Margot Z. presented a great morning report where we discussed the work-up of an adolescent with throat pain. There was a lot of great discussion regarding the work up and diagnosis of infectious mononucleosis. Here are some of the highlights:
Infectious mononucleosis refers to the triad of fever, tonsillar pharyngitis, and lymphadenopathy traditionally caused by the Epstein-Barr Virus. Primary CMV infectious account for 7-10 percent of mononucleosis syndromes. Also consider HIV and toxoplasmosis.
Common findings: sore throat, bilateral posterior cervical lymphadenopathy (anterior is possible), fever, fatigue, tonsillar enlargement, splenomegaly (50-60% present, however insensitive on physical exam 27-58% depending on experience)
Monospot has a sensitivity of 63-84% and specificity of 84-100%; 25% false negative rate in the first week of illness
The EBV specific antibodies are 97% sensitive and 94% specific - this takes longer and is more costly
The presence of atypical lymphocytes greater than 10% of the differential has a specificity of 92%
Given the above statistics the following pathway is reasonable:
If history and exam suggest infectious mononucleosis get a monospot; if positive the diagnosis is confirmed
If negative obtain EBV specific antibodies for final diagnosis
Some pathways suggest getting a CBC with differential PRIOR to obtaining EBV antibodies and only drawing antibodies if there is a high atypical lymphocyte count or ALC > 4,000
Patients with IM should be withdrawn from contact or collision sports for at least 4 weeks after onset of symptoms
Fatigue and myalgias may persist for several months
Tom R and Sally Y presented a case of a 5-year-old presenting with two episodes of seizure like activity in the setting of URI symptoms and fevers.
Convulsion associated with temperature greater than 38°C
Age 6 months to 5 years
No CNS infection or inflammation
No acute systemic metabolic abnormality
No previous afebrile seizures
Rate of rise of fever vs maximum height of fever
There is debate about which is the main determinant of risk
Viral infections more common than bacterial
Genetic predisposition
In children with febrile seizures, 10 to 20 percent of their parents and siblings also have had or will have febrile seizures
Stephanie K presented a wonderful morning report where we discussed a teenage patient that was admitted with hypoglycemia after an unknown ingestion of pills. There are several drugs that should be considered as a cause for hypoglycemia that are included in the table to the right.
Sulfonylureas are particularly important to think about because a single 2mg sulfonylurea pill can be sufficient to cause hypoglycemia - "One and Done!"
This patient's admission was complicated by recent significant weight loss and distorted body image, leading to a discussion about her increased risk for refeeding syndrome.
It is difficult to define refeeding syndrome, but most commonly it is defined as “electrolyte depletion, fluid retention, and altered glucose homeostasis that occurs in malnourished patients on commencing oral, enteral, or parenteral nutrition.”
There are several other risk factors for feeding syndrome including the following:
Psychiatric: Anorexia nervosa, depression, chronic drug use
Chronic Malnutrition: Prolonged fasting (>4 days), failure to thrive, complex health needs, malignancy
Renal/Endocrine: Diabetic hyperosmolar states, chronic diuretic use
GI Losses: Inflammatory bowel disease, chronic pancreatitis, short bowel syndrome, significant vomiting/diarrhea
Other: Child abuse, food insecurity, acute weight loss of greater than 10% in 1-2 months, chronic infectious diseases, cystic fibrosis, congenital heart disease
Finally - a quick review of the physiology (to the left) and associated electrolyte abnormalities that occur with refeeding syndrome:
HypOphosphatemia
HypOkalemia
HypOmagnesemia
Being born is hard work!
Thanks Jaclyn B for this high yield Newborn Morning Report! We talked about a newborn who presented at 12 hours of age with a mass on the occiput. He was AGA at 41 weeks, and delivered vaginally after a prolonged labor which required vacuum extraction. The area had a fluid wave with palpation, and the fluid shifted based on the infants position.
The child was diagnosed with a Subgaleal Hemorrhage. This develops when veins are sheared or severed as a result of traction on the scalp during delivery, and blood accumulates in the loose tissue in the space between the periosteum of the skull. The mortality with these bleeds is 25% because these babies are at high risk of blood volume loss. It presents as a diffuse, fluctuant swelling of the head that may shift with movement and extend to the neck. Expansion of the swelling due to continued bleeding may occur hours to days after delivery. Affected neonates may have tachycardia and pallor due to blood loss, although blood loss may be massive before signs of hypovolemia become apparent. Early recognition is key, as newborns must be monitored with frequent hemoglobin and coagulation studies. Serial head circumferences are also indicated.
#KnowledgeNugget: Vacuum extraction is a significant risk factor for subgaleal bleeds & these babies have high mortality from blood loss!
It's important to consider the anatomy of the head when examining newborns. There are three key features to examine: fontanelles, sutures, and extra-cranial findings:
Fontanelles: Palpate with the newborn in the sitting position. Both fontanelles should be soft and flat. A tense and bulging fontanelle in a sitting infant who is not crying may be an indication of raised intracranial pressure (ICP), which may be present in patients with a subdural hematoma or bacterial meningitis.
Sutures: Palpate the main sutures of the skull (sagittal, coronal, lambdoid, and metopic). Passage through the birth canal may result in molding. An asymmetric skull that persists for longer than two to three days after birth or a persistent palpable ridge along the suture line may suggest craniosynostosis.
Extra-cranial findings: Inspection of the head includes noting the size and shape of the head and the presence of abnormal hair or whirls, scalp defects, unusual lesions or protuberances, lacerations, and abrasions or contusions.
Bonus finding: Craniotabes! Craniotabes is a soft area of skull bone, usually in the parietal region, that gives a sensation of a ping-pong ball when depressed. It commonly is found in preterm infants, and can occur in a term infant whose head rested on the maternal pelvic brim during the last few weeks of gestation. Craniotabes can be a pathologic finding in syphilis and older kids with rickets, although it usually occurs in normal infants.
Over-Riding Sutures/Molding
Common - baby has to get out somehow! Usually noted on palpation: the ridges develop when one bone overlaps the adjacent one during delivery. Over-riding sutures are part of molding. Resolve with time.
Caput Segundum
Common - Scalp edema that can cross over suture lines, but often unilateral. Produces pitting edema when pressed. Maximum size at birth, resolves quickly.
Cephalohematoma
Less Common - Blood under the periosteum. Does not cross suture lines. If more than one bone is affected, there will be a separation between the two areas at the suture line as seen here. Fluctuent on palpation.
Subgaleal Hematoma
Rare = Worrisome! Feels like a water balloon. Area between the scalp and skull is a large space, can lose significant blood volume. A fluid wave is typically seen and is positional.
Maddie P presented a case of a school aged child who presented with ~5 days of abdominal pain, a painful L sided erythematous abdominal rash, as well as anasarca and significant proteinuria. Additional labs were consistent with Nephrotic Syndrome- but what about that rash? Given its band like distribution, the differential was bacterial cellulitis as well as Zoster we wondered whether nephrotic patients are at risk for viral infections also.
There are a few contributing reasons nephrotic patients are at higher risk for infection:
Low serum concentrations of immunoglobulin G
Impaired ability to make specific antibodies
Low levels of alternative complement
Immunosuppressive therapy
What this means is nephrotic patients are at high risk for infections, particularly with encapsulated organisms, and Children are at increased risk of viral infections too, especially varicella, and especially if they are also on immunosuppressive medications.
In fact Infection was the most common cause of death before antibiotics were available (a study published in Pediatrics sites a mortality rate of 40% prior to 1940!) and this UptoDate article notes that they are particularly at risk for recurrent URIs, UTIs, peritonitis and sepsis especially from Strep pneumo.
Our patient was started on steroids, acylovir and antbiotics and responded well, but never developed vesicles- so the team favored a bacteria cause of the rash.
Kelly S presented an interesting case of late-onset Group-B Strep sepsis in a 2-month-old. This unimmunized, term infant presented with one day of fevers and sleepiness. Her mother was noted to be GBS positive, but did not receive any intrapartum antibiotics due to a precipitous birth. Initial laboratory testing including CBC and BMP were unremarkable, but blood culture later came back positive for GBS.
Although our patient's mother was unable to have her GBS treated appropriately during labor, as figure 1 demonstrates, appropriate intrapartum antibiotic prophylaxis for GBS does not seem to have an effect on the number of infants with late onset GBS disease.
Figure 1. The figure above, is data from the Active Bacterial Core Surveillance project at the Centers for Disease Control and Prevention, which demonstrates the reduction in early-onset GBS disease since the introduction of screening and intrapartum antibiotic prophylaxis in the 1990's.
This critical care morning report was a collaborative effort between the admitting night team, day team, and consult toxicology staff! We heard about a toddler admitted over the weekend with concern for seizure after she woke her mother "kicking like crazy." Upon arrival in the field, EMS found bradycardia, and an O2 sat of 10% with bradypnea. In the ED, she was no longer seizing, was stabilized and found to have non-reactive, 4mm pupils, with a GCS of 3. Head CT was normal, but on Chest/Ab imaging she was found to have a 1.5cm radiolucent object in her descending colon. After more history it was learned the only medication in the home was Carbamazepine, and toxicology became involved for concern for ingestion.
In our Toxicology Block Ed on 11/1/19, Dr. Abby Montague reminded us that urine drug screens are almost never indicated in teenagers! This is because you know they're probably taking a cocktail of things, there's a lot of cross reactivity, and it's rarely going to change your management. HOWEVER, in infants, their urine drug screen should be totally normal so if ingestion is suspected, there is utility in a urine drug screen. But you have to know how to interpret cross-reactivity! So in this child a urine drug screen was obtained -- and found the carbamazepine level to be 62 (normal <8)!!
Management for carbamazepine toxicity is activated charcoal. Because Keppra works on a different receptor, it's safe to use in carbamazepine overdose, so the patient was loaded on this without any new seizure activity. Unfortunately, after several days the patient remains unstable and critically ill despite a now normal carbamazepine level.
Carbamazepine comes in many different capsules and formulations, but interestingly, the capsules are radiolucent. The significance of the finding on XR is unclear at this point -- it doesn't really look like a pill capsule -- but interestingly the family also recently returned from Liberia, where jewelry and other trinkets are often made of toxic heavy metals. So while carbamazepine ingestion is the likely cause of this patients presentation, heavy metal toxicity could not be ruled out as a contributing factor to her illness. The heavy metal screen is pending.... stay tuned for updates!
UPDATE: One week later, the heavy metal screen was normal. Still critically ill and unable to intubate due to severe ARDS.
Thanks Emma Pabarcus for this high yield morning report! She presented a case of a young boy who came in overnight with fever and four days of pain in his left arm. He refused to move, but he did have passive range of motion when distracted. His neurologic exam was normal but his XR was concerning for a new bone lesion, most concerning for osteomyelitis.
How does infection happen? It's most often the result of hematogenous seeding of bacteria to the metaphyseal region of bone. About 30% of patients report local trauma which likely increases the risk of bacterial seeding.
Why is it always the metaphyseal region? Well, the blood flow in metaphyseal capillaries is sluggish due to sharp turns. This results in venous sinusoids which give bacteria time to lodge in this region. PLUS the low pH and low oxygen tension around the growth plate assist in the bacterial growth. Once a bacteria is established in the bone, it spreads via the Haversian and Volkmann canal systems.
Risk factors? In addition to regional trauma, children with diabetes, hemoglobinopathies, rheumatoid arthritis, chronic renal disease, immune compromise, or varicella infection are at greater risk
Tell me about the bugs! Staph. Staph. Staph. It's the most common cause of osteomyelitis in kids. Staph aureus is #1, so always be thinking about MRSA.
Aren't there other bugs that cause osteomyelitis too? Heck yes there are! Here's what you need to know about them:
Group B Strep: The most common cause of osteomyelitis in neonates.
Kingella kingae: Gram [-], seen in kids 6-36 months. Difficult to grow, so often cultures have no growth until days 4 or 5. Often affects non-tubular bones (spine, sternum, etc)
Pseudomonas: Think about this in puncture wounds to the foot, particularly through a "rubber-soled" shoe. Pseudomonas forms biofilms on rubber.
Salmonella: remember that Salmonella has a capsule, so you have to worry about this in your asplenic patients (Sickle Cell, TPIAT kids)
Mycobacterium TB: TB in children is more likely to be extra-pulmonary, so we do see TB osteomyelitis in children. Watch for those acid-fast bacilli in immigrant children or kids with significant travel history.
What do I start them on? Because of the severe implications of bone infections, we often start with empiric coverage as soon as possible (but after blood and fluid cultures!). Treat based on the probable pathogen for the child's age and your hospital antibiogram.
What about surgical management For most kids with osteomyelitis, IV antibiotics are usually sufficient. Sometimes surgery is needed when there is failure to improve after 48-72 hours, devitalized bone, extension into the soft tissue or joint capsule, or extensive bony involvement.
Thanks Caleb Hocutt for this interesting case of digital swelling! A school-aged boy with a history of rheumatic fever who recently immigrated from Northern Africa, came in with a one day history of worsening swelling of the left thumb. His vital signs were normal and he was in mild pain. His thumb was edematous without lesions, but did have significant erythema, limited motion of the digit, and streaking up the wrist. Laboratory testing was within normal limits. We discussed the importance of keeping a broad differential in cases with unusual travel history or exposures.
Cutaneous Anthrax
Bacillus anthracis
Bacterial. Common in low-middle income countries. Starts as a boil-like skin lesion that forms a painless ulcer with eschar. Treatment: Amox or Cipro
Sporotrichosis
Sporothrix schenckii
"Rose Gardener's Disease" Fungal. Affects children playing with soil. Nodular lesions along lymph nodes and vessels. Treatment: Itraconazole
Juvenile Idiopathic Arthritis
"Stills disease"
Characterized by daily fever in a quotidian pattern, rash, and arthritis. Peak incidence is one to three years of age. Treatment: NSAIDS first, then biologics
Dactylitis
Secondary to Sickle Cell
Vaso-occlusive severe pain in the small bones of the hands and feet that typically occurs 6mos-5yrs. Treatment: hydration, analgesics, warm packs
While thinking about the exotic and scary things is important, remember that common things are common. Given his history and exam, the working diagnosis for this child was non-purulent cellulitis, likely secondary to Strep (GAS is the #1 cause). He was started on Cefazolin.
#KnowledgeNugget: Hands are special. Surgery should evaluate any child with hand pathology because of the risk of necrotizing fasciitis and compartment syndrome. There are many facial planes and even a small amount of swelling can develop into compartment syndrome with vascular compromise. Don't forget the consult!
Phil P presented of a school aged girl who presented with 6 months of constipation, polydipsia/polyphagia and hair loss. She eventually presented to the ED with sweating, fatigue, headache, photophobia and pain with eye movement. When she arrived to the ED she was febrile, hypertensive to 140/100, tachycardic to 160, and the tachycardia and hypertension persisted after she defervesced. Infectious workup was reassuring but her TSH was undetectable with a FT4 of 6.04. They got her started on treatment right away for thyrotoxicosis (definition: the clinical manifestations of too much thyroid hormone- either T3 or T4) but what is the most serious complication we need to be watching for in someone with hyperthyroidism?
Treatments
Beta Blockers- to control symptoms of increased adrenergic tone
Methmizole (1st line) or Propothyouriacil (if fails other therapies)- inhibits the production of new thyroid hormone
Iodine- inhibits the release of thyroid hormone
Steroids- inhibits conversation of T4 to T3
Thyroidectomy- if fails or there are contraindications to above therapies
Thyroid Storm
A Thyroid storm is the manifestation of thyrotoxiosis- it's pretty rare (1% in adults), but life threatening. It can happen in longstanding uncontrolled hyperthyroidism- most often Graves Disease in Children- but is typically precipitated by an event such as infection. Storms happen hormone levels no more elevated than what you'd typically see with thyrotoxiosis but also have the following:
Signs of multisystem organ failure (nausea, vomiting, diarrhea, liver damage, heart failure)- which is often the cause of death
Shock like vital signs and hyperpyrexia (often 104-106 F)
Altered mental status- (agitation, delirium, psychosis, stupor, coma)
There's a validated scorning system in adults to evaluate for impending storm. These patient usually need ICU level of care for cardio respiratory support, aggressive thyroid treatment and cooling.
Jen Signor presented a 14-year-old patient with Lyme carditis with associated 1st degree AV block for EKG rounds. We discussed the basic steps to take when reading an EKG:
1. Rate:
Start with an R wave on a heavy marked line and count 300, 150, 100, 75, 60, 50 for each big box until the next R wave
2. Rhythm:
Sinus rhythm if ALL of the following:
P wave before every QRS
QRS after every p
Normal P wave axis (positive P wave in lead II), meaning the electrical signal is coming from the sinus node
3. Axis:
Normal axis will have positive QRS in leads I and avF (at least for a 14-year-old!)
4. Intervals:
PR: Upper limit of normal: 0.12 sec (newborn) to 0.2 sec (adult)
QRS: Upper limit of normal: 0.08 sec (less than 1yo) to 0.12 sec (adult)
QTc: Upper limit of normal: 0.47 sec (newborn), 0.44 sec (<6 mo), 0.44 sec (adult male), 0.46 sec (adult female)
5. Voltages:
RAE: P wave in II or V1 >3mm
LAE: P wave in II >0.1sec or biphasic in V1
RVH & LVH: you will have to look up normals for age!
This patient has 1st degree AV block with the EKG above showing a prolonged PR interval
Thanks to Kayla Olson for adding in some interesting facts about Lyme carditis as well, including the following:
Lyme carditis occurs in about 1% of all patients with Lyme disease in the U.S
AV conduction block of varying degrees is the most common feature of Lyme carditis, but depressed cardiac function can also occur
The degree of AV block can fluctuate and patients can progress from first degree to second degree or complete AV block within minutes
AV block can persist up to 6 weeks
Alex Muhar presented an interesting case of a well-appearing toddler sent to the ED from clinic for a concerning inguinal rash. The red-brown area appeared over several hours, and had blanching on the periphery but not in the center. There was no fluctuation or warmth, and the child had full range of motion and no pain with palpation. No other skin lesions were present.
UPDATE: The patient was discharged the day of admission after an NAT evaluation and no change in rash presentation. At Dermatology follow-up two days later, biopsy of the lesion demonstrated "outer and eccrine necrosis, with neutrophil predominant inflammatory infiltrate. With this pathology, external trauma (pressure necrosis or thermal injury) is the most likely etiology, however DIC and necrotic arachnidism (arthropod bite) cannot be excluded."
2nd UPDATE: During outpatient follow-up with Safe and Healthy Children, it was discovered that Mom works at a nail salon, and there are nail/salon strength chemicals in the home. Mother noted that some had spilled and she changed the child's diaper after cleaning it up. There is an exothermic reaction that can happen with certain salon chemicals and diaper products. According to S&HC, this child's presentation is quite consistent with this. We figured it out!!
While non-accidental trauma was a significant part of our discussion, it was important for us to consider non-traumatic etiologies with rapid onset purpura. Our differential diagnosis included:
erythema multiforme (not always a classic targetoid appearance!)
burns and frostbite (seen with aerosolized canisters)
Henoch-Schonlein purpura (it can look variable at the beginning!)
immune or ideopathic thrombocytic purpura
And a few rare causes which are good to know exist: infantile acute hemorrhagic edema, papular-purpuric gloves and socks syndrome (Parvo B19).
What does "non-blanching" tell us?
A lot, actually! Understanding the skin layers are key to understanding blanching. Ecchymoses, petechei, and purpura are all non-blanching rashes. They tend to be darker in color and occur from areas of hemorrhage into the dermis. This can be from trauma (bruises) or pathologic vascular leak (HSP, menningococcus, ITP). Let's compare this to sunburns: radiant injury causes inflammation, but the underlying vasculature is still intact - so they blanch!
And don't forget about TIME: Rashes evolve over time and it can be a nice clue to diagnosis. Is this day 1? Or is it really day 4 but the patient/parent didn't notice it? Timing matters.
Morgan Boes presented a case of fever in a patient with sickle cell disease and asthma. We discussed the work up and management for this patient, along with acute chest syndrome and how asthma affects the prognosis of a patient with sickle cell disease.
Fever in a patient with sickle cell disease is a medical emergency!
These patients are at high risk for invasive pneumococcal disease
Evaluation of fever should always include: physical exam (any localizing symptoms?), CBC, and blood culture
Empiric antibiotics should be given to cover pneumococcus. Ceftriaxone is the antibiotic of choice
What causes acute chest syndrome (ACS)?
While about 45% of patients with ACS have no identifiable cause, about 30% of patients will have ACS due to infection. The most common infectious causes include Chlamydia pneumoniae, viral infections, and Mycoplasma pneumoniae. Other causes include pulmonary infarction and fat embolism.
Asthma and Sickle Cell Disease
In patients with sickle cell disease, a diagnosis of asthma is associated with higher rates of ACS, vaso-occlusive crisis, and early death.
Andrea Lyle presented a case of a teenager who presented with a few days of fever, chills and vomiting/diarrhea, a history of significant unintentional weight loss over ~4 months. Eventually during the workup chest CT revealed diffuse ground glass opacities, interlobular septal thickening and mediastinal/hilar lyphadenopathy. The differential was pretty broad and included things like opportunistic viral/fungal infections, sarcoidosis, a hypersensitivity pneumonitis; after more workup these lung findings are likely due to a chronic vaping injury- the patient has been using commercially available vape liquid several times a day, most days of the week for the majority of the past year. We've seen quite a few of these cases recently.
Ground glass opacities, which is a non-specific term describing an area of increased attenuation in the lung with sparing of the bronchial and vascular markings, should point you toward an alveolar or interstitial process. It can be a buzzword for a few disease processes depending on the age/clinical context. In neonates we see this finding with respiratory distress syndrome or meconium aspiration. In an immunosuppressed patient it could point you towards pneumocystis, CMV, HSV, aspergillosis. We see this pattern in chemical pneumonitis, which is an inflammatory rather than infectious process, and occurs a substance gets into the lower respiratory tract that shouldn't be there, like in this patient. Vaping is relatively new, but we commonly see chemical pneumonitis in processes such as aspiration, GERD, burn patients with inhalational injury.
Nathan Wegmann presented a case of a child with an enlarged anterior cervical lymph node and fevers, leading to a great discussion about the causes and management of lymphadenitis.
We discussed the most common causes of lymphadenitis are Staph aureus and group A streptococcus. While Staph and Strep species account for about 80% of cases, there are others to consider such as anaerobic organisms, Yersinia pestis, Bartonella henselae (cat-scratch disease), Mycobacterium tuberculosis, and atypical mycobacteria, depending on the patient's history and exam. The management of lymphadenitis often differs between the outpatient and inpatient setting, as well as the suspected cause of lymphadenitis.
Thanks Tricia Paul for the excellent Morning Report reviewing the physiology, etiology, and management of stridor!
We started by listening to the breathing of a patient with stridor and had a great discussion detailing how the phase of "noisy breathing" can tell us the location of obstruction (see graphic below). The high pitched, rhythmic pattern of breathing is what is important to appreciate in these children. The most common cause of stridor in young children is viral croup, but it's important to keep a broad differential. While stridor is typically a clinical diagnosis and self-limited with clinical improvement, sometimes laryngoscopy, bronchoscopy or chest and neck imaging are needed to further evaluate the source.
Note: Stridor is NOT Stertor. Stertor is a heavy, low-pitched inspiratory snoring-type sound associated with naso- or oropharynx obstruction.
Nasreen Quadri, Med-Peds Global Health Chief, presented a powerful morning report about the refugee crisis affecting over 50 million people worldwide. Diving into the geopolitical and historical context for the crises in the Congo, Myanmar, Burma and Honduras, we learned that when caring for these displaced families and children, it's imperative to recognize the trauma associated with their experience and the incredible resilience needed to survive. ASK about their story, and ADVOCATE for their health and well-being.
Check out these fantastic interactive visualizations about global refugee populations:
This week, Nasreen will be traveling to refugee camps in Jordan and the Tanzania-DRC border with the International Organization for Migration (IOM) to help teach physical exam entrance assessments. If you are interested in this work or have any questions, contact her at quadr015@umn.edu. Thanks Nasreen!
Thanks Brian Leyva for the great trauma teaching case! We talked about a teenager who was brought in after being found on the side of the road with his bike after being struck by a car. He had lost consciousness, but was alert upon arrival. He was clinically stable, and complained of headache and right ankle pain.
Our discussion involved several aspects of imaging decisions in pediatric trauma management:
The Pediatric Emergency Care Applied Research Network (PECARN) is a research collaboration of pediatric emergency departments across the U.S. that has developed criteria to help identify children at very low risk of a clinically significant TBI in whom head CT may be unnecessary.
In their study, children under 2 years of age with zero of the six predictors, risk of clinically significant TBI was less than 0.02%, and no child classified as low risk had a clinically significant TBI.
They found in children over 2, the risk of clinically significant TBI was slightly higher, at 0.05%.
By using PCARN as a guide, we can be reassured that patients classified as ‘low risk’ can safely forego a head CT with a very low risk of missing a clinically significant TBI.
Our patient was moderate risk given the severe mechanism of injury and loss of consciousness. His CT scan was normal.
For more information, check out this well referenced blog/podcast about pediatric head injury.
In morning report, we discussed a 11 month old child who had a fever for the past 7 days. There were no associated symptoms other than mild fussiness and high spiking fevers with a Tmax of 104.7 degrees Fahrenheit, not amenable to Tylenol. Initially, reassurance was provided by his primary care provider, but as the fever progressed the clinician drew a CBC significant for elevated platelets and an urinalysis. He was sent to the ED for further workup. Exam upon presentation was normal.
This case highlights and interesting differential spanning hematology , infectious disease, and oncology. Ultimately, the biggest concern for this child was incomplete Kawasaki Disease (KD). Affecting 10 out of every 100,000 children, the clinician should have a high index of suspicion for KD given the possibility that the child may develop a coronary aneurysm. Please refer to the 2018 AHA Kawasaki Guidelines for further information.