Croup vs. Epiglottitis (Peds.)

Pediatrics (neonates to school age; adolescence is another topic) is probably my least favorite specialty to deal with and they are one of the hardest to help at times with all the elements that go with the patient. Whether it is dealing with the sick child or the distraught parents, we must sift through the physical findings and the information from the parents to understand what is going on. This gets especially sticky when it comes to some upper airway complications in the younger group.

Two very common upper airway problems in the younger populations include Croup and Epiglottitis. Both can be dangerous, but require different management when treatment is concerned. This article will give you a brief overview of the pathophysiology, signs and symptoms, treatments, and key points to remember.


Pathophysiology: Commonly a viral infection (RSV, adenovirus, influenza A and B, etc.) of the upper respiratory system for ages 6 to 36 months. Major inflammation has occurred in the larynx, trachea, bronchi, bronchioles, and lung parenchyma; causing obstruction of the airway. As the swelling progresses supraglottic the patients with begin show signs of respiratory distress. Further along, the patient’s lower airway may begin to begin having atelectasis, due to the lack of air keeping the alveoli open.

Croup is a slow progression of inflammation. Noticing early that the patient has upper respiratory issue is key in the management. Due to the smaller airway of children, we must not hesitate to seat

Signs and Symptoms: The most common sign of croup will be the seal like bark with inspiratory stridor. With this means that the patient is in respiratory distress and quickly heading to failure. If you hear the seal like bark, check the lower lung fields for crackles, because possible atelectasis may have begun.

Commonly more serious during night, awakening them from sleep. Other signs to know include:

  • Tachypnea
  • Retractions
  • Cyanosis
  • Shallow respirations
  • Fever

Treatment: Emergency treatment for croup is a humidified air and a dose of corticosteroids. If in further destress, racemic epinephrine will assist with edema. ETCO2 and O2 readings will help determine if there is retention of gasses, which may lead to acidosis. ABGs will be needed to confirm this as well.

Usually, patients will be able to return home to be monitored. Family should watch for difficulty breath and be using humified air. Antipyretics will assist in keeping fevers down as well.


Pathophysiology: Influenza type B, streptococcus pneumoniae or aureus may cause epiglottitis. The epiglottis is a small flap above the glottic opening, which is used to prevent foreign objects entering the trachea. When the epiglottis is infected, with will swell, narrowing the airway for the patient. Increased work of breathing may occur and soon my might have a patient in respiratory failure.

Epiglottitis is a more acute problem, with sudden onset and quick changes to mentation form the restriction of airflow.

Signs and symptoms: As the epiglottis swells, the child may begin to develop stridor. When stridor occurs, we must ask the question is this an object or is this medical. Other signs that might point you towards epiglottitis will be:

  • Sore throat
  • fever
  • Odynophagia
  • Drooling
  • Irritability
  • Cyanosis
  • Tripoding or nasal flaring

Treatment: The most important thing with these patients is to ensure they have an airway. Do not try and examine the patient, especially if you are a paramedic on scene (Load and go). When gathering a medical history, it is especially important to ask for vaccination in the pediatric population. Today, Influenza vaccinations are given to children, but we do have a set population now that do not vaccinate their children. X-rays of neck will be done and a visual examination may be performed. Keep the patient calm at this time, further agitation may cause the airway to swell more.

Patient will commonly receive an antibiotic, such as ceftriaxone, to help with the bacteria. ET tubes may be places in severe cases and usually remain for 24 to 48 hours. Trachostomes may be required, if a ET tube cannot pass the glottic opening.

Key Points

  • Both Croup and Epiglottitis can be dangerous to pediatric patients. If you have a child that has stridor and any signs of distress, they will need immediate attention.
  • Out of hospital, assume epiglottitis and rule it out when you can. This load and go for you
  • Croup X rays may show steeple sign, but epiglottitis won’t

Written by: MEDDAILY

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Urinary Tract Infections

Definition of UTI

  • Pathologic bacteria in urine
    • Asymptomatic patients: growth of > 10^5 (100,000) CFU/mL
    • Symptomatic patients: 10^2 (100) CFU/mL

Classification of UTI

  • Lower tract infections: urethritis, cystitis
  • Upper tract infections: pyelonephritis, prostatitis
  • Community-acquired
  • Nosocomial: catheter-related


  • E. coli - most common
  • Gram negative rods
  • Adenovirus - children


  • Colonization of external genetalia
  • Bacteria can ascend into the urinary tract 
  • Upper tract infection most common complication of lower tract infection
  • Hematogenous spread - S. aureus

Who gets UTIs?

  • Females > males
  • Increased incidence with sexual activity
  • Childhood: M > F

Female Patients

  • Vaginal introitus and distal urethra normally colonized by gram positive organisms
  • Female urethra more prone to gram negative infection 
    • Close to anus
    • Short length 
  • Risk factors
    • Hygiene issues
    • Sexual activity
      • Void after intercourse decreases this risk

Male Patients

  • Rare
  • > 50 years of age, BPH is main cause

Other Risk Factors

  • Pregnancy
  • Unsterile or prolonged catheterization
  • Obstruction
  • Vesicourethral reflux


  • Most common manifestation of UTI
  • Infection/inflammation of bladder
  • Most commonly E. coli, can be adenovirus
  • Clinical presentation
    • Irritative voiding 
    • Supraspubic discomfort
    • Other urinary complaints?
  • PE
    • Unremarkable
    • No CVA tenderness
  • Lab
    • Urinalysis
      • (+) LES
      • (+) Nitrites
    • Urine gram-staining
      • E. coli
      • Contamination possible
  • Acute urethral syndrome
    • “Painful voiding syndrome”
    • Dysuria with sterile culture
    • Irritants, trauma, etc.
  • Management
    • Antimicrobials
      • Short-term (< 7 days) for uncomplicated cases
      • Longer therapy (7-10 days) for DM, recurrent UTI, over 65, Men
    • Symptomatic treatment
  • Follow-up
    • Repeat urine C&S 3-5 days after antibiotics finished


  • Infection/inflammation of renal parenchyma and pelvis
  • Most commonly E. coli or Proteus sp. 
  • Presentation
    • Flank pain
    • Fever
    • Chills
    • Toxic appearance
    • CVA tenderness
  • Lab
    • Urinalysis
      • (+) LES
      • (+) Nitrites
      • WBC casts
    • Urine gram stain
      • E. coli
      • Contamination possible
    • CBC
      • Leukocytosis with left shift
  • Imaging
    • Only done in complicated cases
  • Complications
    • Sepsis/shock
    • Scarring/fibrosis
      • Chronic pyelonephritis
  • Management
    • Usually treated as outpatient
    • Empiric therapy
      • Broad-spectrum antibiotics
        • IV 
        • PO quinolone
        • No nitrofurantoin
        • Watch resistance for Augmentin and Bactrim 
      • 14+ days
        • Inpatient: 24 hours after fever resolves
        • Outpatient: 14 days
  • Follow-up
    • Repeat urine C&S 1-2 weeks after treatment completed
    • Treatment failure
      • Imaging or referral

UTIs in Pregnancy

  • Asymptomatic bacteriuria very common - treat due to risk of complications to fetus
  • Cystitis
    • No fluoroquinolones
    • Recheck urine C&S
  • Pyelonephritis
    • Hospitalization
    • Empiric IV therapy, then PO
    • No fluoroquinolones
    • Recheck urine C&S

Nosocomial UTIs

  • Foley catheters 
  • Care for UTIs not reimbursed by Medicare/Medicaid 

Recurrent Infections: more than 2-3 per year

Vesicoureteral reflux (VUR)

  • Reflux of urine from bladder into ureters/renal pelvis
  • Common cause of UTI in children
  • Renal scarring due to volume and duration of reflux
  • Presentation
    • Weight loss
    • Nocturnal enuresis
    • Failure to thrive
  • Labs
    • Urinalysis
      • (+) LES
      • (+) Nitrites
    • Urine gram stain
      • E. coli
    • Cast formation
  • Imaging
    • Voiding cystourethrogram (VCUG)
    • Management of VUR
      • Mild
        • Spontaneous resolution usually
        • Antibiotics until puberty
      • Severe
        • Surgical intervention
        • Antibiotics into condition corrected

riverrr-the-writer  asked:

What are some illnesses/reasons for someone to cough up blood continuously? ( and not just for a few hours, I mean like for years?) is there anything that is more low key than tuberculosis and it'll take a lot of tests to figure out?

Well, dearest diggory, you’ve been waiting a long, long time indeed for this. And I’m sorry. You shouldn’t have to. Scripty has been slow-pokey on the uptake when it comes to the older asks of late. I’ve been skipping around to see what’s interesting, and not getting to the stuff that came in first.

But this is an ask whose time has come. And because you’ve waited so long, I’m going to cook you up something good.

First, the medical term for up-coughy of bloody mess is hemoptysis (hemo – blood; ptysis – sputum). Hemoptysis is caused by several things, but those things can be organized categorically.

You’re looking for something “more low-key than tuberculosis” and “requiring a lot of tests”. I can give you a couple of options, but none of them are low-key. I’ll be honest, dearest diggory, coughing up blood is usually an indicator of a serious problem.

First, yes, tuberculosis is known far and wide as the diseases that makes you cough up the red gooeys.

There are two reasons to cough up blood.

1) You’ve irritated something in the lining of the airways, and you’re getting flecks of blood from somewhere.

2) You’ve got blood in the actual lung parenchyma (tissue), and when y’cough, y’get y’blood y’in y’mouth. (Note: y’in is not a word.)

If the cause is something from 1), an issue with the actual airway (bronchi or bronchioles), it will definitely get seen on a bronchoscopy. This is when a doctor sedates a patient (or numbs the back of the throat), puts a tube down the windpipe, and sticks a camera down that tube to look at the actual airway to check for structural damage. Penetrating trauma to the chest could do this, inhaling food at some point could do this (especially if it’s a small piece of something sharp, like a bone), irritation from constant coughing like a persistent bronchitis could do this. But it’s easy to see, because you can stick a camera in the patient and physically see it.

If your character has a problem inside the lung itself, however, it’s going to be harder to spot.

The top two contenders in the “lung parenchyma” end of thing are, of course, tuberculosis and lung cancer. Non-small-cell lung cancer could start with coughing, which could have a little bit of blood in it, and simply get missed on x-ray and bronchoscopy; the prognosis for it is actually relatively good, assuming the disease is caught early. However, we said “MORE low key than TB”, not, y’know, goddamn cancer. So let’s back up a sec.  

There are a few autoimmune disorders that will give your character recurrent hemoptysis. House is always looking for Behcets and Wegener’s granuloma, but if you want a true weird-ass diagnosis that didn’t even crop up in the most esoteric medical show ever written, try idiopathic pulmonary hemosiderosis.

Say it out loud. Idiopathic pulmonary hemosiderosis. I’ll wait.

Now say it again, but faster.

Good. Now faster.

Idiopathicpulmonaryhemosiderosis! Idiopathicpulmonaryhemosiderosis!

IPH is a disease of unknown cause (hence idiopathic), that causes diffuse bleeding in the alveoli (the grape-like sacs in the lung that do gas exchange), and some fibrosis (toughening) of the lungs. It’s primarily a disease of children, but that doesn’t mean adults can’t get it, it just means they don’t get it frequently.

It’s not a one-in-a-million disease. It’s about a one-in-four-million disease, at least amongst the Swedes (?). Then, because 80% of the patients are kids, an adult with this disease is about… 1 in 20 million. Congrats! Your character is a case study!

It starts with a cough that may slowly turn bloody. Your character could have on-and-off symptoms for years, or they could hack up blood daily with little explanation. They’ll be short of breath when they exercise or run—you’ll find this with anything that causes long-term bloody cough—and it will likely get worse over time. They’ll also likely develop anemia, because of the constant bleeding.

Your character will have batteries of tests. And I mean batteries of them, if they’re being treated in a modern US healthcare setting. Because there’s no one thing that can make the doctors say “Ah-HAH! It’s IPH! Why didn’t I think of it before?” It’s a diagnosis of exclusion, meaning it’s what’s left when they’ve ruled out everything else. Your character will get:

  • Lung function tests
  • Blood tests
  • Bronchoscopies
  • Lung biopsies
  • V/Q (ventilation/perfusion) tests
  • Test to re-test what the last tests tested
  • Tests to re-re-test the results of the last test

And so many more.

So relax. Go nuts. Rock the one-in-20 million, sit back, clasp your hands behind your head like a godsdamned champ, and write the character hacking up blood.

xoxo, Aunt Scripty


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Caffeine in Migraine!

Does Caffeine play a role in therapy of migraine? Or does it cause migraine?

Asking a doctor, he said yes caffeine heals pain in migraine attack. OK yea fine. But it can cause an attack too!! This is what I found something Amazing!

Migraine is a disorder characterised by acute pulsating headache, usually restricted to one side of head. Pulsatile dilatation of cranial blood vessels is the immediate cause of pain.

But we know headache is usually caused by vasoconstriction of cranial vessels and not vasodilation!
Actually, excess vasoconstriction or vasodilation, both cause less blood to reach brain parenchyma. This makes brain tissue cry for its necessary nutrients from blood!

In migraine there’s excessive vasodilation of the vessels. So is the cause of acute pain. Caffeine constricts cranial blood vessels ( all other systemic vessels are dilated ). It is a CNS stimulant. (That’s why we have more coffee at night while studying). :p

Now here comes the point. 1-2 cups of coffee (100-200mg) heal the pain by vasoconstriction. More than this will tend to decrease blood flow and so less supply to brain tissue.
That’s why some people, who are in a habit of taking excess coffee or soft drinks, are more prone to headaches!

》 Caffeine is one of the constituents of medicines specific for treating migraine.

MIGRIL: Ergotamine 2mg, Caffeine 100mg, cyclizine 50mg tab.

VASOGRAIN: Ergotamine 1mg,  Caffeine 100mg, Paracetamol 250mg, Prochlorperazine 2.5mg tab.

PS: Remember, the moment you feel migraine symptoms, have coffee. It is the best and most effective way to heal pain, without significant side effects.

That’s all
Thanks :)

Some cactus science, if you are so inclined:

“One defining feature of cacti is having clusters of spines. Numerous plants have spines of course, but in cacti, spines occur in clusters in the axil of leaves, even though the leaves are usually microscopic. Most cactus morphologists have concluded that cactus spines are either modified leaves or modified bud scales (the difference is inconsequential because bud scales themselves are modified leaves). The leaf-nature of spines is certainly understandable from the point of view of location: spine primordia look just like leaf primordia and are produced at a location where we would expect leaf primordia – at the base of the axillary bud’s shoot apical meristem. 

“Evolution appears to have been more complex than would be expected: mature cactus spines do not contain any of the cells or tissues characteristic of leaves, and conversely leaves lack all features characteristic of spines. The two organs have little in common other than developing from leaf primordia. Spines consist of just a core of fibers surrounded by sclereid-like epidermis cells. They have no stomata, no guard cells, no mesophyll parenchyma, no xylem, no phloem. When mature, all cells in a spine are dead, and even when the spine is still growing it has living cells only at its base. Cactus leaves on the other hand … have parenchymatous epidermis cells, guard cells, spongy mesophyll, chlorenchyma, xylem and phloem. So the evolutionary conversion of cactus leaves into spines did not involve a mere reduction of the lamina and then further reduction of midrib and petiole, it instead involved the suppression of all leaf-cell type genes and activation of genes that control formation of fibers, the deposition and lignification of secondary walls, and then programmed cell death. These fiber morphogenesis genes are not activated in any cactus leaf (none at all has fibers), but they are activated of course in the development of wood. It would appear that after an axillary bud apical meristem initiates spine primordia, most leaf genes remain suppressed and instead wood fiber genes are activated. This does not involve all wood genes because vessels are never produced in the spines, just wood fibers. This would be a type of homeotic evolution.”

Mauseth, J. D. 1982. Development and ultrastructure of extrafloral nectaries in Ancistrocactus scheeri (Cactaceae). Botanical Gazette 143: 273 – 277.