UMEM Educational Pearls

Pediatric Septic Shock

• Sepsis is the most common cause of pediatric deaths worldwide.
• Recognition is paramount!  Delayed Dx = Higher Mortality
  • Hypotension is a late finding. 
  • Look for other signs of End Organ Hypoperfusion
    • Prolonged Cap Refill, Change in MS
    • Tachycardia, Tachypnea
    • Elevated Lactate / unexplained metabolic acidosis
• Management strategy is similar to that of adults
  • Get access (Don’t forget your I/O’s if necessary)!
  • Fluid Resuscitation is the most important aspect of the management
    • Get 20-60ml/kg infused within the first 15 minutes
    • Children with septic shock who get >40ml/kg before the first hour have increased survival compared to those who do not.
      • They may require 60-200ml/kg over the first few hours.
  • Get your Abx on board quickly
  • Currently there are Protocols that are based on the Adult Surviving Sepsis Campaign.

Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics.  Pediatr Crit Care Med. 2005 Jan;6(1):2-8.

GHB

• Sedating and amnestic, has become notorious in chemical submission (date rape)
• Very fast onset and rapid resolution though respiratory depression can occur 
• Difficult to test for with few labs and quickly eliminated through urine 
• Best chance to catch it is if the patient's first urine void is collected and tested

According to ACEP's clinical policy, a non-contrast head CT is only indicated in mild traumatic brain injury under the following circumstances:  

1)  headache
2)  vomiting
3)  age over 60
4)  drug or alcohol intoxication
5)  short-term memory deficits
6)  physical evidence of injury above the clavicle
7)  seizure

A recent study came out which confirms what we already knew... that MRSA infections are no longer confined to ICUs but are spreading to the community. What the new study does show, is that it affects particular populations disproportionately and Baltimore City, more than any other study population. The full article is attached below, or can be obtained for free from the JAMA website.

"Unadjusted incidence rates of all types of invasive MRSA ranged between approximately 20 to 50 per 100 000 in most ABCs sites but were noticeably higher in 1 site (site 7, Baltimore City) (TABLE 2)." "... we calculated interval estimates excluding site 7 (Baltimore City) to allow the reader to interpret a range of estimates reflecting different metropolitan areas. Regarding the high observed incidence rates reported by site 7, we conducted an evaluation to determine whether these results were valid, including a review of casefinding methods, elimination of cases to include only those with zip codes represented in the denominator, contamination in any laboratory, and other potential causes for increased rates; however, none were in error."

Attachments

• 0710170948_jama_mrsa.pdf (129 Kb)

Hyperammonemia in the Critically Ill

• Patients with acute hyperammonemia have significant morbidity and mortality 
• Fulminant hepatic failure is the most common cause of acute hyperammonemia in adult ICUs
• Other causes include TPN, GI hemorrhage, steroid use, trauma, multiple myeloma, infection with urease-splitting organisms, and drugs (salicylates, valproate) 
• Cerebral edema, intracranial hypertension, seizures, and herniation are the most significant effects
• Initial management should focus on treating intracranial hypertension - mannitol, hypothermia, N-acetylcysteine have been used
• Lactulose has not been shown to reduce mortality in acute hyperammonemia but is unlikely to be harmful

Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest 2007;132:1368-1378.

There is no good evidence for what type of workup an asymptomatic hypertensive patient should get in the ED.  An ECG is likely to show LVH, a cxr will be normal in most cases, and many patients will have some degree of proteinuria.

So, what is a safe and reasonable strategy to workup these patients?

• Consider checking a serum creatinine. I say consider because even this recommendation isn't terribly evidence-based. Elevated creatinine may NOT indicate that a hypertensive emergency is present, but if the creatinine is elevated it might persuade you to choose a different antihypertensive agent (HCTZ won't lower BP effectively if the creatinine near 2.0, and many of us would be a little hesitant to start an ACE-I if the creatinine is elevated). Although there is one study that showed absence of proteinuria and hematuria was correlated with a normal serum creatinine, many patients with asymptomatic HTN will have proteinuria.
• Repeat the BP several times. One study has shown that as many as 1/3 of patients with high BP in the ED do not have elevated BP when followed up as an outpatient. Many patients' BPs will spontaneously decline (regression to the mean).
• In the asymptomatic patient a CXR and ECG will likely not help you manage a patient, so don't waste your time and the patient's money getting it.

American College of Emergency Physicians 2006 Guidelines on the evaluation of asymptomatic HTN.

 

 

New onset atrial fibrillation is rarely the sole manifestation of myocardial infarction. In other words, in the absence of accompanying chest pressure, dyspnea, diaphoresis, or other anginal equivalents, a rule-out ACS workup in not supported by the literature and is not cost-effective.

The two exceptions to the statement above are elderly and diabetic patients, in whom subtle presentations of ACS are common with or without atrial fibrillation.

Pediatric Strain versus Fracture

• Due to the fact that tendons are much stronger than the physeal growth plate in pre-pubescent children, one should be extremely cautious when diagnosing a strain/sprain. 
• Pre-pubescent pediatric patients should be treated as if they have a Salter Harris I fracture with an appropriate splint and close follow up.

Review of Salter Harris Fractures

1. A fracture through the physeal growth plate. Typically can not be seen on x-ray unless they growth plate is widened.
2. A fracture through the physeal growth plate and metaphysis.
3. A fracture through the physeal growth plate and epiphysis.
4. A fracture through the physis, physeal growth plate and metaphysis.
5. A crush injury of the physeal growth plate.

Please click here for a pictorial of Salter Harris Fractures from FP Notebook.

Foreign Bodies
•    No object should be left in the esophagus for >24 hrs
•    Unusual FB’s:
        ==>    Very Sharp or pointed objects may perforate the GI tract and should be removed endoscopically.
        ==>    Long objects (>6cm) or wide (>2cm) objects may not pass and should  be remove  endoscopically.
•    Button Batteries
        ==>    9% of cases involve more than one battery (x-ray mouth to anus)
        ==>    Hazards:
                    (1)    Heavy metal leakage (Mercury) – low risk but real
                    (2)    Electrical Discharge (Local tissue injury)
                    (3)    Pressure Necrosis
                    (4)    Leakage of Corrosives
        ==>    85% Pass without symptoms
                    (1)    No intervention if pass the esophagus and pt is without symptoms

•    Consider Heliox as a temporizing measure in children with respiratory distress, while awaiting endoscopy/bronchoscopy.

Valproic Acid (Depakote) - Increased use for both seizure disorder, migraine prophylaxis and bipolar disorder - Causes hyperammonemia with or without hepatic insufficiency (Liver enzymes could be normal!) - Hyperammonemia can occur at therapeutic concentrations and overdose - If the patient is sedated and has hyperammonemia, consider carnitine therapy antidotal - Carnitine IV or PO: 50-100 mg/kg bolus or divided bid, safe to give

• The most common (80%) cause of non-traumatic subarachnoid hemorrhage (SAH) = ruptured saccular (berry) aneurysm.
• Saccular aneuryms are thought to be present in up to 5% of the population.
• There is a strong familial association with cerebral aneurysms, and prevalence is increased in people with Marfan Syndrome and Polycystic Kidney Disease.
• Other causes of non-traumatic SAH include:  AV malformation, cavernous angioma, mycotic aneurysm, and blood dyscrasia. 

[RESENT - STILL FIXING CODE - THESE TEST EMAILS SHOULD CEASE SHORTLY... SORRY FOR THE INCONVENIENCE]

• Abdominal compartment syndrome (ACS) is increasingly identified in the critically ill medical patient population
• ACS is defined as a sustained intra-abdominal pressure > 20 mmHg associated with new organ dysfunction
• Primary organs adversely affected by ACS include cardiac, pulmonary, GI, and renal
• To date, associated mortality rates have ranged from 27% to 50%
• Risk factors for ACS include:
  • massive fluid resuscitation ( >10 L crystalloid in 24 hours)
  • massive transfusion ( > 10 U PRBCs in 24 hours)
  • severe sepsis or septic shock from any cause
  • mechanical ventilation
  • PEEP > 10 cm H20
• Intravesicular (bladder) pressures are currently the standard monitoring modality
• Decompressive laparotomy is the current standard for management of ACS

Suspect an aortoenteric fistula in patients who present with an upper GI bleed if they have ever had a AAA repair. This occurs when a fistula forms between the abdominal aorta and the GI tract (most commonly the duodenum). Patients may present stable or may present critically-ill. Unstable patients with an upper GI bleed and a history of AAA repair should proceed to the OR for laparotomy.

Stable patient may undergo CT scanning and/or endoscopy. Bottom line: If a patient with a history of AAA repair presents with an upper GI bleed, rally your troops (GI, Surgery, etc) ASAP and don't mess around. If you are wrong, and the patient doesn't have a fistula, no big deal. If you are wrong, and the patient does have a fistula, the patient may very well die on you as you struggle to get a regular ICU bed.

 

 

In the treatment of an acute ST-elevation MI, there are three major signs of successful reperfusion:

1. T-wave inversion within the first 4 hours. If the T-wave inversions occur beyond 4 hours, it's uncertain.
2. Resolution of the STE by at least 70% in the lead with maximal STE.
3. Development of a "reperfusion arrhythmia," most notably accelerated idioventricular rhythm (AIVR), which looks like V.Tach but the rate is only 60-120. Remember, V.Tach should have a rate > 120.

Persistent pain/symptoms OR absence of STE resolution by 90 minutes warrants strong consideration of rescue angioplasty.

Low Back is one of the most common complaints that we see in the Emergency Department.  Our first priority is to rule out those causes that can lead to paralysis or death (i.e.: epidural abscess, pathological fracture, cauda equina syndrome, etc…).  However, most of the back pain that we will see is musculoskeletal in origin.

The American College of Physicians (ACP) and the American Pain Society (APS) recently released some joint recommendations on the evaluation of treatment of individuals with back pain.

In summary their key recommendations are:

1. Routine imaging is not required. However, diagnostic imaging and testing should be obtained for patients with low back pain when severe or progressive neurologic deficits are present or when serious underlying conditions are suspected.
2.  For patients with low back pain, clinicians should consider the use of medications with proven benefits in conjunction with back care information and self-care. For most patients, first-line medication options are acetaminophen or nonsteroidal anti-inflammatory drugs.
3. Medications that have good evidence of short-term effectiveness for low back pain are NSAIDs, acetaminophen, skeletal muscle relaxants (for acute low back pain), and tricyclic antidepressants (for chronic low back pain).

Links to the Clinical Guidelines are listed below:

• Evaluation and Treatment
• Nonpharmacologic Therapies for Acute and Chronic Low Back Pain
• Medications for Acute and Chronic Low Back Pain

Concussions

• Symptoms
  • HA, Dizziness, Confusion, Tinnitus, Nausea, Vomiting, Vision changes
• 3 grades of Concussions
  • Grade 1 = transient concussion symptoms.  No amnesia.  No LOC. 
  • Grade 2 = transient concussion symptoms with amnesia.  No LOC.
  • Grade 3 = + LOC of any durations
• Return to Play Guidelines 
  • (there is no consensus statement. What follows is based on the most conservative approach)
  • Grade 1: Remove from game, Examine q 5 min.
    Return to game when asymptomatic for 20 minutes.
  • Grade 2: Remove from game until asymptomatic for 1 week.
  • Grade 3: ED evaluation.  No contact sports for 1 month once asymptomatic for 2 weeks. 
    • These apply to first concussions.  Increase concern with 2nd concussion.
• Second-Impact Syndrome
  • Occurs when a player returns to contact sport before symptoms of 1 concussion have fully  resolved.
  • Even a minor blow to the head can result in loss of brain’s autoregulation of blood flow.  
    • Leads to vascular engorgement and subsequent herniation.

Colorado Medical Society School and Sports Medicine Committee. Guidelines for the management of concussion in sports. Colo Med 1990;87:4.

I have made some improvements to the educational pearl interface. This required recoding several sections to change the text formatting from plain text to html...

Why do you care?
Well, many email clients will block html, or messages that have lots of capitals, decorations, etc...

Our first priority is to get you the information and beat anti-spam auto-filtering. If you notice that you are not getting the educational emails. 

• Add admin@umem.org  and umem.org to your safe senders list

Notes to authors Do not use a lot of colors like this post Do not use allcaps, lots of bolding, etc...

thanks
dan

Isopropanol (Commonly Rubbing Alcohol)

• Rubbing alcohol is 70% isopropanol, like drinking Bacardi 151 (151 proof)
• This is NOT a toxic alcohol in the traditional sense
• This causes a large ketosis, large osmol gap but NO anion gap and no acidosis
• This is because isopropanol is metabolized to acetone (a ketone) not an acid
• Toxicity: inebriation, hemorrhagic gastritis, sedation to the point of death/intubation

Horner's Syndrome Deficit in descending sympathetic pathways Miosis + Ptosis + Anhidrosis Associated with lateral medullary infarctions, which are caused by disrupted flow to the posterior inferior cerebral artery (PCA) (i.e. Wallenberg Syndrome)

DIC is the simultaneous occurrence of widespread (micro) vascular thrombosis, leading to compromised blood supply to vital organs Although major bleeding can be seen in some, the more common complication of DIC is organ failure DIC is not a disease itself but secondary to an underlying disorder Sepsis, solid and hematologic malignancies, severe trauma, and obstetrical emergencies (amniotic fluid embolism, abruption) are the most common disorders associated with DIC A prospectively validated scoring system (Toh CH, et al. J Thromb Haemost 2007;5:604-6.) is used for diagnosis and is comprised of platelet count, fibrin split products, PT, and fibrinogen level The key to treating DIC is vigorous treatment of the underlying disorder Platelet transfusion is generally only given for patients with major bleeding (i.e. intracranial) with platelets counts < 50 k