Major Traumatic Brain Injury

Traumatic Brain Injury - TBI Initial ManagementWhile the weird, wild, and unusual conditions that affect our pediatric patients deserve our attention, traumatic injuries unquestionably demand much of our clinical attention.  We have certainly discussed many trauma topics previously (ex, Abdominal Trauma, Aortic Trauma, Damage Control ResuscitationDental Trauma), but the one region of the body that, when injured, leads to the most significant problem is the head. While much of the time we are afforded the opportunity to discuss limiting medical radiation in the setting of Minor Head Injury, there are times when it isn’t a minor problem. Let us take a minute to ensure we are taking simple steps to help those with Major Traumatic Brain Injury:


Not Minor. TBI is a Major Problem!

  • In the USA, traumatic brain injury (TBI) leads to > $1 billion in total hospital charges annually. [Schneier, 2006]
  • Adolescents develop TBI primarily from motor vehicle collisions.
  • Younger children are exposed to TBI often from falls.
  • Sadly, non-accidental trauma must always be consider as well.


Prevent Secondary Injury!

Much of the work done for pediatric closed head injury has focused on how to risk stratify those who have had minor head impacts and are at Low Risk for having a substantial intracranial injury. While this is important, Major Traumatic Brain Injury is devastating and we need to know some basic steps to help these patients.

  • Primary Injury vs Secondary Injury
    • The primary insult (ex, blunt impact, penetrating missile, blast, rapid acceleration-deceleration) can create a severe injury.
      • Some will lead to Epidural or Subdural hematomas that warrant neurosurgical intervention.
      • Some will lead to irreversible damage (ex, Diffuse Axonal Injury).
    • The secondary insult evolves as a consequence of the primary insult and is what clinicians need to be mindful to prevent.
      • The injured brain is very susceptible to additional injury.
      • Hypotension and/or hypoxia will further stress the tenuous regions around the primary injury.
  • Prevent Hypotension and Hypoxemia.
    • Both will worsen secondary brain injury.
    • RSI with C-Spine stabilization should be done early.
    • Get access! Give fluids. Stop Bleeding.
    • Consider Hypertonic Saline for volume resuscitation.
  • Consider Head Positioning
    • Head of Bed at 30 degrees will aid in venous drainage.
    • Ensure head is Midline to ensure one side’s venous flow is not being constricted.
  • Avoid additional physiologic stressors that can increase mortality risk! [Smith, 2012; Davis, 2009; McHugh, 2007]
    • Avoid Hyperthermia
    • Avoid Hypoglycemia and Hyperglycemia
    • Avoid Hypocapnea
    • Avoid Hyperoxia
  • Make the patient sedated and paralyzed!
    • The patient fighting and struggling will increase ICP.
    • Agitation, anxiety and stress will all exacerbate the problem.
    • Be mindful, though, of inducing hypotension.
      • Consider Etomidate if lower BPs
      • Ketamine has also been shown to be safe for patients with TBI. [Bar-Joseph, 2009].
      • Thiopental is an alternative for patients who have higher BPs.
  • Many will choose to use Lidocaine as a pretreatment medication for RSI.
    • Good idea… but really needs to be given several minutes before intubation.
    • If you have time to use it, feel free to.  If you don’t, don’t waste time waiting for it. {that’s my 2 cents}


Moral of the Morsel

  • While avoiding unnecessary CT in patients with Low Risk for significant traumatic brain injury is important, remembering to do some rather basic steps is crucial for our patients who have major TBI!
  • Basics are Best! Check that Head of Bed angle.
  • Keep that ICP low and that BP normal! Cerebral Perfusion depends on it!



Brenkert TE1, Estrada CM, McMorrow SP, Abramo TJ. Intravenous hypertonic saline use in the pediatric emergency department. Pediatr Emerg Care. 2013 Jan;29(1):71-3. PMID: 23283268. [PubMed] [Read by QxMD]

Agbeko RS1, Pearson S, Peters MJ, McNames J, Goldstein B. Intracranial pressure and cerebral perfusion pressure responses to head elevation changes in pediatric traumatic brain injury. Pediatr Crit Care Med. 2012 Jan;13(1):e39-47. PMID: 21242856. [PubMed] [Read by QxMD]

Smith RL1, Lin JC, Adelson PD, Kochanek PM, Fink EL, Wisniewski SR, Bayir H, Tyler-Kabara EC, Clark RS, Brown SD, Bell MJ. Relationship between hyperglycemia and outcome in children with severe traumatic brain injury. Pediatr Crit Care Med. 2012 Jan;13(1):85-91. PMID: 21499170. [PubMed] [Read by QxMD]

Bar-Joseph G1, Guilburd Y, Tamir A, Guilburd JN. Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. J Neurosurg Pediatr. 2009 Jul;4(1):40-6. PMID: 19569909. [PubMed] [Read by QxMD]

Davis DP1, Meade W, Sise MJ, Kennedy F, Simon F, Tominaga G, Steele J, Coimbra R. Both hypoxemia and extreme hyperoxemia may be detrimental in patients with severe traumatic brain injury. J Neurotrauma. 2009 Dec;26(12):2217-23. PMID: 19811093. [PubMed] [Read by QxMD]

McHugh GS1, Engel DC, Butcher I, Steyerberg EW, Lu J, Mushkudiani N, Hernández AV, Marmarou A, Maas AI, Murray GD. Prognostic value of secondary insults in traumatic brain injury: results from the IMPACT study. J Neurotrauma. 2007 Feb;24(2):287-93. PMID: 17375993. [PubMed] [Read by QxMD]

Schneier AJ1, Shields BJ, Hostetler SG, Xiang H, Smith GA. Incidence of pediatric traumatic brain injury and associated hospital resource utilization in the United States. Pediatrics. 2006 Aug;118(2):483-92. PMID: 16882799. [PubMed] [Read by QxMD]

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Poor Utility of WBC Count for the Evaluation of Fever

WBC Count is Last Bastion of Intellectually DestituteWhen I was a resident (Not that long ago people! Come on!!), I was taught by Dr. Mattu (@amalmattu) that the WBC Count is “the last bastion of the intellectually destitute.” These words were meant to encourage me to avoid reflexively ordering a WBC to determine whether a patient had “an infection.”  Often, it is aimed at the evaluation of the patient with abdominal pain and possible appendicitis. Recently, there have been other labs that have be used in a similar fashion (ex, Lactate Level), but the WBC count still has a strong association, in many people’s minds, with “infection” or general “sickness.” Some days I spend half of my clinical time discussing my disdain for the WBC count and this perceived association. Recently, one of my fantastic PEM Fellows, Dr. Mary Grady, alerted me to an article published that helps add justification for my position and Dr. Mattu’s mantra. Let’s review the Accuracy of WBC Count in Evaluation of Fever:


The WBC Count: Beliefs

  • Our patients’ perceive the WBC Count as being useful measure of health.
    • Abnormal WBC = Badness; Normal WBC = Wellness.
    • A quick internet search of “WBC Count” will lead you to the conclusion that an abnormal WBC count is:
      • Concerning.
      • Associated with infection…
      • Also associated with Inflammation, Trauma, Allergy, “Disease.”
    • I wouldn’t classify this as “Alternative Facts,” but it is certainly not the entire story and we need to realize that our patients are consuming this information prior to seeing us in the ED.
  • We are part of the problem.

Ok, before we get on our high horses and ride off into the sunset. realize that the misconceptions of medical testing are our creations… and reinforced by our poor communication.

    • We like certainty and dislike difficult conversations.
      • Obtaining tests, and playing the favorable odds of them supporting our already formed conclusions, is often easier than discussing the limitations of tests.
      • It is difficult to discuss sensitivities and specificities of lab tests, particularly when I have a hard time understanding that myself.
      • It is also difficult to discuss uncertainty and describe reasonable approaches to mitigating risk.
    • We like to please people…
      • Many people want “something done” and testing is typically equated with “doing something.”
      • Spending a few minutes education patients/families can really help realign everyone’s goals… and is actually “doing something.”
        • There may be a perception that they need a Plastic Surgeon, but that facial laceration is best closed by me at 3am.
        • There may be a perception that their child needs IV fluids for dehydration, but they need to be educated about the potential pitfalls of that as well as how Oral Rehydration Therapy is faster.
    • We have been conditioned.
      • Just like a Pavlovian response, many of us have had our medical training link “Infection” with “Abnormal WBC Count.”
      • Each time I was asked for the WBC count when discussing a child with appendicitis a subconscious link was generated.
      • It takes effort to decondition the Pavlovian Response.


The WBC Count: Not Alternative Facts

  • Abnormally high or low WBC counts can be important when…
  • Isolated abnormal WBC Count is not often helpful in ruling in or out a diagnosis.
    • Isolated abnormal WBC does not equate to Septic Arthritis, and it’s absence doesn’t negate the diagnosis.
    • Appendicitis can exist with normal WBC count and abnormal WBC count does not diagnose appendicitis.
    • The clinical question helps determine the utility of the test.


The WBC Count: Fever Evaluation in Infants

  • Fever is one of the most common presenting complaints in children in the ED.
  • The CBC is the most commonly obtained test in their evaluation.
  • In September of 2017, JAMA published a PECARN study that looked at the Utility of the CBC for Evaluation of Fever in Infants. [Cruz, 2017]
    • Design:
      • Prospective enrollment of infants <61 days of age in 26 EDs
      • Included infants with fever, Blood Cultures, and CSF cultures (or telephone follow-up)
      • Excluded critically ill and premature and those with significant comorbidities or recent antibiotic exposure.
    • Found:
      • Of the 4313 who met inclusion criteria, 97 (2.2%) had invasive bacterial infections (bacteremia or meningitis — not UTI).
        • Bacteremia – 73
        • Meningitis – 24 (11 with concurrent bacteremia)
        • 57 were Neonates (< 29 days of age) – 4.3% of neonates
        • 40 were 29-60 days of age – 1.4% of this group.
      • No CBC parameter (leukocytosis, leukopenia, ANC, thrombocytosis) distinguished between infants with invasive bacterial infections and those without infection.
      • Using widely accepted normal ranges for WBC counts would have missed 63% of cases.
    • Conclusions:
      • A minority of infants with invasive bacterial infections have abnormal WBC counts.
      • WBC count is a poor discriminator of infants with and without invasive bacterial disease in the post-vaccination era.
      • “… we need to question our continual reliance on a test whose greatest strength may simply be in its ready availability in clinical practice.” [Cruz, 2017]


Moral of the Morsel:

  • The WBC Count is still the last bastion of the intellectually destitute. It does not equate to presence or lack of infection.
  • No test is perfect. All must be performed in relation to a clinical question and compared to pre-test probabilities.
  • Educate others! Take the time to discuss with your patients/families about the real limitations of testing.



Cruz AT1, Mahajan P2, Bonsu BK3, Bennett JE4, Levine DA5, Alpern ER6, Nigrovic LE7, Atabaki SM8, Cohen DM3, VanBuren JM9, Ramilo O10, Kuppermann N11; Febrile Infant Working Group of the Pediatric Emergency Care Applied Research Network. Accuracy of Complete Blood Cell Counts to Identify Febrile Infants 60 Days or Younger With Invasive Bacterial Infections. JAMA Pediatr. 2017 Nov 6;171(11):e172927. PMID: 28892537. [PubMed] [Read by QxMD]

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Pulmonary Hypertensive Crisis

Pulmonary Hypertensive CrisisCaring for children can be rather challenging. Yes, there is a fair amount of finding ways to avoid saying “It’s Just a Virus” while conveying the fact that the child is doing just fine; however, there are also a number of children who require overt Critical Care. We have previously discussed critical presentations involving hypertension (ex, Hypertensive Crisis, Eclampsia, PheochromocytomaThyroid Storm), but there is another that involves the lungs that we need to add to the library. Let’s review Pulmonary Hypertensive Crisis:


Pulmonary Hypertension

  • Pulmonary Hypertension is not a specific disease.
  • It is the clinical picture of: [Del Pizzo, 2016]
    • Decreased pulmonary vasculature function
    • Elevated right ventricle pressure
    • Can progress to right heart failure.
  • Largely results from one or more of the following: [Del Pizzo, 2016]
    • Interruption of pulmonary vasculature maturation
      • Adult number of alveoli don’t develop until ~ 4years of age.
      • ex, congenital diaphragmatic hernia
    • Lung destruction from inflammation
    • Vasodilator/vasoconstrictor imbalance
  • Can be associated by numerous conditions and factors: [Del Pizzo, 2016]
    • Examples:
      • Acquired and Congenital heart disease
      • Respiratory distress syndrome of the newborn
      • Pulmonary veno-occlusive disease
      • Hypoxia
      • Cystic fibrosis
      • Hypercoagulable states (ex, Nephrotic Syndrome)
      • HIV infection
      • Inhaled toxins
      • Sickle Cell Disease
      • Genetic factors – Trisomy 21 is the most common.
    • Can also be idiopathic – accounts for the majority of cases
  • Presentation and diagnosis is often delayed.
  • Initial symptoms can be non-specific.
    • Dyspnea, cough, chest pain, fatigue, syncope, palpitations
    • RED FLAGS for undiagnosed Pulmonary Hypertension: [Del Pizzo, 2016]
      • Dyspnea with exertion
      • Syncope with exertion
      • Abdominal pain with exertion
      • Look for these associated with known concerning comorbidities (ex, sickle cell disease, connective tissue disorder)
  • Can present with critical distress. [Del Pizzo, 2016]
      • Patients with pulmonary hypertension walk a tenuous tightrope where stability can be quickly jeopardized.
      • They do not tolerate hypovolemia well – but volume overload is also problematic.
      • They do not tolerate arrhythmias well, especially bradycardia!


Pulmonary Hypertensive Crisis: Basics

  • Occurs when pulmonary vascular resistance increases to the point that it: [Kaestner, 2016; Del Pizzo, 2016]
    • Right Ventricle (RV) pressure and volume increase.
      • Causes septum to be displaced leftward reducing Left Ventricle (LV) volume
      • Ventricular filling pressures increase as well as compensatory tachycardia and decreases in systemic vascular resistance occur.
      • Leads to drop in cardiac output and coronary blood flow and metabolic acidosis.
    • Pulmonary blood flow decreases.
      • Leading to pulmonary arterial distension, mechanically obstructing small airways
      • Pulmonary edema develops
      • These increase Dead Space and worsen V/Q mismatch -> hypoxia and respiratory acidosis.
  • Can be triggered by: [Del Pizzo, 2016]
    • Fever
    • Hypovolemia (ex, good ol’ fashioned viral gastroenteritis)
    • Increased cardiac demand
    • Interruption of continuous prostanoid infusion
  • Presents with:
    • Tachycardia, hypotension, cool extremities, poor perfusion, and altered mental status.
    • Essentially, looks like Cold Shock, but with hyperdynamic right ventricle.
      • May hear loud single S2, holosystolic murmur.
      • May palpate engorged liver edge.


Pulmonary Hypertensive Crisis: Management

  • Primary goals: [Kaestner, 2016; Cunningham, 2016; Del Pizzo, 2016]
    • Reduce pulmonary vascular resistance
    • Augment RV preload and cardiac output
    • Resolve systemic hypotension and maintain coronary artery flow
    • Avoid tachyarrhythmias  
  • Primary therapies: [Kaestner, 2016; Del Pizzo, 2016]

See [Kaestner, 2016] for a nice treatment algorithm

    • Supplemental Oxygen
      • Use if Pulse Ox is < 95%
      • Adjust to typical baseline for those with congenital heart diseases.
    • Judicious fluid administration
      • Need volume to support output, but too much will exacerbate right heart failure
      • Aliquots of 5 – 10ml/kg with vigilant reassessment is advised. [Del Pizzo, 2016]
    • Inhaled Prostanoids / prostacyclin
      • Iloprost can be given IV as well.
      • Inhaled therapies have benefit in the spontaneously breathing patient
        • Can be started without IV,
        • Have less impact on systemic blood pressure.
          • May need concomitant vasopressor therapy.
          • Norepinephrine or Vasopressin [Siehr, 2016; Kaestner, 2016]
          • Dobutamine, epinephrine, or milrinone may also be needed.
    • Inhaled Nitric Oxide (NO)
      • NO at 20 – 40 ppm via nasal cannula can work rapidly
      • If intubated, need to have inhaled NO continued via circuit.
    • Sildenafil
      • Can potentiate NO effects
      • Can be given orally or IV, but in critical states, IV makes more sense.
    • Normalizing blood pH
      • Acidosis causes vasoconstriction.
      • Treating acidosis with IV bicarbonate is described.
      • Goal serum pH of 7.44 has been recommended. [Kaestner, 2016]
    • Avoiding bradycardia
      • If heart rate is noted to be dropping, start chronotropic medications early.
      • Isoproterenol, a pure beta agonist, is a good choice.
  • Additional therapeutic considerations:
    • Treat the inciting event / trigger (ex, fever).
    • If a patient is on chronic IV therapies, these should be continued during treatment.
    • Sedation, anesthesia, and intubation are known risk factors for pulmonary hypertensive crisis. [Del Pizzo, 2016]
      • Avoiding intubation is best, but if required, used medications that have the least influence on hemodynamics.
      • Be prepared to give vasopressor support for pronounced fall in systemic vascular resistance!
    • ECMO may be considered. [Kaestner, 2016]


Moral of the Morsel

  • Chest Pain / Abdominal Pain / Syncope with exertion is Bad! Add Pulmonary Hypertension to the list of scary things that cause this.
  • Children with Pulmonary Hypertension walk upon a thin tightrope. Be ready to catch them when they fall.
  • Reduce the Pressure in the Pulmonary Vascular beds… breath in the meds!



Del Pizzo J1, Hanna B. Emergency Management of Pediatric Pulmonary Hypertension. Pediatr Emerg Care. 2016 Jan;32(1):49-55. PMID: 26720067. [PubMed] [Read by QxMD]

Kaestner M1, Schranz D2, Warnecke G3, Apitz C1, Hansmann G4, Miera O5. Pulmonary hypertension in the intensive care unit. Expert consensus statement on the diagnosis and treatment of paediatric pulmonary hypertension. The European Paediatric Pulmonary Vascular Disease Network, endorsed by ISHLT and DGPK. Heart. 2016 May;102 Suppl 2:ii57-66. PMID: 27053699. [PubMed] [Read by QxMD]

Cunningham ME1, Berger JT. Pediatric Pulmonary Hypertensive Crisis Medications: A Stepping Stone for the Future. Pediatr Crit Care Med. 2016 May;17(5):465-6. PMID: 27144695. [PubMed] [Read by QxMD]
Siehr SL1, Feinstein JA, Yang W, Peng LF, Ogawa MT, Ramamoorthy C. Hemodynamic Effects of Phenylephrine, Vasopressin, and Epinephrine in Children With Pulmonary Hypertension: A Pilot Study. Pediatr Crit Care Med. 2016 May;17(5):428-37. PMID: 27144689. [PubMed] [Read by QxMD]

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