. Serum amylase and/or lipase levels 3x or greater the upper limit of nromal
3. Characteristic findigns on US or CT scan.

Amylase and lipase for acute pancreatitis

Amylase (6-12hr). At 3x upper normal has 67-83% sensitivity, 85-98% specific. Could be normal in hypertriglyceride-mediated pancreatitis

Lipase (4-8hr, peak 24) - sensitivity/specificity 82-100%. More sensitive in alcohol, longer half life (good for >24hr after presentation) --> preferred lab!!

Imaging for acute pancreatitis

Plain films - not sensitive or specific. CXR may show free air, pleural effusions.

U/S - Edematous, swollen pancreas. May also identify pseudocysts or abscesses. Gas-filled bowel loops often limit its view of the pancreas. It is good for identification of cholelithiasis and dilation of the biliary tree.

Abd CT - Test of choice when clinical signs and lab results do not provide a secure diagnosis, to exclude other stuff, and to identify complications and severity --> pancreatic nerosis. Very eary scans may underestimate severity of pancreatitis.

Management of mild pancreatitis

Oral analgesics, clear liquid diet. No evidence of systemic complciation can be discharged home if they can toelrate oral liquids and if pain is controlled.

F/u in 24-48 hours.

Management of severe pancreatitis

ICU admissin with aggressive fluid resuscitation, IV pain control, bowel rest, parenteral feeding possibly. Antibiotics are debated. In the absence of infectious complications their use is not encouraged.

Unstable angina i.e. possible ACS, what meds and in what order?

1. ASA first line, 325mg, Clopidogrel alternative
2. O2 if Sat<90%
3. Nitroglycerin sublingual, if relief, then transdermal or IV nitro therapy

If patient still appropriate for possible ACS classification but has not transferred to definite ACS....
4. Nitrates with Beta blockers if not contraindicated

If still experiencing symptoms...
5. Morphine

Acute MI medications

ASA first and most important
BBs within 24 hours of presentation...

Aortic dissection classification

Type A - ascending aorta
Type B - descending aorta

Risk factors for aortic dissection

Systemic hypertension - 72%
Atherosclerosis - 31%
Preexisteing aneurysm for younge rpatients
Aortic coarctation s/p surgery
Vasculitides - Giant cell arteritis, Takayasu, RA, Syphilis
Collagen disorders - Marfan, Ehlers-Danlos
Bicuspid aortic valve

Drugs used for management of atrial fibrillation

If the patient is stable, the first priority is to achieve ventricular rate control. In patients without evidence of heart failure or a bypass tract, -blockers and nondihydropyridine (rate-controlling) calcium channel blockers are first-line agents. The peak response to diltiazem is seen in 2 to 7 minutes. If -blockers and calcium channel blockers are ineffective, IV amiodarone can be used. IV digoxin or amiodarone are the treatment of choice in patients with heart failure without an accessory pathway, The onset of action of digoxin is slow, with a mean time >11 hours to achieve ventricular rate control. Calcium channel blockers can exacerbate heart failure in these patients.

Special Circumstances
Pregnant patients with atrial fibrillation who are unstable should be electrically cardioverted. Calcium channel blockers, -blockers, and digoxin can be used in stable pregnant patients with atrial fibrillation. Patients with AMI and LV dysfunction who are hemodynamically stable should be controlled with amiodarone.

Treatment of a ruptured aortic aneurysm

IV access --> two large bore IVs or a central line
Lab studies --> type and cross match
Treat shock with IV crystalloids followed by whole blood ASAP
Transfer to OR ASAP as mortality is virtually 100% without surgical intervention.

Acute pulmonary edema, what drugs needed for its management, and what drugs will not give you immediate effects

Management: Nitroglycerian to IV nitroprusside. Furosemide or bumetamide. Ace inhibitor
Beta blockers

The latter

Limitations of imaging in abdominal discomfort


Pros: Fast, low rad. Good for perforated viscus (PUD), obstruction/volvulus
Cons: bad for basically everything else


Pros: no rad. Good for AAA, ectopic, RUQ pain, intussusception, pyloric stenosis, hydronephrosis, pelvic stuff
Cons: limited penetration, can be slow


Pros: test of choice for most. Good for appendicitis, diverticulitis, stones, trauma
Cons: lot of rad. Need good kidney fxn.

Strep throat criteria

- Tonsillar exudate
- Painful adenopathy
- Absence of cough
- Fever
- Age<15 +1, Age>=45 -0

0-1 pts, not strep
2-3 pts, tke culture, treat if +
4-5 pts, treat empirically

Seizures, what drugs in what order

If new seizure, check glucose, Na, K, Mg
Drug levels if old

Benzos first
Phenytoin, fosphenytoin as well
If seizures still happening, consider pyridoxine, Can induce a coma with midazolam, propofol, etc.

Testicular torsion, clinical findings

Swollen, tender, high riding testis, with an abnormal transverse lie.
Absence of cremasteric reflex

Prehn sign

Pain relief when elevating testicle supposed to be present with epididymitis, known to be not sensitive for differentiating the two.

Time frame for torsion

<6 h, generally good.

Criteria for febrile seizure

No post-ictal
<15 minutes

Scrotal pain other than torsion

Torsion of testicular appendage

Appy vs ruptured appy, who is at risk

Elderly --> atypical presentations
Institutionalized patients
Pregnant women

Neonatal sepsis organisms

E. coli

Kawasaki disease, aka

aka Mucocutaneous lymph node syndrome... generalized systemic vasculitis of unknown cuase...

Signs of Kawasaki disease

Bilateral nonexudative conjunctivitis
Erythema of the mucous membranes
Extremity changes

Affects infants and young children, can occur in endemic and community-wide epidemic forms...

Most severe sequelae of Kawasaki disease

Cardiac: Coronary artery aneurysms, myocarditis, pericarditis, pericardial effusion, valvular dysfunction, left ventricular dysfunction, and arrhythmias.

CA aneurysms or ectasia 15-25% of untreated children, and can lead to myocardial infarction, sudden death, or ischemic heart disease... LV dysfunction is seen in almost half of patients with this disease. Most aneurysms develop during the 3-4 week of illness.

Most common cardiac findings in Kawasaki disease

TAchy out of proportion to fever
Gallop rhythm
Valve incompetence --> murmur

Ages of Kawasaki disease

KD peaks at 18-24 months, is rare below age of 4 months or after 5 yo.

Criteria for classic Kawasaki disease

FEver >5 days --> must have
Four other findings:
- bilateral nonexudative conjunctivitis
- cervical LAD - 40% of cases
- erythema of lips and oral mucosa
- various skin changes of the extremities
- rash

Incomplete Kawasaki. Fever, at least two of the clinical symptoms of classic disease but with supportive lab findings:
- Elevated CRP or ESR
- Albumin <3
- Anemia for age
- Elevated ALT
- Platelets >450
- WBC >12
- Presence of pyuria

Treatment of Kawasaki disease

High dose ASA 80-100mg/kg/d in four doses for 14 days, then 3-5mg

Antibiotics for neonatal sepsis

Coverage for GBS, E. coli, Klebsiella, H flu.
Ampicillin --> GBS and Listeria
Gentamicin --> E. coli and other GNs

If GN meningitis suspected, Replace Gent with Cefotaxime or Ceftazidiem, which have better CNS penetration.

Matenral hx of herpes or suspicious CSF findings, or ill-appearing --> Acyclovir

Neonatal sepsis s/s

Temp instability
CNS dysfunction
Respiratory distres
Feeding disturbance
Fever, hypothermia
Lethargy, irritability, seizures
Apnea, tachypnea, grunting
Vomiting, poor feeding, gastric distention, diarrhea

FEbriel well appearing child 3-36 months

Empiric Ceftriaxone treatment

Strept treatment in PCN allergic kids


Kawasaki disease age

<5 yo

Signs of a posterior MI on a standard EKG

High R in V1-V3 with ST depression in V1-V3 >2mm

Anterior MI: ST elevation, depression reciprocal, and possible coronary artery

No real reciprocal changes

Septal MI: ST elevation, depression reciprocal, and possible coronary artery

Disappearance of septum Q in leads V5,V6
No reciprocal changes
LAD-septal branches

Lateral MI: ST elevation, depression reciprocal, and possible coronary artery

I, aVL, V5, V6
II, III, aVF reciprocal changes

Inferior MI: ST elevation, depression reciprocal, and possible coronary artery

I, aVL reciprocal changes
RCA 80% or RCX 20%

Posterior MI: ST elevation, depression reciprocal, and possible coronary artery

High R in V1-V3 with ST depression V1-V3 >2 mm (mirror view)
RCX coronary artery

Right ventricular MI

I,aVL reciprocal changes

What percent of PE patients describe symptom onset as sudden


2/ PE.... prevalence, among whom

Certain types of surgery, incuidng ortho surgery of the hip and knee, gynecologic cancer surgery, major trauma, craniotomy for brain tumor.

May occur as late as a month after discharge

Things that may your d-dimer rise...

Acute MI
Metastatic cancer
Recent surgery

PE clinical signs

Nonspecific: dyspnea, tachypnea, chest pain, or tachycardia..
Life threatening--> dyspnea, sycnope, or cyanosis rather than chest pain.
<1/3 -> DVT

Massive PE suspected in whom

Hypotensive patients with predisposing factors
Clinical findigns of acutecor pulmonale --> distended neck veins, S3 gallop, right ventricular heave, tachy, tachypnea.

PE with severe chest pain or hemoptysis, where is the clot?

Anatomically small PE near the periphery of the lung.... this is where innervation is greatest, and where pulmonary infarction is most likey to occur from a dearth of collateral bronchial circulation.

ECG s/sx

New S1Q3T3
New incomplete RBBB
Right axis deviation
Right ventricular ischemia or strain with ST-depressions in the right precordial leads.

Trop leak with a PE

May result from acute right ventricular microinfarction due to pressure overload, impaired coronary artery blood flow, or hypoxemia caused by the PE.

PERC rule criteria

O2 >94% on RA
No prior history of DVT/PE
No recent trauma or surgery
No hemoptysis
No exogenous estrogen
No clinical signs of DVT

Corticosteroids in COPD

Use of a short course 7-14 days improves FEV1 in acute COPD exacerbations... decreases rate of return visits....

Antibiotics for CAP in pediatric population

Betalactams for outpatient: Amoxicillin, cefuroxime, cefdiinir
Macrolides in most school-aged chidlren

HAP antibitocs

Optimal combinations include meropenem or doripenem plus either levofloxacin or aztreonam. Alternately, antipseudomonal penicillin (eg, piperacillin) in combination with levofloxacin, meropenem, aminoglycoside, or aztreonam, may provide equal efficacy.

Toxic dose of acetaminophen

Max total daily dose in adults 4gm
75mg/kg in kids...

Toxic expsure Adult >10g or 200mg/kgas a single ingestion... or that ove r a 24 horu period. or >6 g opr 150mg/kg for at least 2 consecutive days...

Patient report of >12 g was associated with a 30% incidence of 4h acetaminophen level above 200mg/dl.... 6% incidence of hepatotoxiciy...

Stages of acetaminophen toxicity

First 24 hours --> stage 1, minimal and nonspecifi csymptsom of toxicity, maybe some hypokalemia..

2-3 days --> hepatotoxicity

3-4 --> fulminant failure.... for some, others will recover without sequelae...

Metabolic acidosis, coagulopathy, renal failure, encephalopathy....

Those who survive --> recover ove rnex t2 weeks, complete resoultion in 1-3 months

Calculating on the Rumack Matthews nomogram

Original nomogram line separating possible toxicity from unlikely toxicity was bsed on a 4h acetaminophen level of 200mcg/ml... moved down to 150mcg/ml

4h-24h other 20h window.

Above 200--> 60% risk of hepatotoxiicy, 1% risk of renal failure, 5% risk fo mrotality...

Below line... 1%

NAC administered 8h post treatment cut down levels

ASA managemnet

Fluid volume with K
Sodium bicarb boluses

Check salicylate and electrolyte concentratiosn q1-2 hours... once serum salicylate and electrolyte concentrations peaks an dbegins to decrease, repeat measurement can be obtained q4-6 hours.


Clinical presentation of ASA toxicity

Hearing loss


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